[encoded data, 112169 characters]\" alt=\"\"></p></div></div><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1655221639);
INSERT INTO `mdl_page` VALUES (12,13,'Pioneers of Neurotherapy','',1,'<p></p><p>This section will cover:<br></p><p>1. Pioneers in EEG and Neurofeedback&nbsp;</p><p>2. Discussion of the highlights of the seminal studies in neurofeedback&nbsp;</p><p><img src=\"@@PLUGINFILE@@/Old%20Brain.png\" alt=\"Old Brain Drawing\" width=\"750\" height=\"1431\" class=\"img-responsive atto_image_button_text-top\"></p><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1669051167),(13,13,'The Definition and Basics of Neurotherapy','',1,'<p>This section will cover:</p><p>1) The fundamentals of electroencephalography</p><p>2) The difference between neurology and psychophysiology, and</p><p>3) The clinical fundamentals of the application of neurofeedback and neurotherapy modalities.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/EEG.jpg?time=1612552683711\" alt=\"EEG\" width=\"500\" height=\"313\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1669051150),(14,13,'Ancient Antiquity\'s Influence','',1,'<p></p><p>Between 460 and 379 B.C.&nbsp;<b>Hippocrates</b>&nbsp;first proposed the brain was the source of sensation, emotions and human intelligence. Within a few years (387 B.C.)&nbsp;<b>Plato</b>&nbsp;followed suit, noting the brain was the seat of mental processes. Between 335 and 280 BC Herophilus noted that the ventricles were the seat of human intelligence.</p><p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Galen.png\" alt=\"Galen\" width=\"300\" height=\"495\" class=\"img-responsive atto_image_button_left\">In 177A.D.,&nbsp;</span><b style=\"font-size: 1rem;\">Galen&nbsp;</b><span style=\"font-size: 1rem;\">lectured “On the Brain” and developed a hypothesis that the brain had ventricles that contained a liquid substance that controlled how a person behaved or thought.&nbsp; He believed that the grey matter and the rest of the brain were not important.&nbsp; (This was of course the cerebral spinal fluid (CSF) that fills the brain ventricles and flows up and down the spinal cord.</span></p><p>Research into the brain came to a halt in the fourth century when the church declared dissection of a human body to be punished by torture or death. In 1347, the Black Plague led to the loss of a third of Europe’s population.&nbsp; At that point, the church lost credibility and released its ban on human research.&nbsp; The Renaissance followed, and between 1500-1600&nbsp;<b>Leonardo da Vinci,</b>&nbsp;as well as a whole host of European anatomical explorers began to dissect and name structures of the brain.</p><p></p><p>In 1543,&nbsp;<b>Andreas Vesalius&nbsp;</b>was the first to question the doctrine that cerebro-spinal fluid in the brain was the substance that controlled thought.&nbsp; He stated that because the ventricles were the same in both humans and lower animals, they could not be the source of human intelligence and thought.&nbsp; Vesalius believed that the larger and more developed cerebral cortex of the brain (the &nbsp;grey matter) was the source of intelligence. This thought was later reinforced by the anatomist,&nbsp;<b>Thomas Willis.</b></p><p><b><img src=\"@@PLUGINFILE@@/Ventricles.png\" alt=\"Ventricles\" width=\"300\" height=\"283\" class=\"img-responsive atto_image_button_right\"></b></p><p>In the seventeenth century, philosopher&nbsp;<b>Rene’ Descartes&nbsp;</b>endorsed a belief in dualism, better known as the Cartesian divide. Descartes&nbsp;purported that the body and the soul were separate; the soul was a gift from God, as well as the controller of thought and emotion. The soul, said Descartes, was provided stored in the brain’s pineal gland.&nbsp; He was the first to attempt to assign a function to a portion of the brain. &nbsp;</p><p><img src=\"@@PLUGINFILE@@/Pineal%20Gland.png\" alt=\"Pineal Gland\" width=\"300\" height=\"235\" class=\"img-responsive atto_image_button_left\"><span style=\"font-size: 1rem;\">After Descartes successfully divided the mind and the brain up into two&nbsp;essentially different substances, he found difficulty reconciling their causal interactions&nbsp;(Kim, 1993). The “</span><b style=\"font-size: 1rem;\">hard problem of consciousness</b><span style=\"font-size: 1rem;\">,” as it has been dubbed in academic&nbsp;circles, still remains as a question over the division of mind and the brain. One camp believes the mind and the brain are indivisible—that is, the mind is simply the reaction of neurotransmission, neuronal firings, and the flow of blood and hormones (Churchland, 1989; Dennett, 1993, 2003, 2014; Graziano, 2013). The other camp believes there is something else involved—that mind is not simply chemical and hormonal actions and interactions—and there is something much more meaningful at work (Chalmers, 1995, 1996, 2002; Nagel, 1974,&nbsp;1986, 2012). This paradox is akin to the physics paradox that light is both a wave and a&nbsp;particle, where the mind is a wave, yet the brain is an identifiable particle. Modell (2012)&nbsp;believes this type of thinking must pervade our conception as it pertains to the&nbsp;intersection of neuroscience and psychoanalysis. It is indeed interesting in the light of applied psychophysiology</span></p><img src=\"@@PLUGINFILE@@/Wave%20and%20Particle.png\" alt=\"Galen\" width=\"600\" height=\"621\" class=\"img-responsive atto_image_button_left\" style=\"text-align: center;\"><p style=\"text-align: center;\"><br></p><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',3,1653942456),(15,13,'The Beginnings of Electroencephalography','<p></p><p><br></p><p></p>',1,'<p></p><p>The early roots of EEG can be traced to two Italians, <b>Luigi Galvani </b>(1737-1798) and <b>Alesandro Volta</b> (1755-1832), and two Englishmen,&nbsp;<b>George Ohm </b>(1787-1832) and <b>Michael Farad</b>ay (1791-1867) (Collura, 1993, p. 476).&nbsp;Their discoveries have provided the understanding of electrical potential and current, and how it applies to muscular activity.&nbsp;<img src=\"@@PLUGINFILE@@/Volta%20and%20Galvani.png\" alt=\"Volta and Galvani\" width=\"420\" height=\"243\" role=\"presentation\" class=\"atto_image_button_left\"><br></p><p><img src=\"@@PLUGINFILE@@/Ohm%20and%20Faraday.png\" alt=\"Ohm and Faraday\" width=\"420\" height=\"348\" class=\"img-responsive atto_image_button_right\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><b style=\"font-size: 1rem;\"><br></b></p><p><b style=\"font-size: 1rem;\"><br></b></p><p><b style=\"font-size: 1rem;\">Richard Caton</b><span style=\"font-size: 1rem;\"> (1842–1926) was the first electroencephalographer, as he was the first to record electrical activity from the exposed brains of rabbits and monkeys, using a mirrored galvanometer (Collura, 1993, p. 479).</span><br></p><p><img src=\"@@PLUGINFILE@@/Caton.png\" alt=\"Caton\" width=\"193\" height=\"252\" class=\"img-responsive atto_image_button_left\"></p>In his 33rd year, Caton reported his\r\ninitial findings to the British Medical Association in 1875. In 1877 these were reported\r\nmore fully in a supplement to the British Medical Journal, and\r\nagain in 1887 to the Ninth International\r\nMedical Congress in Washington DC.&nbsp;<p></p><p>In his experiments, Caton\r\nplaced unipolar electrodes on the surface of\r\nboth hemispheres of the exposed animals\' brain, or one electrode on the exposed cerebral cortex and the other\r\non the surface of the skull. Currents were\r\nmeasured via Thomson\'s galvanometer by optical magnification of the\r\nmeniscus.<img src=\"@@PLUGINFILE@@/Galvanometer.png\" alt=\"Galvanometer\" width=\"500\" height=\"856\" class=\"img-responsive atto_image_button_right\"></p><p>Caton found that the currents of the brain increased with sleep.\r\nThese currents were vulnerable to anoxia and\r\nanaesthesia, and they disappeared by the\r\nanimal’s death. Caton also found that strong\r\ncurrent variations occurred when light was\r\nshone into the eyes. He also discovered\r\ncerebral potential change evoked by sensory\r\nstimulation. Caton did not recieve much notoriety in his lifetime for his experiments with brainwaves; in his obituary in the Lancet, Caton’s\r\ncontribution to electrophysiology was not mentioned (Haas, 2003).</p><p>EEG recordings were presented to the public at the same time as ECG\r\n(electrocardiogram), but while the ECG, which was built by a man named\r\nEinthoven, won the Nobel Peace Prize, the EEG remained unnoticed.&nbsp; In fact, none of the pioneers of EEG ever\r\nreceived a similar honor, not even Caton. One of the reasons for this was the\r\ninitial and long-standing doubt that recording was actually showing brain\r\nactivity (Stam, 2006).<br></p><p></p><p>In 1924, German neurologist <b>Hans Berger </b>recorded the first<b>&nbsp;</b>EEG\r\non the brains of humans using a ballistic galvanometer (today, differential\r\namplifiers are used for this collection). The importance, for him, was based on\r\na parapsychological incident. His sister had a dream that he had fallen off a\r\nhorse and died, and wrote him a fearful letter about it. At the time of her\r\ndream, he had, in fact, fallen off a horse and broken his leg. This synchronistic event encouraged\r\nhis belief that pursuing the EEG would uncover the mysteries of telepathy,\r\nwhich he conceived was a phenomenon carried by the brain’s electrical activity\r\n(Buzsaki, 2006, p. 4). He wanted to figure out the physiological basis for psychic phenomena. Additionally, he intended the EEG as a new technique for\r\npsychiatric diagnosis and research (Ulrich, 2013, p. 1). He worked out of the University of Jena, in Germany, where he was the director of the psychiatric clinic\r\nand a Professor of Neurology and\r\nPsychiatry by 1919.<img src=\"@@PLUGINFILE@@/Berger.png\" alt=\"Berger\" width=\"448\" height=\"454\" class=\"img-responsive atto_image_button_left\"></p>\r\n\r\n<p>It was Berger coined \"electroencephalogram\" who first discovered a 10 Hz rhythm, which he dubbed\r\n“alpha,” especially prominent when individuals closed their eyes. His second\r\nEEG discovery was “beta,” which he found rarely co-existed with the alpha\r\nrhythm (The delta rhythm was discovered in 1937 by <b>W.\r\nGrey Walter</b>, who also later identified the theta wave in 1953).</p><p></p><p>Berger was excessively self-conscious about his initial findings\r\non EEG, so much so that he undertook five years of testing and surveying the\r\nresults of his studies on EEG before he released it to the public in report\r\nform, in 1929 (during the years 1929-1938 he published 23 reports about his\r\nstudies of EEGs, and much of our modern knowledge of the subject, especially in\r\nthe middle frequencies, is due to his research).<a href=\"#_ftn1\" name=\"_ftnref1\" title=\"\"><!--[if !supportFootnotes]-->[1]<!--[endif]--></a>Sadly,\r\nwhen released his paper Über\r\ndas Elektrenkephalogramm des Menschen (On the\r\nEEG in humans) in 1929,&nbsp;it was received with disbelief and derision from\r\nthe scientific community. He described normal and abnormal findings,&nbsp; associated with attention and mental effort, as well as cerebral injury. In 1934, Adrian and Matthews confirmed his basic observations in 1934, and thereafter&nbsp;EEG was accepted\r\nand embraced with the advent of the first ink-writing oscillograph, called the\r\n“neurograph,” by engineer J. F. Toennies.<a href=\"#_ftn2\" name=\"_ftnref2\" title=\"\"><!--[if !supportFootnotes]-->[2]<!--[endif]--></a></p>\r\n\r\n<p>After Berger’s, the first experiments of EEG\r\nwere conducted at the Bradley Hospital in Providence, Rhode Island in 1933 by\r\nHerbert Jasper (Collura, 1993, p. 488). Berger’s findings were duplicated and\r\nconfirmed by Edgar Douglas Adrian (Lord Adrian), an English\r\nelectrophysiologist, which thrust EEG into scientific literature, and Jasper\r\npursued the development of an EEG lab in Montreal at the request of Wilder\r\nPenfield, a neurosurgeon, who was the first to use EEG activity to localize\r\nseizure activity using EEG. </p>\r\n\r\n<p>In short\r\ntime, neurology adopted the EEG for psychiatric diagnostics and EEG became the\r\ncentral tool for neurological electrodiagnosis, centering around epileptic\r\nconditions. Even today, EEG is used primarily in clinical neurophysiology and\r\nneurology. However, Berger wanted EEG to be used in “psychophysiology,” a term\r\ncoined by him to denote a new basic discipline of psychiatry.&nbsp;&nbsp;</p><div>\r\n\r\n<p>Throughout\r\nthe 1930s and 1940s, EEG was explored at many medical institutes, including\r\nHarvard Medical School, the University of Chicago, MIT, the Mayo Clinic, and\r\nthe University of Iowa.&nbsp; During World War\r\nII, the EEG was used widely in neurological and psychological studies, and in\r\nthe 1940s and 1950s, many EEG instrument companies appeared in the United\r\nStates, Europe, and Japan (Collura, 1993). In 1958, Jasper lead a committee to\r\nstandardize the international 10/20 system that is used for electrodes today. This system is based on a set of latitudinal and\r\nlongitudinal arcs upon the surface of a spherical cranium. The positions of\r\nelectrodes are determined by measurements from standard landmarks (i.e.,\r\nnasion, inion, and pre auricular points) on the skull. Electrodes are then\r\nplaced at locations 10%, 20%, 20%, 20%, 20%, and 10% along each of these arcs.</p>\r\n\r\n<h3><img src=\"@@PLUGINFILE@@/10%20-%2020%20system.png\" alt=\"10-20 system\" width=\"333\" height=\"320\" class=\"img-responsive atto_image_button_left\"></h3><p>In the 1960’s, Neal Miller and Leo DeCara carried out a series of\r\ndramatic animal experiments, which demonstrated the possibility of operant\r\nconditioning with a variety of internal autonomically regulated physiologic\r\nprocesses, including: blood pressure, cardiac function, and intestinal\r\nactivity. Prior to their research, physiologists generally assumed that\r\norganisms only had control over voluntary processes and not involuntary\r\nprocesses. Their research provided the ground work for Barry Sterman’s sleep\r\nresearch training the EEG, the Sensory Motor Rhythm (SMR), in cats.</p><br clear=\"all\">\r\n\r\n<hr align=\"left\" size=\"1\" width=\"33%\">\r\n\r\n<!--[endif]-->\r\n\r\n<div id=\"ftn1\">\r\n\r\n<p><a href=\"#_ftnref1\" name=\"_ftn1\" title=\"\"><!--[if !supportFootnotes]-->[1]<!--[endif]--></a>\r\nKaiser, David A. \"Basic Principles of\r\nQuantitative EEG.\" <i>Journal of Adult\r\nDevelopment</i>, Vol. 12, Nos. 2/3, August 2005</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn2\">\r\n\r\n<p><a href=\"#_ftnref2\" name=\"_ftn2\" title=\"\"><!--[if !supportFootnotes]-->[2]<!--[endif]--></a>\r\nAn electroencephalograph is the instrument for recording,\r\nElectroencephalography is the process of recording, and an electroencephalogram\r\n<i>is</i> the recording, itself.</p></div></div><br><p></p><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1655222319),(17,4,'Readings Required by the International QEEG Certification Board, only available in print','',1,'<p>Collura, T. F. (2013). <a href=\"https://www.amazon.com/Technical-Foundations-Neurofeedback-Thomas-Collura/dp/1138051896/ref=sr_1_1?dchild=1&amp;keywords=collura+technical+foundations&amp;qid=1614715687&amp;sr=8-1\">Technical Foundations of Neurofeedback.</a> Routledge. Chapters 1-6</p><p><a href=\"https://www.amazon.com/Rowans-Primer-EEG-Lara-Marcuse-dp-0323353878/dp/0323353878/ref=dp_ob_title_bk\">Rowan, J. &amp; Tolunsky, E. (Eds). (2003). Primer of EEG: WIth a mini-atlas. Philadelphia, PA: Elsevier.</a></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1614715886),(18,15,'Montage Options and Their Characteristics','',1,'<p></p><p>Montages are logical and orderly\r\narrangements of channels (electrode pairs, with waveforms representing the\r\npotential difference between the two electrodes).</p><p>One never records from a single\r\nelectrode, but the difference of voltage between&nbsp; (at least) two electrodes (the active and the\r\nreference electrode). Each EEG channel records variations in double ended\r\nvoltage differences.&nbsp;<b>Common Mode Rejection</b>:&nbsp;The ability of the amplifier to suppress voltages&nbsp;<b>common</b>&nbsp;to both electrodes, i.e. varying together over time, is called the&nbsp;<b>common mode rejection</b>. An example is the noise from a 50 or 60 Hz line current.</p>There are two classifications of montages: monopolar (aka referential) and bipolar. <u>(</u>The term monopolar is a misnomer, since all recording must come from the difference of two channels). The use of two channels is what makes a \"differential amplifier\" differential. It is measuring the difference between two electrodes, and by way of that removing all common noise or signals between the two to highlight their differences.<p></p><p><img src=\"@@PLUGINFILE@@/Montages.jpg\" alt=\"Montages\" width=\"600\" height=\"344\" class=\"img-responsive atto_image_button_middle\"></p><p><b>Average montages</b> (such as laplacian, average, hjorth, current source density, and weighted average). These are good for identifying focal issues.</p><p><b>Bi-polar montages</b> are from one scalp site to another scalp site. They can be widely spaced or closely spaced. More widely spaced electrodes should give greater amplitude because there is less data in common and thus, less common mode rejection. These are also good for focal findings.</p><p><b>Referential montages</b> use sites like singular (right or left) ear, ipsilateral ear, contralateral ears linked ears, Cz (the exception to the rule, as it is a scalp reference), mastoids, or the nose as a point of reference. With linked ears, for instance, the activity at the T3 and T4 electrodes will be of lowest voltage, because of the greatest common mode rejection with the reference site. These are good for global findings.</p><p>Every montage has its benefits and its shortcomings.&nbsp; In a general sense, referential montages will have the least amount of cancellation of activity and will then show a purer signal, but bi-polar montages can localize more subtle deficits.</p><p>A Cz montage can dull and diminish activity at the sites surrounding that central electrode (in as such, C3, C4, F3, Fz, F4, P3, P4, Pz will all have lower amplitudes, however the activity at the temporal lobes will be magnified, since the ears are removed from the common mode rejection equation).</p><h3>Shared Variance in Linked Ears Montages</h3><p>One of the oft-overlooked and most insidious artifacts found in EEG comes from \"contaminated ear references\" in any referential montage using the ears. This phenomenon is best explained with an anology. Imagine that there is very high amplitude, slow activity, stemming from the temporal lobe. If the activity is of sufficient size, the ear lobe will also reflect the same EEG finding (i.e. it will cease to be a \"neutral\" reference). Then, two things will happen: 1) the actual focus of the slow wave at T3 will be <u>removed</u>&nbsp;from the T# electrode via common mode rejection, and the slow wave will be distributed in all of the other channels not proximal to the actual source of the slow wave.&nbsp;</p><p>The image on the left is a screen shot of the artifact of shared variance. The image on the left is the shared activity between the left ear and the T3 electrode.</p><p><img src=\"@@PLUGINFILE@@/Shared%20Variance.png\" alt=\"Shared Variance\" width=\"1000\" height=\"565\" class=\"img-responsive atto_image_button_middle\"><br></p><p><span style=\"font-size: 1rem;\">The image below is an easier one to grok, in term of shared variance. In the below image, there is a cardiac artifact that is obvious in the EEG record. We know it to be cardiac, for sure, by its rhythmicity (once per second, just like a heartbeat). It is appearing in every channel because the origin of the heartbeat is the ear lobe, itself. Thus, this is different from every channel on the scalp and showing up in every channel on the scalp, due to common mode rejection.&nbsp;</span><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/heartbeat%20shared%20varnace.png\" alt=\"heartbeat shared variance\" width=\"1104\" height=\"668\" class=\"img-responsive atto_image_button_middle\"><br></p><p><span style=\"font-size: 1rem;\">Here is a video showing one of the most common impostors in shared variance, erroneous diffuse alpha. In this video, the montage is switched from Linked Ears (which shows false global alpha) and current source density (which localizes the alpha waveform).</span><br></p><p><a href=\"@@PLUGINFILE@@/Shared%20Variance.mp4\">Shared Variance.mp4</a><br></p><p>When the ear electrodes are contaminated, the quantitative EEG can produce erroneous coherences, usually showing as hypercoherences, such as those seen in the below image.</p><p><br></p><p><img src=\"@@PLUGINFILE@@/Hypercoherences.jpg\" alt=\"Erroneous Hypercoherences\" width=\"517\" height=\"518\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><h3>Bi-Polar Montages</h3><p>Many neurologists use bi-polar montages to look for findings in EEG becuase they are commonly looking for epileptiform discharges in the EEG. The location of these abnormal findings is found in the electrode shared between two pairs.&nbsp;</p><p><img src=\"@@PLUGINFILE@@/Phase%20Reversals.png\" alt=\"Phase Reversals\" width=\"750\" height=\"445\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p>The video below is of a woman dealing with age-related cognitive decline, as seen in phase reversals localizing slowing at her temporal lobes (T5 and T6), once we switch the montages to bipolar montages.</p><p><a href=\"@@PLUGINFILE@@/Phase%20Reversals.mp4\">Phase Reversals.mp4</a><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',5,1654211611),(21,13,'Barry Sterman on Pavlovian Theory ','<p>Applying theories to EEG&nbsp;</p>',1,'<p><br></p>\r\n<p><iframe src=\"https://player.vimeo.com/video/517322186?badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" width=\"880\" height=\"495\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" title=\"STERMAN - EEG and Autonomic Responses\" style=\"font-size: 1rem;\"></iframe><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br>\r\n    <iframe src=\"https://player.vimeo.com/video/509056299?badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" width=\"880\" height=\"495\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" title=\"STERMAN - Pavlovian Theory, Lack of Volition, and Adynamia in Subjects\"></iframe></p>\r\n<p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',9,1669051192),(22,13,'Learning Theory','<p>This chapter will cover the basics of how humans learn, including habituation, classical and operant conditioning, discrimination, shaping, generalization and extinction.</p>',1,'<h3><iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/PRdCowYEtAg\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><br><b><br></b></h3><h3><b>Operant Conditioning vs. Classical Conditioning</b></h3><p>\r\n    </p><p>We learn many of our psychophysiological responses through the unconscious processes of perceptual learning, classical conditioning, and operant conditioning, and the conscious process of relational learning.&nbsp;Thus, through neurofeedback and biofeedback\r\n        one can learn physiological self-regulation.</p>\r\n\r\n    <p><b>Operant conditioning, sometimes called\r\ninstrumental learning,</b> is the use of a behavior\'s antecedent and/or its consequence to influence the occurrence and form of behavior. Operant conditioning is distinguished from&nbsp; classical (also called “Pavlovian conditioning”) in that operant\r\n        conditioning deals with the <a href=\"http://en.wikipedia.org/wiki/Behavior_modification\">modification of\r\n\"voluntary behavior\"</a> or operant behavior. Operant behavior \"operates\" based on the rules of an environment and is maintained by the consequences of following or breaking those rules.&nbsp;</p>\r\n    <p><span style=\"font-size: 1rem;\">Classical conditioning deals with the conditioning of reflexive</span><span style=\"font-size: 1rem;\">&nbsp;behaviors. Reflexive behaviors are involuntary and nearly instantaneous movements in response to a stimulus.</span>\r\n        <span style=\"font-size: 10.5px;\"> </span><span style=\"font-size: 1rem;\">A reflex is made possible by pathways in the brain called reflex arcs,</span><span style=\"font-size: 1rem;\">&nbsp;which can act on an impulse before that impulse reaches the brain. The reflex is then an automatic response to a stimulus that does not receive or need conscious thought which are elicited by antecedent</span>\r\n            <span style=\"font-size: 1rem;\">&nbsp;conditions. <b><span><span style=\"\"><i style=\"\">Behaviors conditioned via a classical\r\nconditioning procedure are not maintained by consequences.</i></span></span></b></span></p><p><span style=\"font-size: 1rem;\"><b>\r\n        </b>\r\n        </span>\r\n    </p>\r\n\r\n    <p>Reinforcement and punishment are the main building blocks of operant conditioning. Although it is confusing, positive and negative rewards have nothing to do with good or bad. With <u>positive reinforcement,</u>&nbsp;the reinforcement is delivered\r\n        following a response. With&nbsp;<u>&nbsp;negative reinforcement</u>&nbsp;the reinforcement is withdrawn following a response. For instance, lets say I want my two-year old to eat his vegetables for dinner. There is a chocolate cake sitting on\r\n        the table for dessert once he\'s eaten his dinner. In a scenario of positive reinforcement, I would reward him with dessert after he\'s eaten his vegetables. In a scenario of negative reinforcement, I would remove the chocolate cake from the table,\r\n        denying it to him upon his failure to eat his vegetables.<br></p><p><img src=\"@@PLUGINFILE@@/Operant%20Conditioning.png\" alt=\"Operant Conditioning\" width=\"544\" height=\"424\" class=\"img-responsive atto_image_button_left\"></p><p><span style=\"font-size: 1rem;\">This creates a total of four basic consequences, with the addition of a fifth procedure known as </span><a href=\"http://en.wikipedia.org/wiki/Extinction_%28psychology%29\" style=\"background-color: rgb(255, 255, 255); font-size: 1rem;\">extinction</a><span style=\"font-size: 1rem;\"> (i.e. no change in consequences following a response).</span></p><p></p><p><b>Extinction</b> occurs if, over time, if actors interaction with the stimulus\r\nobject does not provide sufficient reward or punishment. This concept\r\nmeans that the individual disengages from the behavior that resulted from\r\nconstant reinforcement.&nbsp;</p><p>In classical conditioning, extinction results from the unconditioned stimulus (the involuntary drooling) NOT occurring after the conditioned stimulus (bell ringing) is presented over time. In operant\r\nconditioning it results from some response by the organism no longer being\r\nreinforced (for example, you keep getting your dog to sit on command, but you\r\nstop giving it a treat or any other type of reinforcement. Over time, the dog\r\nmay not sit every time you give the command).<br></p><p><br></p><p>This pattern has led some to be concerned that the\r\nchange in EEG patterns learned from neurofeedback would extinguish over time.\r\nHowever, the case is not so simple. Extinction varies with the type of behavior\r\nlearned. Just as learning to ride a bicycle does not extinguish over time,\r\nlearning the new EEG pattern does not extinguish. Lubar (1995) and Peniston\r\n(1999) found that the new EEG patterns still remained after ten or more years.&nbsp;</p><p></p>\r\n\r\n    <p>It\'s important to note that actors are not spoken of as being reinforced, punished, or extinguished; it is the actions that are reinforced, punished, or extinguished. Additionally, reinforcement, punishment, and extinction are not terms whose use\r\n        is restricted to the laboratory. Naturally occurring consequences can also be said to reinforce, punish, or extinguish behavior and are not always delivered by people.</p><h4><b>History of Operant Conditioning</b></h4>\r\n\r\n    <div>\r\n        <!--[if !supportFootnotes]--><p><img src=\"@@PLUGINFILE@@/Edward%20Thorndike.jpg\" alt=\"Thorndike\" width=\"283\" height=\"178\" class=\"img-responsive atto_image_button_left\">Operant\r\nconditioning was first extensively studied by <a href=\"http://en.wikipedia.org/wiki/Edward_L._Thorndike\">Edward L. Thorndike</a> (1874–1949), who observed\r\nthe behavior of cats trying to escape from home-made puzzle boxes.<a href=\"#_ftn1\" name=\"_ftnref1\" title=\"\"><!--[if !supportFootnotes]-->[1]<!--[endif]--></a>\r\nWhen first constrained in the boxes, the cats took a long time to escape. With\r\nexperience, ineffective responses occurred less frequently and successful\r\nresponses occurred more frequently, enabling the cats to escape in less time\r\nover successive trials.&nbsp;</p><p><span style=\"font-size: 1rem;\">In his </span><a href=\"http://en.wikipedia.org/wiki/Law_of_effect\" style=\"font-size: 1rem; background-color: rgb(255, 255, 255);\">law of effect</a><span style=\"font-size: 1rem;\">, Thorndike theorized that successful responses,\r\nthose producing </span><i style=\"font-size: 1rem;\">satisfying</i><span style=\"font-size: 1rem;\">\r\nconsequences, were \"stamped in\" by the experience and thus occurred\r\nmore frequently. Unsuccessful responses, those producing </span><i style=\"font-size: 1rem;\">annoying</i><span style=\"font-size: 1rem;\"> consequences, were </span><i style=\"font-size: 1rem;\">stamped\r\nout</i><span style=\"font-size: 1rem;\"> and subsequently occurred less frequently. In short, some consequences </span><i style=\"font-size: 1rem;\">strengthened</i><span style=\"font-size: 1rem;\"> behavior and some\r\nconsequences </span><i style=\"font-size: 1rem;\">weakened</i><span style=\"font-size: 1rem;\"> behavior.\r\nThorndike produced the first known learning curves through this procedure. </span><a href=\"http://en.wikipedia.org/wiki/B.F._Skinner\" style=\"font-size: 1rem; background-color: rgb(255, 255, 255);\">B.F. Skinner</a><span style=\"font-size: 1rem;\"> (1904–1990) formulated a more detailed\r\nanalysis of operant conditioning based on reinforcement, punishment, and\r\nextinction.&nbsp;</span></p><p></p><p>\"Operant\r\nconditioning\" was coined by behaviorist&nbsp;<a href=\"https://www.verywell.com/b-f-skinner-biography-1904-1990-2795543\">B.F. Skinner</a>, which is\r\nwhy you may occasionally hear it referred to as Skinnerian conditioning. As a behaviorist,\r\nSkinner believed that it was not really necessary to look at internal thoughts\r\nand motivations in order to explain behavior. Instead, he suggested, we should\r\nlook only at the external, observable causes of human behavior. Skinner was more interested in how the&nbsp;<strong>consequences</strong>&nbsp;of people\'s actions influenced their behavior.&nbsp;<span>Skinner used the term&nbsp;</span><em>operant</em><span>&nbsp;to refer to any \"active behavior that operates upon the environment to generate consequences\" (1953). In other words, Skinner\'s theory explained how we acquire the range of learned behaviors we exhibit each and every day.</span></p><p><span style=\"font-size: 1rem;\">Through the\r\nfirst part of the 20th-century, behaviorism had become a major force within\r\npsychology. The ideas of&nbsp;</span><a href=\"https://www.verywell.com/john-b-watson-biography-1878-1958-2795550\" style=\"background-color: rgb(255, 255, 255); font-size: 1rem;\">John B.\r\nWatson</a><span style=\"font-size: 1rem;\">&nbsp;dominated\r\nthis school of thought early on.&nbsp;</span><a href=\"http://www.simplypsychology.org/behaviorism.html\" style=\"font-size: 1rem; background-color: rgb(255, 255, 255);\">Behaviorism</a><span style=\"font-size: 1rem;\">&nbsp;as a movement in psychology appeared in 1913 when Watson published the classic article&nbsp;</span><a href=\"http://psychclassics.yorku.ca/Watson/views.htm\" target=\"_blank\" style=\"font-size: 1rem; background-color: rgb(255, 255, 255);\"><i>psychology as the behaviorist views it</i></a><span style=\"font-size: 1rem;\">.&nbsp;</span><span style=\"font-size: 1rem;\">John Watson proposed that the process of classical conditioning (based on&nbsp;</span><a href=\"http://www.simplypsychology.org/pavlov.html\" style=\"font-size: 1rem; background-color: rgb(255, 255, 255);\">Pavlov’s</a><span style=\"font-size: 1rem;\">&nbsp;observations) was able to explain all aspects of human psychology. He thought that e</span><span style=\"font-size: 1rem;\">verything from speech to emotional responses were simply patterns of stimulus and response. Watson denied completely the existence of the mind or consciousness. Watson believed that all individual differences in behavior were due to different experiences of learning. He famously said:&nbsp;</span></p><p></p></div><div class=\"editor-indent\" style=\"margin-left: 30px;\"><div><p></p><p><span style=\"font-size: 1rem;\"></span></p><div><p>\"Give me a dozen healthy infants, well-formed, and my own specified world to bring them up in and I\'ll guarantee to take any one at random and train him to become any type of specialist I might select - doctor, lawyer, artist, merchant-chief and, yes, even beggar-man and thief, regardless of his talents, penchants, tendencies, abilities, vocations and the race of his ancestors” (Watson, 1924, p. 104).</p></div><p></p><p></p></div></div><div>\r\n\r\n<p>The first\r\nscientific studies identifying <a href=\"http://en.wikipedia.org/wiki/Neuron\">neurons</a> that responded in ways that suggested they encode\r\nfor conditioned stimuli came from work by <a href=\"http://en.wikipedia.org/w/index.php?title=Mahlon_deLong&amp;action=edit&amp;redlink=1\">Mahlon deLong</a><a href=\"#_ftn3\" name=\"_ftnref3\" title=\"\"><!--[if !supportFootnotes]-->[3]<!--[endif]--></a>&nbsp; &nbsp;and by R.T. \"Rusty\" Richardson.<a href=\"#_ftn4\" name=\"_ftnref4\" title=\"\"><!--[if !supportFootnotes]-->[4]<!--[endif]--></a>\r\nThey showed that <a href=\"http://en.wikipedia.org/wiki/Nucleus_basalis\">nucleus basalis</a> neurons, which release <a href=\"http://en.wikipedia.org/wiki/Acetylcholine#Neuromodulatory_Effects\">acetylcholine</a> broadly throughout the <a href=\"http://en.wikipedia.org/wiki/Cerebral_cortex\">cerebral cortex</a>, are activated shortly\r\nafter a conditioned stimulus, or after a primary reward if no conditioned\r\nstimulus exists.</p><p><img src=\"@@PLUGINFILE@@/Nucleus%20Basilis.jpg\" alt=\"Nucleus Basilis\" width=\"800\" height=\"506\" class=\"img-responsive atto_image_button_left\"><br></p><p>These neurons are equally active for positive and negative\r\nreinforcers, and have been demonstrated to cause <a href=\"http://en.wikipedia.org/wiki/Neuroplasticity\">plasticity</a> in many <a href=\"http://en.wikipedia.org/wiki/Cerebral_cortex\">cortical</a> regions.<a href=\"#_ftn5\" name=\"_ftnref5\" title=\"\"><!--[if !supportFootnotes]-->[5]<!--[endif]--></a>\r\nEvidence also exists that <a href=\"http://en.wikipedia.org/wiki/Dopamine#Functions_in_the_brain\">dopamine</a> is activated at similar\r\ntimes. There is considerable evidence that dopamine participates in both\r\nreinforcement and aversive learning.<a href=\"#_ftn6\" name=\"_ftnref6\" title=\"\"><!--[if !supportFootnotes]-->[6]<!--[endif]--></a>\r\nDopamine pathways project much more densely onto <a href=\"http://en.wikipedia.org/wiki/Frontal_cortex\">frontal cortex</a> regions. <a href=\"http://en.wikipedia.org/wiki/Cholinergic\">Cholinergic</a> projections, in contrast, are dense even in the\r\nposterior cortical regions like the <a href=\"http://en.wikipedia.org/wiki/Primary_visual_cortex\">primary visual cortex</a>. A study of patients with\r\n<a href=\"http://en.wikipedia.org/wiki/Parkinson%27s_disease\">Parkinson\'s disease</a>, a condition attributed\r\nto the insufficient action of dopamine, further illustrates the role of\r\ndopamine in positive reinforcement.<a href=\"#_ftn7\" name=\"_ftnref7\" title=\"\"><!--[if !supportFootnotes]-->[7]<!--[endif]--></a>\r\nIt showed that while off their medication, patients learned more readily with\r\naversive consequences than with positive reinforcement. Patients who were on\r\ntheir medication showed the opposite to be the case, positive reinforcement\r\nproving to be the more effective form of learning when the action of dopamine\r\nis high.</p></div><h3><b><br></b></h3><h3><b><br></b></h3><h3><b>Generalization</b></h3><div><p></p><p><a href=\"http://www.simplypsychology.org/pavlov.html\">Ivan Pavlov</a>&nbsp;showed that classical conditioning\r\napplied to animals.&nbsp; Did it also apply to humans? In a famous (though\r\nethically dubious) experiment, Watson and Rayner (1920) showed that it did. This is the story of Albert, classical conditioning, and \"generalization.\"</p>\r\n\r\n<p>Little Albert was a 9-month-old infant\r\nwho was tested on his reactions to various stimuli. He was shown a white rat, a\r\nrabbit, a monkey and various masks. Albert described as \"on the whole\r\nstolid and unemotional\" showed no fear of any of these stimuli. However,\r\nwhat did startle him and cause him to be afraid was if a hammer was struck\r\nagainst a steel bar behind his head. The sudden loud noise would cause\r\n\"little Albert to burst into tears.</p>\r\n\r\n<p>When Little Albert was just over 11\r\nmonths old the white rat was presented and seconds later the hammer was struck\r\nagainst the steel bar.&nbsp; This was done 7 times over the next 7 weeks and\r\neach time Little Albert burst into tears. By now little Albert only had to see\r\nthe rat and he immediately showed every sign of fear. He would cry (whether or\r\nnot the hammer was hit against the steel bar) and he would attempt to crawl\r\naway.&nbsp;<span style=\"font-size: 1rem;\">In addition, the Watson and\r\nRayner found that Albert developed phobias of objects which shared\r\ncharacteristics with the rat; including the family dog, a fur coat, some cotton\r\nwool and a Santa Claus mask. This process is know as </span><b style=\"font-size: 1rem;\">generalization.</b></p>\r\n\r\n<p>Watson and Rayner had shown\r\nthat classical conditioning could be used to create a phobia. A phobia is an\r\nirrational fear, i.e. a fear that is out of proportion to the danger. Over the\r\nnext few weeks and months Little Albert was observed and 10 days after\r\nconditioning his fear of the rat was much less marked. This dying out of a\r\nlearned response is called extinction. However, even after a full month it was\r\nstill evident, and the association could be renewed by repeating the original\r\nprocedure a few times.</p><p><b>\r\n\r\n</b></p><h3><b><a name=\"_Toc58156758\"><b>Components of Operant Conditioning: Reinforcement</b></a></b></h3><b>\r\n\r\n<p><a href=\"https://www.verywell.com/what-is-reinforcement-2795414\"><b>Reinforcement</b></a>&nbsp;is any event that strengthens or increases the\r\nbehavior it follows. There are two kinds of reinforcers:</p>\r\n\r\n<ol start=\"1\" type=\"1\">\r\n <li><a href=\"https://www.verywell.com/what-is-positive-reinforcement-2795412\"><b>Positive reinforcers</b></a>&nbsp;are\r\n     favorable events or outcomes that are presented after the behavior. In\r\n     situations that reflect positive reinforcement, a response or behavior is\r\n     strengthened by the addition of something, such as praise or a direct\r\n     reward.</li>\r\n <li><a href=\"https://www.verywell.com/what-is-negative-reinforcement-2795410\"><b>Negative reinforcers</b></a>&nbsp;involve\r\n     the removal of an unfavorable events or outcomes after the display of a\r\n     behavior. In these situations, a response is strengthened by the removal\r\n     of something considered unpleasant.</li>\r\n</ol>\r\n\r\n<p>In both of\r\nthese cases of reinforcement, the behavior&nbsp;<strong>increases.</strong></p>\r\n\r\n<h3><a name=\"_Toc58156759\"><b>Punishment</b></a></h3>\r\n\r\n<p><a href=\"https://www.verywell.com/what-is-punishment-2795413\"><b>Punishment</b></a><strong>&nbsp;</strong>is the\r\npresentation of an adverse event or outcome that causes a decrease in the\r\nbehavior it follows. There are two kinds of punishment:</p>\r\n\r\n<ol start=\"1\" type=\"1\">\r\n <li><a href=\"https://www.verywell.com/what-is-positive-punishment-2795411\"><b>Positive punishment</b></a>, sometimes referred to as punishment by application,\r\n     presents an unfavorable event or outcome in order to weaken the response\r\n     it follows.</li>\r\n <li><a href=\"https://www.verywell.com/what-is-negative-punishment-2795409\"><b>Negative punishment</b></a>, also known as punishment by removal, occurs when a\r\n     favorable event or outcome is removed after a behavior occurs.</li>\r\n</ol>\r\n\r\n<p>In both of these\r\ncases of punishment, the behavior&nbsp;<strong>decreases.</strong></p>\r\n\r\n<h3><a name=\"_Toc58156760\"><b>Reinforcement\r\nSchedules</b></a></h3>\r\n\r\n<p>Skinner also\r\nfound that when and how often behaviors were reinforced played a role in the\r\nspeed and strength of acquisition. He identified several different&nbsp;<a href=\"https://www.verywell.com/what-is-a-schedule-of-reinforcement-2794864\">schedules of\r\nreinforcement</a>:</p>\r\n\r\n<ol start=\"1\" type=\"1\">\r\n <li><strong><u>Continuous reinforcement</u></strong>&nbsp;involves\r\n     delivery a reinforcement every time a response occurs. Learning tends to\r\n     occur relatively quickly, yet the response rate is quite low. Extinction\r\n     also occurs very quickly once reinforcement is halted.</li>\r\n <li><strong><u>F</u><u>ixed-ratio schedules</u></strong><u>&nbsp;</u>are\r\n     a type of partial reinforcement. Responses are reinforced only after a\r\n     specific number of responses have occurred. This typically leads to a\r\n     fairly steady response rate.</li>\r\n <li><strong><u>Fixed-interval schedules</u></strong>&nbsp;are\r\n     another form of partial reinforcement. Reinforcement occurs only after a\r\n     certain interval of time has elapsed. Response rates remain fairly steady\r\n     and start to increase as the reinforcement time draws near, but slow\r\n     immediately after the reinforcement has been delivered.</li>\r\n <li><strong><u>Variable-ratio schedules</u></strong>&nbsp;are\r\n     also a type of partial reinforcement that involve reinforcing behavior\r\n     after a varied number of responses. This leads to both a high response\r\n     rate and slow extinction rates.</li>\r\n <li><strong><u>Variable-interval schedules</u></strong><b>&nbsp;</b>are\r\n     the final form of partial reinforcement Skinner described. This schedule\r\n     involves delivering reinforcement after a variable amount of time has\r\n     elapsed. This also tends to lead to a fast response rate and slow\r\n     extinction rate.</li></ol></b><div>\r\n\r\n<hr align=\"left\" size=\"1\" width=\"33%\">\r\n\r\n<!--[endif]-->\r\n\r\n<div id=\"ftn1\">\r\n\r\n<p><a href=\"#_ftnref1\" name=\"_ftn1\" title=\"\"><!--[if !supportFootnotes]-->[1]<!--[endif]--></a>\r\nThorndike, E.L. (1901). Animal intelligence: An\r\nexperimental study of the associative processes in animals. Psychological\r\nReview Monograph Supplement, 2, 1–109.</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn2\">\r\n\r\n<p><a href=\"#_ftnref2\" name=\"_ftn2\" title=\"\"><!--[if !supportFootnotes]-->[2]<!--[endif]--></a> Mecca Chiesa (2004) Radical Behaviorism: the\r\nphilosophy and the science</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn3\">\r\n\r\n<p><a href=\"#_ftnref3\" name=\"_ftn3\" title=\"\"><!--[if !supportFootnotes]-->[3]<!--[endif]--></a> \"Activity of pallidal neurons during\r\nmovement\", M.R. DeLong, <i>J. Neurophysiol.</i>, 34:414–27, 1971</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn4\">\r\n\r\n<p><a href=\"#_ftnref4\" name=\"_ftn4\" title=\"\"><!--[if !supportFootnotes]-->[4]<!--[endif]--></a> Richardson RT, DeLong MR (1991): Electrophysiological\r\nstudies of the function of the nucleus basalis in primates. In Napier TC,\r\nKalivas P, Hamin I (eds), <i>The Basal Forebrain: Anatomy to Function</i> (<i>Advances\r\nin Experimental Medicine and Biology</i>, vol. 295. New York, Plenum, pp.\r\n232–252</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn5\">\r\n\r\n<p><a href=\"#_ftnref5\" name=\"_ftn5\" title=\"\"><!--[if !supportFootnotes]-->[5]<!--[endif]--></a> PNAS 93:11219-24 1996, Science 279:1714–8 1998</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn6\">\r\n\r\n<p><a href=\"#_ftnref6\" name=\"_ftn6\" title=\"\"><!--[if !supportFootnotes]-->[6]<!--[endif]--></a> Neuron 63:244–253, 2009, Frontiers in Behavioral\r\nNeuroscience, 3: Article 13, 2009</p>\r\n\r\n</div>\r\n\r\n<div id=\"ftn7\">\r\n\r\n<p><a href=\"#_ftnref7\" name=\"_ftn7\" title=\"\"><!--[if !supportFootnotes]-->[7]<!--[endif]--></a> Michael J. Frank, Lauren C. Seeberger, and Randall C.\r\nO\'Reilly (2004) \"By Carrot or by Stick: Cognitive Reinforcement Learning\r\nin Parkinsonism,\" Science 4, November 2004</p></div></div></div><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1654220999),(24,15,'3) Comparison of EEG to Other Neuroimaging Techniques','',1,'<p></p>\r\n<p>Clinical psychophysiology (also known as applied psychophysiology) aims to correlate the objective data with the subjective report, for example, linking EEG with behavior.&nbsp;Whereas the scientist-physician will link the EEG to neurological pathologies,\r\n    the neurotherapist will link the EEG to psychopathology and sometimes to physical pathology.&nbsp; The neurotherapist uses psychophysiological measures, such as<b> EEG</b> and <b>quantitative EEG</b>, to assess the client, and later treats the client\r\n    with applied psychophysiology (i.e. neurofeedback, neurotherapy, and biofeedback), while the neurologist looks at the neurophysiology for assessment purposes, alone, typically prescribing pharmaceuticals or surgery as treatment.&nbsp;&nbsp;</p>Neuroscientific\r\ntechnology has exploded in the past 20 years, however, and the fields of applied psychophysiology, experimental psychology, and medical neuroscience are three separate fields&nbsp;that are accessing the tremendous advancements in viewing the brain and\r\nits activity. Today, there is a proliferation of scientific psychological research involving brain imaging technology. The <b>MRI (magnetic resonance imaging)</b>—a 3D view of the brain from various cuts—has led to the <b>fMRI (functional magnetic resonance imaging)</b>,\r\nwhich reveals every region’s activity and how much those parts of the brain are being used. <b>Diffusion tensor imaging (DTI)</b> has evolved to diffusion tensor magnetic resonance imaging tractography, which allows us to see and understand connections\r\nin the brain. And <b>Positron Emission Tomography (PET)</b> scans have revolutionized our capability of viewing the activity of the brain by showing metabolic and vascular activity in real time.<br><p><br></p><p>The poor signal to noise ratio and expense of MEG make this technology impractical for most imaging situations. qEEG provides a much better signal to noise ratio and is far cheaper and easier to use. PET scans and SPECT scans require radioactive injections and SPECT scans have less spatial resolution than fMRI. The most popular imaging method for medical clinical imaging today is fMRI. At this point in time qEEG, using sLORETA analysis methods, has close to the same spatial resolution and superior temporal resolution with respect to MRI. It is also far cheaper and easier to use. The main drawback is its inability to image subcortical structures, however new methods of cortical analysis are being developed to make it possible to assess subcortical function based on cortical dynamics (Yehudit Meir-Hasson et al., 2013).</p><h5><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\"><b>Quantitative EEG</b>&nbsp;(qEEG)</b></h5>\r\n<p><b>Quantitative EEG</b>&nbsp;uses fast fourier transform (FFT) and other algorithms to decompose EEG data into subsets of frequencies (integers) and connectivity measures. Sometimes these measures are displayed relative to a \"normative database\" of individuals\r\n    who are healthy for their age (in these cases, the clinician can compare their patient\'s EEG to see how deviant it is from the same-aged \"norm\"). Other quantitative databases simply quantify EEG data, but do not compare the data to a norm in order\r\n    to indicate standard deviations from the normal same-aged demographic. EEG and qEEG can only provide data from cortical sources of brainwaves. It cannot directly measure subcortical structures and activity. EEG is the sum of dipoles representing pyramidal\r\n    cells oriented perpendicular to the surface of the scalp.&nbsp;</p>\r\n<p><b>Below are two separate images from QEEGs</b></p>\r\n<p><img src=\"@@PLUGINFILE@@/raw%20vs.%20QEEG.png\" alt=\"raw vs. QEEG\" width=\"700\" height=\"422\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n<p><span><b style=\"font-weight: bold;\"><img src=\"@@PLUGINFILE@@/QEEG.png\" alt=\"QEEG\" width=\"500\" height=\"330\" class=\"img-responsive atto_image_button_right\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><span><b style=\"font-weight: bold;\"><br></b></span></p>\r\n<p><br></p>\r\n<p><br></p><p></p><h3><b style=\"font-size: 1rem;\">Magnetoencephalography (MEG) (see image below) i</b><span style=\"font-size: 1rem;\">s a technique for mapping brain activity by recording magnetic fields produced by electrical currents occurring naturally in the brain, using arrays of SQUIDs (superconducting quantum interference devices).</span></h3><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/MEG%20%282%29.jpg\" alt=\"MEG\" width=\"300\" height=\"452\" class=\"img-responsive atto_image_button_left\">Applications of MEG include localizing regions affected by pathology before surgical removal, determining the function of various parts of the brain, and neurofeedback. MEG</span><span style=\"font-size: 1rem;\">&nbsp;is\r\n    the sum of magnetic fields from dipoles of neurons parallel to the surface of the scalp located in the sulci of the cortex and is consequently complementary to EEG analysis. One measures perpendicular sources of electromagnetic activity and the other\r\n    measures tangential sources of magnetic activity.</span><br><p></p>\r\n<p><img src=\"@@PLUGINFILE@@/MeG.png\" alt=\"MEG2\" width=\"600\" height=\"335\" class=\"atto_image_button_middle\"><br></p><p><b style=\"font-size: 1rem;\"><b>Magnetic Resonance Imaging (MRI) (see image below)</b>&nbsp;</b><span style=\"font-size: 1rem;\">uses a strong magnetic field to align the protons of hydrogen atoms in the water of the body, it generates a radio wave pulse that knocks them out of alignment and then measures the radio waves that the protons emit as they realign. Protons in different tissues realign at different rates or \"relaxation times\" and can be used to construct images of the tissue.&nbsp;</span><br></p><p><img src=\"@@PLUGINFILE@@/MRI%20Images.jfif\" alt=\"MRI Images\" width=\"600\" height=\"336\" class=\"img-responsive atto_image_button_left\"><br></p><p><b><img src=\"@@PLUGINFILE@@/MRI2.jfif\" alt=\"MRI2\" width=\"500\" height=\"333\" class=\"atto_image_button_middle\"><br></b></p><p><b style=\"font-size: 1rem;\">Functional Magnetic Resonance Imaging (fMRI)</b><span style=\"font-size: 1rem;\">&nbsp;uses this same technology but applies it to cerebral blood flow. It monitors changes in magnetization between oxygen rich and oxygen depleted blood which is then color coded graphically. When neurons become active, the oxygen rich blood increases within two seconds and reaches a peak in about 4 seconds. To generate 3D density distribution patterns, special mathematical image reconstruction methods are used.</span><br></p><p><img src=\"@@PLUGINFILE@@/fMRI%20%282%29.jfif\" alt=\"fMRI\" width=\"700\" height=\"284\" class=\"atto_image_button_middle\"></p><p><span style=\"font-size: 1rem;\">When a brain area is more active it consumes more oxygen and to meet this increased demand blood flow increases to the active area. FMRI can be used to produce activation maps showing which parts of the brain are involved in a particular mental process.</span></p><p>Oxygen is delivered to neurons by haemoglobin in capillary red blood cells. When neuronal activity increases there is an increased demand for oxygen and the local response is an increase in blood flow to regions of increased neural activity.</p><p>Haemoglobin is diamagnetic when oxygenated but paramagnetic when deoxygenated. This difference in magnetic properties leads to small differences in the MR signal of blood depending on the degree of oxygenation. Since blood oxygenation varies according to the levels of neural activity these differences can be used to detect brain activity. This form of MRI is known as blood oxygenation level dependent (BOLD) imaging.</p><p>One point to note is the direction of oxygenation change with increased activity. You might expect blood oxygenation to decrease with activation, but the reality is a little more complex. There is a momentary decrease in blood oxygenation immediately after neural activity increases, known as the “initial dip” in the haemodynamic response. This is followed by a period where the blood flow increases, not just to a level where oxygen demand is met, but overcompensating for the increased demand. This means the blood oxygenation actually increases following neural activation. The blood flow peaks after around 6 seconds and then falls back to baseline, often accompanied by a “post-stimulus undershoot”.<br></p>\r\n<p><br></p>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/rJjHjnzmvDI\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n<p></p><p></p><img src=\"@@PLUGINFILE@@/PET%20scan.jpg\" alt=\"PET Scan\" width=\"1000\" height=\"386\" class=\"img-responsive atto_image_button_middle\"><b>Positron Emission Tomography (PET)</b>&nbsp;scans are dependent on the injection of radioactive isotopes into the blood. Regions that use more blood as they are activated emit positrons that can be measured by special sensors placed around the head. The\r\n    resolution is not as good as MRI.<p></p>\r\n<p><b>Single photon emission computed tomography (SPECT, or less commonly, SPET)</b>&nbsp;is a nuclear medicine tomographic imaging technique using gamma rays. It is very similar to conventional nuclear medicine planar imaging using a gamma camera. However,\r\n    it is able to provide true 3D information. This information is typically presented as cross-sectional slices through the patient, but can be freely reformatted or manipulated as required.<img src=\"@@PLUGINFILE@@/SPECT.jpg\" alt=\"SPECT Scan\" width=\"800\" height=\"450\" class=\"img-responsive atto_image_button_middle\"></p>\r\n<p></p>\r\n<p>The basic technique requires injection of a gamma-emitting radioisotope into the bloodstream of the patient. Occasionally the radioisotope is a simple soluble dissolved ion, such as a radioisotope of gallium(III), which happens to also have chemical properties\r\n    which allow it to be concentrated in ways of medical interest for disease detection. However, most of the time in SPECT, a marker radioisotope, which is of interest only for its radioactive properties, has been attached to a special radioligand, which\r\n    is of interest for its chemical binding properties to certain types of tissues. This marriage allows the combination of ligand and radioisotope to be carried and bound to a place of interest in the body, which then allows the ligand concentration\r\n    to be seen by a gamma-camera because the properties of radioligand bind it to certain types of tissues.&nbsp;A gamma camera captures the emissions from several different angles which can be used to generate a 3D image of the tissue that the radioligand\r\n    binds with.</p><p><b style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/SPECT%20scans.jpg\" alt=\"SPECT Scan 2\" width=\"500\" height=\"335\" class=\"img-responsive atto_image_button_right\"></b></p><h3><b style=\"font-size: 1rem;\">SPECT in Functional Brain Imaging</b></h3><p></p>\r\n\r\n<p>Because blood flow in the brain is tightly coupled to local brain metabolism and energy use, an isotope is used to assess brain metabolism regionally, in an attempt to diagnose and differentiate the different causal pathologies of dementia. In meta analysis,\r\n    SPECT was superior to clinical exam and clinical criteria in being able to differentiate Alzheimer\'s disease from vascular dementias. This latter ability relates to SPECT\'s imaging of local metabolism of the brain, in which the patchy loss of cortical\r\n    metabolism seen in multiple strokes differs clearly from the more even or \"smooth\" loss of non-occipital cortical brain function typical of Alzheimer\'s disease.</p>\r\n\r\n<p><br></p>\r\n\r\n<p><br></p>\r\n\r\n<p><br></p><br><br>\r\n<p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',25,1654212303),(25,13,'Concepts of Control and Feedback in biological systems','',1,'<p></p><h4></h4><h2><strong>Feedback in Biology</strong></h2><b></b>\r\n\r\n<p>\r\n\r\n</p><p>Feedback is defined as the information gained about a\r\nreaction to a product, which will allow the modification of the product.\r\nFeedback loops are therefore the process whereby a change to the system results\r\nin an alarm which will trigger a certain result. This result will either\r\nincrease the change to the system or reduce it to bring the system back to\r\nnormal.</p>\r\n\r\n<h4><b><h2><strong>Feedback Loops</strong></h2></b></h4>\r\n\r\n<p>A feedback loop is a biological occurrence wherein the output\r\nof a system amplifies the system (positive feedback) or inhibits the system\r\n(negative feedback). Feedback loops are important because they allow living\r\norganisms to&nbsp;<strong>maintain homeostasis</strong>.&nbsp;Homeostasis&nbsp;is the mechanism that enables us to keep our\r\ninternal environment relatively constant – not too hot, or too cold, not too\r\nhungry or tired. The level of energy that an organism needs to maintain\r\nhomeostasis depends on the type of organism, as well as the environment it\r\ninhabits. For example, a cold-blooded fish keeps its temperature at the same\r\nlevel as the water around it, and so doesn’t need to control its internal\r\ntemperature. Compare this to a warm-blooded whale in the same environment: it\r\nneeds to keep its body temperature higher than that of the water around it, and\r\nso it will expend more energy in temperature regulation.</p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Predator%20Prey%20Cycle.png\" alt=\"Predator Prey Cycle\" width=\"555\" height=\"258\" class=\"img-responsive atto_image_button_left\">Feedback loops can also occur to a larger degree: at the ecosystem level, a form of homeostasis is maintained. A good example of this is in the cycle of predator and prey populations: a boom in prey population will mean more food for predators, which will increase predator numbers. This will then lead to over predation, and the prey population will again decline. The predator population will decline in response, releasing the pressure on the prey population and allowing it to bounce back.&nbsp;</p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\">Positive Feedback Loops</strong><br></p><p><span style=\"font-size: 1rem;\">A positive feedback loop occurs in nature when\r\nthe product of a reaction leads to an increase in that reaction. If we look at\r\na system in homeostasis, a positive feedback loop moves a system further away\r\nfrom the target of equilibrium. It does this by amplifying the effects of a\r\nproduct or event and occurs when something needs to happen quickly.</span></p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Greenhouse%20Gases.jpg\" alt=\"Greenhouse Gases\" width=\"650\" height=\"384\" class=\"img-responsive atto_image_button_left\">Positive feedback loops are inherently unstable systems. Because a\r\nchange in an input causes responses that produce continued changes in the same\r\ndirection, positive feedback loops can lead to runaway conditions. The term\r\npositive feedback is typically used as long as a variable has an ability to\r\namplify itself, even if the components of a loop (receptor, control center and\r\neffector) are not easily identifiable. In most cases, positive feedback is\r\nharmful, but there are a few instances where positive feedback, when used in\r\nlimited fashion, contributes to normal function.&nbsp;</p>\r\n\r\n<h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b>Positive Feedback Loop Example 1: Fruit Ripening</b></h4>\r\n\r\n<p>There is a surprising effect in nature where a tree or bush will\r\nsuddenly ripen all of its fruit or vegetables, without any visible signal. This\r\nis our first example of a positive biological feedback loop. If we look at an\r\napple tree, with many apples, seemingly overnight they all go from unripe to\r\nripe to overripe. This will begin with the first apple to ripen. Once ripe, it\r\ngives off a gas known as ethylene (C<sub>2</sub>H<sub>4</sub>) through its skin. When\r\nexposed to this gas, the apples near to it also ripen. Once ripe, they too\r\nproduce ethylene, which continues to ripen the rest of the tree in an effect\r\nmuch like a wave. This feedback loop is often used in fruit production, with\r\napples being exposed to manufactured ethylene gas to make them ripen faster.</p>\r\n\r\n<h4><strong style=\"font-size: 1.286rem;\">Positive Feedback Loop Example 2: Childbirth</strong><br></h4>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Oxytocin%20Feedback%20Loop.jpg?time=1621544152196\" alt=\"Oxytocin Feedback Loop\" width=\"555\" height=\"453\" class=\"img-responsive atto_image_button_left\">When\r\nlabor begins, the baby’s head is pushed downwards and results in increased\r\npressure on the cervix. This stimulates receptor cells to send a chemical\r\nsignal to the brain, allowing the release of oxytocin. This oxytocin diffuses\r\nto the cervix via the blood, where it stimulated further contractions. These\r\ncontractions stimulate further oxytocin release until the baby is born.</p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">Positive Feedback Loop Example 3: Blood Clotting</strong></p>\r\n\r\n<p>When\r\ntissue is torn or injured, a chemical is released. This chemical causes\r\nplatelets in the blood to activate. Once these platelets have activated, they\r\nrelease a chemical which signals more platelets to activate, until the wound is\r\nclotted.</p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\">Negative Feedback Loops</strong><br></p>\r\n\r\n<p>A\r\nnegative feedback loop occurs in biology when the product of a reaction leads\r\nto a decrease in that reaction. In this way, a negative feedback loop brings a\r\nsystem closer to a target of stability or homeostasis. Negative feedback loops\r\nare responsible for the stabilization of a system, and ensure the maintenance\r\nof a steady, stable state. The response of the regulating mechanism is opposite\r\nto the output of the event.</p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Glucose.jpg\" alt=\"Glucose\" width=\"600\" height=\"338\" class=\"img-responsive atto_image_button_left\">Negative feedback loops are inherently stable systems.\r\nNegative feedback loops, in conjunction with the various stimuli that can\r\naffect a variable, typically produce a condition in which the variable\r\noscillates around the set point. For example, negative feedback loops involving\r\ninsulin and glucagon help to keep blood glucose levels within a narrow\r\nconcentration range. If glucose levels get too high, the body releases insulin\r\ninto the bloodstream. Insulin causes the body’s cells to take in and store\r\nglucose, lowering the blood glucose concentration. If blood glucose gets too\r\nlow, the body releases glucagon, which causes the release of glucose from some\r\nof the body’s cells.</p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\"><br></strong></p><p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Example 1: Temperature\r\nRegulation</strong></p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Body%20Temperature.jpg\" alt=\"Body Temperature\" width=\"555\" height=\"312\" class=\"img-responsive atto_image_button_left\"><span style=\"font-size: 1rem;\">Temperature\r\nregulation in humans occurs constantly. Normal human body temperature is\r\napproximately 98.6°F. When body temperature rises above this, two mechanisms\r\nkick in the body begins to sweat, and vasodilation occurs to allow more of the\r\nblood surface area to be exposed to the cooler external environment. As the\r\nsweat cools, it causes evaporative cooling, while the blood vessels cause convective\r\ncooling. Normal temperature is regained. Should these cooling mechanisms\r\ncontinue, the body will become cold. The mechanisms which then kick in are the\r\nformation of goose bumps, and vasoconstriction. Goosebumps in other mammals\r\nraise the hair or fur, allowing more heat to be retained. In humans, they\r\ntighten the surrounding skin, reducing (slightly) the surface area from which\r\nto lose heat. Vasoconstriction ensures that only a small surface area of the\r\nveins is exposed to the cooler outside temperature, retaining heat. Normal\r\ntemperature is regained.</span></p>\r\n\r\n<p><strong style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\">Positive vs. Negative Feedback</strong></p><h2><b></b></h2>\r\n\r\n<p>The\r\nkey difference between positive and negative feedback is their response to\r\nchange: positive feedback amplifies change while negative feedback reduces\r\nchange. This means that positive feedback will result in more of a product. Negative feedback\r\nwill result in less of a product. Positive feedback moves away from a target point while negative feedback moves\r\ntowards a target.</p><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',11,1654221149),(26,13,'Basic Physiology of Stress and Attention','<h3></h3><br><p></p><p></p>',1,'<p></p><h3><span>I. Stress</span></h3><p><i>Stress is a condition or feeling experienced when a person perceives that \"demands exceed the personal and social resources the individual is able to mobilize.</i>” (attributed to Richard S.Lazarus)<br></p><p>Stress&nbsp;is a situation that triggers a particular biological response. When you perceive a threat or a major challenge, chemicals and hormones surge throughout your body.&nbsp;<span>Stress can trigger your fight-or-flight response in order to fight the stressor or run away from it. Typically, after the response occurs, your body should relax. Too much constant stress can have negative effects on your long-term health.&nbsp;Stress isn’t necessarily a bad thing. It’s what helped our hunter-gatherer ancestors survive, and it’s just as important in today’s world. It can be healthy when it helps you avoid an accident, meet a tight deadline, or keep your wits about you amid chaos.&nbsp;But stress should be temporary. Once you’ve passed the fight-or-flight moment, your heart rate and breathing should slow down and your muscles should relax. In a short time, your body should return to its natural state without any lasting negative effects.</span><br></p><p><span><img src=\"@@PLUGINFILE@@/Stress%20Bellcurve.png\" alt=\"Stress Bell Curve\" width=\"700\" height=\"345\"><br></span></p><h4><span>Good Stress vs. Bad Stress</span></h4><p><span><b>Eustress</b>&nbsp;(acute, physiologically adaptive):&nbsp;</span><span>Increased delayed type hypersensitivity, associated with acute spikes in corticosterone and decreased leukocytes in blood (by movement to skin)&nbsp;</span></p><p><span><b>Distress</b>&nbsp;(chronic, physiologically maladaptive):&nbsp;</span><span>Decreased delayed type hypersensitivity, associated with chronically increased basal corticosterone and less decrease in blood leukocytes (i.e., less movement of leukocytes to skin).</span></p><p><span><br></span></p><h4>According to American Psychological Association (APA), there are 3 different types stress:</h4><p></p><ul><li><b>Acute stress:&nbsp;</b></li><ul><li><span><span>Acute stress happens to everyone. It’s the body’s immediate reaction to a new and challenging situation. It’s the kind of stress you might feel when you narrowly escape a car accident.&nbsp;&nbsp;</span><span>Acute stress can also come out of something that you actually enjoy. It’s the somewhat-frightening, yet thrilling feeling you get on a roller coaster or when skiing down a steep mountain slope.&nbsp;</span><span>These incidents of acute stress don’t normally do you any harm. They might even be good for you. Stressful situations give your body and brain practice in developing the best response to future stressful situations.&nbsp;</span><span>Once the danger passes, your body systems should return to normal.&nbsp;&nbsp;</span></span><span>Severe acute stress</span><span>&nbsp;is a different story. This kind of stress, such as when you’ve faced a life-threatening situation, can lead to&nbsp;</span><span>post-traumatic stress disorder (PTSD)</span><span>&nbsp;or other mental health problems.&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;</span></li></ul><li><b><img src=\"@@PLUGINFILE@@/stress.jpg\" alt=\"stress\" width=\"600\" height=\"336\" class=\"img-responsive atto_image_button_right\"><b>Episodic acute stress</b></b></li></ul><div><p><span>Episodic acute stress is when you have frequent episodes of acute stress.&nbsp;</span><span>This might happen if you’re often anxious and worried about things you suspect may happen. You might feel that your life is chaotic and you seemingly go from one crisis to the next.&nbsp;</span><span>Certain professions, such as law enforcement or firefighters, might also lead to frequent high-stress situations.&nbsp;</span><span>As with severe acute stress, episodic acute stress can affect your physical health and mental well-being.</span></p></div><p></p><ul><li><b>Chronic stress</b></li></ul><div><span>When you have high-stress levels for an extended period of time, you have chronic stress. Long-term stress like this can have a negative impact on your health. It may contribute to:&nbsp;</span><a href=\"https://www.healthline.com/health/anxiety/effects-on-body\">anxiety</a><span>,&nbsp;</span><a href=\"https://www.healthline.com/health/heart-disease/causes-risks\">cardiovascular disease</a><span>,&nbsp;</span><a href=\"https://www.healthline.com/health/depression\">depression</a><span>,&nbsp;</span><span>high blood pressure, and&nbsp;</span><span>a weakened immune system.&nbsp;</span><span>Chronic stress can also lead to frequent ailments such as headaches, an upset stomach, and sleep difficulties.&nbsp;</span></div><b><p></p></b><b><br></b><p><br></p><p></p><p></p><h4>Classical View of the Autonomic Nervous System&nbsp;</h4><p></p><ul><li><u><b>Parasympathetic: Rest and Restoration (also known as Rest and Digest)</b></u></li><ul><li>Integrates the ‘rest &amp; recreation’ (feed &amp; breed) response</li><li>Release of acetylcholine&nbsp;</li><li>Decreased heart rate &amp; blood pressure&nbsp;</li><li>Decreased respiratory rate and bronchial constriction&nbsp;</li><li>Decreased glycogen to glucose in liver&nbsp;</li><li>Pupillary constriction</li><li><span>Increased GI activity&nbsp;</span></li></ul></ul><ul><li><b><u>Sympathetic: Fight or flight</u></b><br></li><ul><li>Integrates the ʻfight or flightʼ response&nbsp;</li><li>Release of norepinephrine &amp; epinephrine&nbsp;</li><li>Increased heart rate &amp; blood pressure&nbsp;</li><li>Increased respiratory rate and bronchial dilation&nbsp;</li><li>Increased glycogen to glucose in liver&nbsp;</li><li>Increased pupil diameter&nbsp;</li><li>Decreased GI activity</li></ul></ul><p></p><p></p><p><br></p><h4>The Biology of Stress<img src=\"@@PLUGINFILE@@/adrenaline.png\" alt=\"qdrenaline\" width=\"500\" height=\"700\" class=\"img-responsive atto_image_button_right\"></h4><p></p><p>When you sense danger, the&nbsp;hypothalamus&nbsp;at the base of your brain reacts. It sends nerve and hormone signals to your&nbsp;adrenal glands, which release an abundance of hormones.</p><p>These hormones are nature’s way of preparing you to face danger and increase your chances of survival.</p><p><br></p><h4><b>Adrenaline</b></h4><p>One of these hormones is&nbsp;<u><b>adrenaline</b></u>. You might also know it as&nbsp;<u>epinephrine</u>, or the fight-or-flight hormone. In rapid fashion, adrenaline works to:</p><ul><li>increase your heartbeat</li><li>increase your breathing rate</li><li>make it easier for your muscles to use&nbsp;glucose</li><li>contract blood vessels so blood is directed to the muscles</li><li>stimulate perspiration</li><li>inhibit&nbsp;insulin&nbsp;production</li></ul><p>While this is helpful in the moment, frequent adrenaline surges can lead to:</p><ul><li>damaged blood vessels</li><li>high blood pressure, or hypertension</li><li>higher risk of&nbsp;heart attack&nbsp;and&nbsp;stroke</li><li>headaches</li><li>anxiety</li><li>insomnia</li><li>weight gain</li></ul><p><br></p><h4><b>Cortisol</b></h4><p></p><p>As the main stress hormone,&nbsp;<b>cortisol</b>&nbsp;plays an essential role in stressful situations. Among its functions are:</p><ul><li>raising the amount of glucose in your bloodstream<img src=\"@@PLUGINFILE@@/Cortisol.jpg\" alt=\"Cortisol\" width=\"700\" height=\"701\" class=\"atto_image_button_right\"></li><li>helping the brain use glucose more effectively</li><li>raising the accessibility of substances that help with tissue repair</li><li>restraining functions that are nonessential in a life-threatening situation</li><li>altering immune system response</li><li>dampening the reproductive system and growth process</li><li>affecting parts of the brain that control fear, motivation, and mood</li></ul><p>All this helps you deal more effectively with a high-stress situation. It’s a normal process and crucial to human survival.</p><p>But if your cortisol levels stay high for too long, it has a negative impact on your health. It can contribute to:</p><ul><li>weight gain</li><li>high blood pressure</li><li>sleep problems</li><li>lack of energy</li><li>type 2 diabetes</li><li>osteoporosis</li><li>mental cloudiness (brain fog) and memory problems</li><li>a weakened immune system, leaving you more vulnerable to infections</li></ul><p><br></p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem;\">Attention</span><br></p><p>Attention can generally be defined as the ability to produce, select, manage and maintain sufficient stimulation at a specific amount of time to process any kind of information. It takes place on the cognitive level and has different types.&nbsp;<span style=\"font-size: 1rem;\">Attention is the key to achieve optimum functionality in our lives. The way to do this is to parse the factors or stimuli we encounter as relevant or irrelevant. Actually, this is when we make the most basic choices regarding the topics we are interested in or not.</span></p><p><span style=\"font-size: 1rem;\">The brain is limited in its capacity to process all sensory stimuli present in the physical world at any point in time and relies instead on the cognitive process of attention to focus neural resources according to the contingencies of the moment. Attention can be categorized into two distinct functions: <b>bottom-up attention</b>, referring to attentional guidance purely by externally driven factors to stimuli that are salient because of their inherent properties relative to the background; and<b> top-down attention</b>, referring to internal guidance of attention based on prior knowledge, willful plans, and current goals.&nbsp;</span><br></p><p><span style=\"\"><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Top%20Down%20and%20Bottom%20Up.png\" alt=\"top down bottom up\" width=\"600\" height=\"479\" class=\"img-responsive atto_image_button_left\" style=\"text-align: center;\"></span></span></p><p style=\"text-align: center;\"><br></p><p></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><br></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\">Over the past few years, insights on the neural circuits and mechanisms of bottom-up and top-down attention have been gained through neurophysiological experiments. Attention affects the mean neuronal firing rate as well as its variability and correlation across neurons. Although distinct processes mediate the guidance of attention based on bottom-up and top-down factors, a common neural apparatus, the frontoparietal network, is essential in both types of attentional processes.</span></p><h3><span style=\"font-size: 1rem;\"><b>General View of Attention Networks</b></span></h3><p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Attention%20Networks.jpg\" alt=\"Attention Networks\" width=\"512\" height=\"425\" class=\"img-responsive atto_image_button_left\">There are many neural nodes and networks involved in the attention process, which are too many and too complex to list here. This diagram to the left gives a depiction of the networks of attention and te&nbsp;</span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4>Determining Factors That Influence the Functioning of Attention</h4><p>Attention is not a one-way process. There are a number of factors for a stimulus to attract our attention. Only a stimulus based on these factors triggers our cognitive functions and can initiate cognitive processing.</p><p>It is possible to examine these factors that attract our attention and maintain focus in two main groups:</p><h5>1.&nbsp;<b>Internal Factors</b></h5><p>These determinants are personal because they depend on the individual\'s own cognitive resources and brain functions. Some of them can be listed as follows:</p><ul><li>Mental condition</li><li>Needs</li><li>Emotions</li><li>Mindset</li><li>Interests</li><li>Motivation</li><li>Physical state</li></ul><h5>2.&nbsp;<b>External Factors</b></h5><p>These determinants are usually based on the characteristics of the stimuli or come from our surroundings. Some of them can be listed as follows:</p><ul><li>Intensity</li><li>Uniqueness</li><li>Size</li><li>Color</li><li>Emotional Burden</li><li>Contrast</li></ul><span style=\"font-size: 1rem;\">There are Four Kinds of Attention<br></span><img src=\"@@PLUGINFILE@@/Attention.png\" alt=\"Attention\" width=\"700\" height=\"413\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"><br><p></p><h3>Selected Attention</h3><p>We are using selected attention al of the time.&nbsp;This is the processes that&nbsp;<b>allow an individual to select and focus on particular input</b>&nbsp;for further processing while simultaneously suppressing irrelevant or distracting information.<img src=\"@@PLUGINFILE@@/selective%20attention.jpg\" alt=\"Selective attention\" width=\"300\" height=\"168\" class=\"img-responsive atto_image_button_left\"></p><p><br></p><h3><br></h3><h3><br></h3><h3><br></h3><h3>Divided Attention</h3><p>We use divided attention while simultaneously paying attention to two or more tasks. This ability is also called multitasking. Divided attention uses mental focus on a very large scale. Nonetheless, this does not allow the brain to fully focus on any task. Therefore, this type of attention does not last for long.<img src=\"@@PLUGINFILE@@/mom.jpg\" alt=\"mom\" width=\"300\" height=\"168\" class=\"img-responsive atto_image_button_left\"></p><br><p></p><br><br><br><br><h3><br></h3><h3>Alternating Attention</h3><p>Alternating attention is the ability to change the focus of your attention and switch between different tasks. In this type of attention, mental flexibility is required so that one task does not limit the performance of others.<img src=\"@@PLUGINFILE@@/cooking.jpg\" alt=\"cooking\" width=\"265\" height=\"190\" class=\"img-responsive atto_image_button_left\"></p><br><br><br><br><br><br><br><h3>Sustained Attention</h3><p>We often use sustained attention for tasks that take a long time or require intense focus. This type of attention allows one to consistently perform a certain mental activity. For example, when children study for an exam, they need to read and acquire the information in a textbook for several hours.</p><img src=\"@@PLUGINFILE@@/Focus.jpg\" alt=\"Focus\" width=\"321\" height=\"157\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',6,1653943556),(27,14,'6) Event Related Potentials and Slow Cortical Poentials','',1,'<h4>Event Related Potentials</h4><p>An ERP is an event related potential.&nbsp;An event-related potential is the measured brain response that is the direct result of a specific sensory, cognitive, or motor event. More formally, it is any stereotyped electrophysiological response to a stimulus. The study of the brain in this way provides a noninvasive means of evaluating brain functioning. ERPs can be used to explore a huge range of topics,\r\nincluding development, visual attention, anxiety &amp;\r\ndepression, individual differences in working memory,\r\nand who will eventually awake from a coma. In an ERP, stimuli are given, again and again, and the participant has to respond to the stimuli, usually by clicking a mouse to indicate recognition of what they\'re directed to note.</p><p><img src=\"@@PLUGINFILE@@/ERP.png\" alt=\"ERP Stimulus and response\" width=\"900\" height=\"537\" class=\"img-responsive atto_image_button_left\"><span style=\"font-size: 1rem;\">To pull out the brain’s\r\nconsist response to some\r\ntype of event, we can simply\r\naverage across the epochs\r\nfor that event type.\r\nWhen we average across\r\nenough epochs, any activity\r\nthat’s consistent from trial to\r\ntrial remains in the average,\r\nand any random noise\r\nsimply averages out.</span></p><p><img src=\"@@PLUGINFILE@@/ERP%20Compilation.png\" alt=\"ERP compilation\" width=\"700\" height=\"559\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p>In a typical ERP\r\nexperiment, we time-lock to\r\nthe onset of a stimulus. In\r\nother words, time zero is\r\nstimulus onset.\r\nWhen we do this, we can\r\ntrack the flow of information\r\nabout the stimulus through\r\nthe brain over a period of\r\nseveral hundred\r\nmilliseconds.<br></p><p><img src=\"@@PLUGINFILE@@/ERP%20decoding.png\" alt=\"ERP Decodinng\" width=\"800\" height=\"716\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p>This method of computational neuroscience is advanced, but very useful for clinicians who are working with a diverse client population. Some of the demographics this testing procedure is particularly useful for include: TBI and Concussion, age-related cognitive decline and dementias, learning disabilities, ADHD, depression and other pathologies where the executive functioning of the individual is thought to be compromised.&nbsp;</p><p>If you are interested in ERPs, check out the Neurofield ERP software program and trainings at ww.neurofield.com.</p><p><br></p><h4>Slow Cortical Potentials</h4><p></p><p><span lang=\"DE\">Slow Cortical Potentials are slow shifts in the EEG that last from 0.3 seconds to several seconds, infra slow oscillations are typically 0.1Hz and lower. These shifts in the EEG reflect the depolarization of large groups of pyramidal cells in the cortex. These slow shifts are caused by the burning of blood glucose, that makes up the hemodynamics of the glial cells.&nbsp;For two decades researchers have proposed that neurons, glial cells, and blood may be regarded as compound generators of these infra-slow bioelectrical phenomena (Hughes, Lőrincz, Parri, &amp; Crunelli, 2011; Zschocke &amp; Speckmann, 1993). Thalamocortical neurons have been observed to exhibit robust infra-slow oscillations (ISOs), in vitro, at approximately 0.005–0.1 Hz (Lőrincz, Geall, Bao, Crunelli, &amp; Hughes, 2009). After a reappraisal of in vivo and in vitro evidence, Crunelli and Hughes (2010) have proposed a three cardinal oscillator model that identifies one cortical and two thalamic sources of infra-slow frequencies. Astrocytes have recently been identified by Hughes et al. (2011) as a source of ISOs in the 0.003–0.1 frequency range. These researchers observed neurons in cat Thalamus succumbing to a cyclic inhibitory influence that they proposed was generated in the slow regime by Thalamocortical astrocytes. These cells create large electro-negative swings when they depolarize. Slow Cortical Potentials (SCP) are changes of cortical polarization lasting several hundred milliseconds to several seconds. SCPs are related to the excitability level of underlying cortical regions. Negative SCP shifts reflect higher cortical excitability while positive shifts reflect reduced excitability or even inhibition. Sheets of cortical neurons are depolarized in the creation of SCPs. It has been hypothesized that in autism spectrum cases, the threshold of depolarization is too high and in ADHD cases, the threshold of depolarization is too low. Additionally, in patients with seizure&nbsp;conditions, large negative potential shifts have been observed moments before a seizure. (ADHD children are taught to increase the negativity of the SCP, while autistic and seizure cases are taught to decrease the negativity of the SCP).<br></span><span lang=\"DE\"></span></p><p><span lang=\"DE\">In Europe Slow Cortical Potential (SCP) neurofeedback is taught by Ute Strehl , who uses a visual to reflect higher arousal (in electro-negative potentials, that is, going up) and lower arousal (in electro-positive potentials, going down). In clinical thresholding, it is important to verbally encourage and reward the patient, especially if they are children.&nbsp;SCP training is a “one size fits all protocol” with the majority of the training done at the vertex. As first developed, the client attempted to produce cortical excitation, a negative DC shift, in the case of ADHD; or cortical inhibition, a positive DC shift, in the case of Epilepsy over the course of many short trials (Birbaumer, 1999; Birbaumer et al., 1994, Kotchoubey et al.,2001 ). More recently SCP training has evolved to train in both negative and positive cortical shifts in the same session with proportions of negative and positive trials dependent on client presentation (Strehl et al., 2006). In clinical interventions, such as epilepsy or ADHD Ute Strehl always implements SCP feedback as a technique in the framework of behavior therapy which is being enumerated by the German statutory health insurance.</span></p><p><span lang=\"DE\">Ute Strehl and colleagues have published extensively in RCT (randomized controlled trials) studies on their work.They have used a slow-wave filter and a 500-millisecond interval moving window. This methodology is available using thought technology equipment and screens (</span><span lang=\"DE\"><a href=\"http://www.thoughttechnology.com/\">www.thoughttechnology.com</a></span><span lang=\"DE\">;&nbsp;<a href=\"https://www.neurocaregroup.com/neuroconn-technologie.html\">https://www.neurocaregroup.com/neuroconn-technologie.html</a>;&nbsp;<a href=\"https://www.mindmedia.com/\">https://www.mindmedia.com/</a>). An important, mandatory feature of SCP feedback is the online artifact control as eye movements and huge EMG actitivty may interfere with EEG activity.</span></p><p><br></p><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',2,1653945057),(28,20,'Alpha Theta Training','',1,'<p></p><h3><a name=\"_Toc3535269\">Alpha-Theta</a></h3><p>Alpha/theta&nbsp;training,&nbsp;in&nbsp;which&nbsp;the&nbsp;goal&nbsp;is&nbsp;to&nbsp;achieve&nbsp;an&nbsp;altered,&nbsp;hypnogogic&nbsp;state&nbsp;of&nbsp;consciousness,&nbsp;useful&nbsp;for&nbsp;therapeutic&nbsp;purposes.&nbsp; During alpha theta training, the participant is typically reclined or laying supine, in a comfortable room in a comfortable position, with their eyes shut, They are listening to auditory feedback (one popular set of sounds is the sounds of ocean waves and the sound of waves upon the shore). The individual in alpha theta training is trained to increased the amplitude of their theta frequencies so that they surpass their alpha frequencies, inducing what is considered a deep state. This increase of theta and decrease of alpha is called a cross-over and is the clinical goal of alpha-theta neurofeedback.</p><p><span style=\"font-size: 1rem;\">Some clinicians use Alpha-Theta neurofeedback only as polish at the end of many neurofeedback sessions, as the accessing of theta while conscious can create abreactions in individuals who are not ready to access the deeper realms where suppressions and repressions reside. On the flip side, this can be a hugely healing protocol for individuals who need to integrate and incorporate the activation behind stress responses.</span></p><h3><a name=\"_Toc35418109\">A diagram showing the concept of an alpha theta crossover, the y-axis related to amplitude</a></h3><p><a name=\"_Toc35418109\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Crossover.png\" alt=\"crossover\" width=\"868\" height=\"476\"><br></a></p><p></p><p>Many of the great minds of our times—artists, musicians, scientists, and geniuses of all sorts—have described arriving at their discoveries and innovations often when in a deep dream-like reverie. The alpha-theta brain wave state that reflects this level of trance teeters on the borderline between consciousness and unconsciousness and is the threshold between alpha and theta—a soft, awake brain wave state. This altered state of consciousness has been called different things by different researchers. Maury (1848) called it “hypnogogia,” Green, Green, &amp; Walters (1970) called it “the reverie state,” and Budzynski (1977) dubbed it “the twilight state.”</p><p>Individuals will often enter this state when daydreaming, resting, meditating, engaging in “mindless” activity (i.e. running, driving long distances), or entering sleep. This state is a calm, relaxed, and unattached presence wherein people report receiving imagery, sounds/music, or thoughts of novelty. Einstein reported coming to the notion of this theory of relativity while daydreaming, observing sunbeams and imagining what it would be like to ride on them (Boyd, 1995). Thomas Edison used to intentionally induce this state to answer his pressing questions by falling asleep in a chair while holding a ball bearing, with a pie tin placed on the ground underneath his hand. Upon entering light sleep, he would drop the ball bearing onto the pie tin, waking him—at which point he would scribble the ideas that arrived in his mind (Robbins, 2000, p. 191).</p><p>In a letter published in 1912, Mozart wrote a colleague about his experience around creativity, music, and this light stage of reverie:</p><p><i>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; When I am . . . completely myself, entirely alone, and of good cheer—say, traveling in a carriage or walking after a good meal, or during the night when I cannot sleep, it is on such occasions that my ideas flow best and most abundantly. Whence and how they come I know not, I cannot force them. . . . All this fires my soul, and provided I am not disturbed, my subject enlarges itself, becoming methodized and defined, and the whole, though it be long, stands almost complete and finished in my mind, so I can survey it, like a fine picture or a beautiful statue, at a glance. Nor do I hear in my imagination the parts successively, but I hear them, as it were, all at once. What a delight this is, I cannot tell! All this inventing, this producing, takes place in a lively dream. (34)</i></p><p>This brain wave state Einstein, Mozart, Edison, and others created their masterpieces in is was likely composed of two frequencies: alpha, which is recorded on an electroencephalogram (EEG) as 9-12 oscillations per second (Hz), and theta, 5-8 oscillations per second (Hz).&nbsp; Alpha theta is used for many clientele populations, including &nbsp;peak performance neurofeedback training. This training is a means of inducing in the performer heightened amplitudes and presence of alpha and theta brain wave states, theorized to bring about “flow” states, or experiences of “being in the zone.” The goal of this type of neurotherapy is to increase the ratio of theta to alpha, encouraging a crossover, whereby the amplitude of theta brainwaves supersedes the amplitude of alpha being produced. In personal neurofeedback practice as clinician, I often incorporate alpha-theta training into neurotherapy sessions once an individual has worked through their major psychological or emotional problems via psychotherapy or other forms of neurofeedback, demonstrating self-regulation. Otherwise there is risk in accessing the unconscious memories residing in theta state and bringing them into conscious awareness while the individual is psychologically unprepared. Alpha-theta training is like a polish, used once a subject displays evidenced psychological readiness to fine-tune their higher-level functioning skills.</p><p>In Egner and Gruzelier’s 2003 study on the enhancement of musicianship in music conservatoires with the aid of neurofeedback, it was discovered that individuals training alpha-theta brainwave states had a positive trend in three criteria of instrumental competence (notably, “perceived instrumental competence, especially rhythmic accuracy”), musicality (notably “stylistic accuracy, interpretive imagination, and expressive range”), and communication (notably “emotional commitment and conviction, ability to cope with the stress of the situation and with deportment”), whereas the study’s control group (without any neurofeedback) evidenced no improvements (p. 3). In the conservatoires’ real-life quantification, the neurofeedback recipients also saw an average a jump of two class grades.</p><p>Another study testing novice singers’ singing abilities as a result of alpha-theta training found similar results in performance communication (specifically “scales of commitment, confidence, enjoyment, attention holding, and deportment”) as well as in the technical areas of “breathing, diction, and pitch.” Lastly, the individuals subject to alpha-theta neurofeedback experienced “increased expressiveness, confidence, and stage presence,” all of which positively corresponded with their respective alpha-theta learning indices (Leach et al., 2008). While these studies are exciting and noteworthy, they are the first of few and there remains to be a lack of science linking alpha-theta brainwave states and musical abilities.</p>Alpha-Theta training is useful for conditions such as alcoholism, PTSD, and trauma, however it behooves the clinician to fully understand the level and depth of the client\'s trauma before beginning treatment. Sometimes when accessing theta content (i.e. during a crossover) a client will have an \"abreaction,\" which is an accessing of repressed memory or emotionally volatile content (e.g. trauma). If your client has a history of developmental trauma or PTSD, it\'s advised they do some psychotherapy before beginning to release traumas.&nbsp; Psychotherapeutic skills like EMDR and Brainspotting are helpful with the traumatized demographic.<br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',4,1654122738),(29,14,'7) Overview of Connectivity','',1,'<p>Synchronization between\r\ncoupled oscillators of whatever kind is known generally as synchrony or\r\ncoupling.&nbsp;In the context of human or animal consciousness, various kinds of neural and\r\nelectromagnetic field synchrony seem to play functional roles. The interaction\r\nbetween oscillations at different frequency bands and at different phase slopes\r\nis generally known as cross-frequency coupling (CFC).&nbsp;</p><p>Connectivity in EEG is measured by coherence, phase, and forms of cross frequency coupling.&nbsp;</p><h4>Coherence</h4><p></p><p>Coherence measures the stability of the phase\r\nrelationship between two time series, calculating the difference between two\r\nsignals measured at the scalp. &nbsp;Coherence\r\nin excess is hypercoherence; coherence in deficiency is hypocoherence. Coherence measures do not\r\nseparate phase and amplitude.&nbsp;</p><p><img src=\"@@PLUGINFILE@@/erroneous%20coherences.png\" alt=\"erroneous coherences\" width=\"600\" height=\"585\" class=\"img-responsive atto_image_button_left\"></p><p>Unfortunately, coherence measures are also apt to be spurious and false positives are likely. The image to the left is of Erroneous coherences.&nbsp; In EEG measures, a linked ears or mastoid reference\r\nused can significantly alter the both the power and phase at each electrode\r\nsite, if a high amplitude source of EEG is at one or more of the temporal\r\nelectrodes. For similar reasons, any common reference coherence data must be\r\ninterpreted cautiously. Even in average references, spuriously large coherences\r\ncan occur from superficial dipoles at large interelectrode differences.&nbsp;&nbsp; Fein et al. (1988) argue the most diligent\r\nway to measure coherences is with reference-free recording methods, while Nunez\r\net al (1997) agree, noting that Laplacians give the best intermediate spatial\r\nrange coherence estimates.&nbsp; Finally , of\r\nimport to valuation of synchrony measures offered, coherence measures do not\r\nseparate phase and amplitude.</p>When coherences are accurate (not false positives), they can indicate the followin<img src=\"@@PLUGINFILE@@/Coherence%20Images.png\" alt=\"Coherence Measures\" width=\"600\" height=\"767\" class=\"img-responsive atto_image_button_left\">g symptoms. Hypercoherence\r\nshows a lack of flexibility in the connection relationships; firings are locked\r\ninto the same rhythm. Imagine soldiers goose-stepping or a crowd clapping in\r\nunison. Hypercoherence is problematic in the sense that it can create “tunnel\r\nvision” or the inability to switch tasks readily. On the other hand, it may\r\nlead to a sort of frenetic distractibility, where nothing gains the complete\r\nattention and the individual always feels “scattered,” “distracted,” and\r\nbusied. The ways in which coherence manifests symptomatically are dependent upon the frequency band they manifest in. Hypercoherence in beta is very different than hypercoherence in alpha, for instance.&nbsp;<br><br><div><!--[if !supportFootnotes]--><h4>LORETA Coherence Measures</h4>\r\n\r\nLoreta computes a&nbsp;<strong>three-dimensional distribution of 2394 voxels of 7x7x7 mm of the generating electric neuronal activity in the grey matter.</strong>&nbsp;A great advantage of this technique is that it isn’t restricted to a certain number of electrodes or electrode locations, and therefore it self-adapts to almost every electrode set-up and EEG measuring device.The measures of coherence and phase can also be taken from Low Resolution Electromagnetic Tomographical Analysis (LORETA), which is a weighted average and the best montage to glean coherences from. Unfortunately, using LORETA in a Z-scored format is a misuse, since inputting scalp z-transformed-maps will not output LORETA (current density) z-transformed-values. This invalid inputs to LORETA violate the mathematics and the physics underlying all computations.</div><div><img src=\"@@PLUGINFILE@@/LORETA%20Coherence%20.png\" alt=\"LORETA Coherence\" width=\"800\" height=\"758\" class=\"img-responsive atto_image_button_left\"><br><hr align=\"left\" size=\"1\" width=\"33%\">\r\n\r\n<!--[endif]-->\r\n\r\n<div id=\"ftn1\">\r\n\r\n<p><br></p>\r\n\r\n</div>\r\n\r\n</div><br><p></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><h4><br></h4><h4>Phase</h4><p>Phase is any one point or portion in a recurring series\r\nof changes, as in the changes of motion of one of the particles constituting a\r\nwave or vibration. There are metrics of phase in EEG an Quantitative EEG, one of the more commonly used is \"phase lag.\" We expect a certain amount of phase lag between oscillations of the brain (for instance, can you see the lag between all three lines below? The black is the first wave, followed by the dark blue and then the light blue. Phase lag metrics are measured by phase reset, which is&nbsp;<img src=\"@@PLUGINFILE@@/Phase.png\" alt=\"Phase\" width=\"600\" height=\"409\" class=\"img-responsive atto_image_button_left\">the&nbsp;<span style=\"font-size: 1rem;\">time it takes for phase to lock (come into coherence) and shift (fall out of coherence) and the begin to lock again. The measure of how long these mechanisms take are measures of phase lag, as seen in normative databases, such as the Neuroguide image of phase lag below.&nbsp;</span></p><p>Blue phase lag is considered \"hypo phase lag\" and that means there is not enough phase lag (too much phase lock), a very similar measure to hypercoherence.&nbsp;</p><p>Red phase lag is considered \"hyper phase lag\" and that means there is too much phase lag (not enough phase lock), very similar to hypocoherence.&nbsp;</p><p><img src=\"@@PLUGINFILE@@/Phase%20Lag.png\" alt=\"Phase Lag\" width=\"700\" height=\"512\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p><br></p><h4>Other Forms of Cross Frequency Coupling (CFC)</h4><p>Cross-frequency couplings are assessed by computing complex-valued coherences between Fourier transform coefficients at different frequencies. This methods detects all forms of amplitude-amplitude, phase-amplitude, and phase-phase coupling / information flow.&nbsp;<br></p><h4>Phase-Phase Cross Frequency Coupling (PPC)</h4><p><img src=\"@@PLUGINFILE@@/Phase%20Phase%20Coupling%20%281%29.png\" alt=\"\" role=\"presentation\"><p>Phase-phase coupling (PPC), also known as cross frequency\r\nphase synchrony (CPS), is one type of CFC that is commonly focused upon as\r\nfunctionally relevant for the workings of the brain and thus for consciousness\r\n(Siebenhühner et al. 2020).\r\nIn phase-phase coupling, we see the phase of a slower carrier wave align with\r\nand serve as the carrier mechanism for a faster wave. This has been seen widely\r\nwith theta carrier waves and gamma waves, a phenomenon that is thought to be\r\nfundamental in the encoding of memory (Scheffer-Teixeira &amp; Tort, 2016) .\r\nPhase-phase coupling is amplitude independent and is reflective of an\r\n“autonomous continuous time system” (Rosenblum et al., 1996). PPC is thought to\r\nbe a frequent type of neural temporal coding (Jirsa and Muller, 2013).&nbsp;</p></p><h4>Amplitude-Amplitude Coupling (aka Power-Power Coupling)</h4><p><img src=\"@@PLUGINFILE@@/Amplitude%20Amplitude%20Coupling.png\" alt=\"Amplitude amplitude coupling\" width=\"300\" height=\"154\" class=\"img-responsive atto_image_button_left\"><p>Most quantitative analyses of EEG and MEG use fast Fourier\r\ntransformation (FFT) to compute power spectral density (PSD). However, this\r\nmeasure fails to show the fast temporal dynamics that EEG brain-imaging is\r\nbest-suited for. This temporal resolution issue has been resolved through calculating\r\nthe spectral covariance of power-power coupling (PPC). Power-power coupling reveals how\r\namplitude (power) modulations in one frequency are affected by amplitude modulations\r\nin the other frequency. The coupling can be found within different frequencies,\r\nor within the same frequency. The measurement of PPC is seen not through the quantitative\r\nanalysis of FFT, but can be seen through Independent Component Analysis (ICA) via\r\nthe -Power-Power Coupling Analysis Toolbox (PowPowCat), a free open-source\r\ntoolbox for EEGLAB (Thammasan &amp; Miyakoshi, 2020).</p>\r\n\r\n<p>&nbsp;<img src=\"@@PLUGINFILE@@/powerpowercoupling.png\" alt=\"poeerpowerciupling\" width=\"700\" height=\"480\" class=\"img-responsive atto_image_button_left\"></p>\r\n\r\n<p>When oscillations of two different frequencies covary in\r\ntime, power-power coupling may occur. This measurement is depicted in a\r\ncomodulogram, also known as a comodugram (Figure xx). The other detail provided\r\nvia this software graphical user interface include the time series of the\r\ncombination of the two selected frequency bins (specified by cursor position);\r\nthe scatter plot of the power spectral diagram, the correlation coefficient of\r\nthe two chosen frequencies, and the power spectrum density by spectrogram. This\r\ntype of measurement is uniquely beneficial in detecting thalamo-cortical\r\ndysrhythmias, as seen in Parkinson’s Disease, tinnitus, depression, and some\r\nforms of neuropathic pain (Vanneste et al., 2018).</p><p><br></p><p><p><i>The above image shows the interactive graphical\r\nuser (GUI) interface of power-power coupling analysis toolbox (PowPowCat),\r\nshowing the spectral covariance in which cross-frequency points within an\r\nindependent component correlate via a correlation coefficient, “r.”</i></p><br></p></p><h4>Phase-Amplitude Coupling (PAC)</h4><p><img src=\"@@PLUGINFILE@@/Phase%20Amplitude%20Coupling.png\" alt=\"Phase Amplitude Coupling\" width=\"300\" height=\"368\" class=\"atto_image_button_left\"><br></p><p><p>Phase is not the only important dynamic of coupled oscillatory\r\nphenomena. The second key variable is amplitude, also known as power. Phase and\r\namplitude can be meaningfully correlated and are functionally relevant to the\r\nworkings of the brain and consciousness (Siebenhühner et al. 2020). PAC usually\r\nrefers to a correlation\r\nbetween the amplitude of faster rhythms (high gamma range) and the phase of\r\nslower rhythms (2-12Hz range) (Florin &amp; Baillet, 2015; Canolty et al.,\r\n2006; Tort et al., 2008, 2009; Voytek et al., 2010).</p>\r\n\r\n<p>Jensen\r\nand Colgin (2007) believe, “gamma oscillations might emerge at a particular\r\nphase of the theta cycle and thereby recruit cell assemblies involved in\r\nprocessing at that time.”&nbsp;\r\nIn most cases of this phenomenon, the slower oscillation exerts influence and\r\nmodulates the amplitude of the faster oscillation. Lakatos et al. (2005)\r\nhypothesized a “hierarchical” organization of EEG oscillations exists in this\r\nregard. This\r\ntype of coupling is commonplace in computational neuroscience, second only to\r\nphase-phase coupling and has been thought of as an “integration mechanism”\r\nbetween rate and temporal coding—rate attributed to amplitude and temporal\r\nattributed to phase (Jirsa et al., 2013).</p>\r\n\r\n<p>An example of PAC has been found\r\nbetween many frequencies. with gamma and theta band CFC. Bagur et al. (2018)\r\nexamines data suggesting that theta frequency band (slower) modulates gamma\r\nfrequency band (faster) amplitude, with each theta cycle comprising a single\r\npacket of gamma information from the sensory cortex. Buzsaki (2010, 2012)\r\nsuggests that these gamma packets may comprise a kind of brain syntax for\r\nordering and integrating information from different parts of the brain, while\r\nDe Ridder (cite) postulates that memory and predictions are encoded in\r\noscillations (memory being the low frequency oscillations and prediction and\r\nprediction error being the high frequency oscillations. Likewise, Lisman (1995)\r\nand Jensen (2006) believe the nesting of fast frequencies into slower one\r\npredicts memory, while others have postulated nesting permits prediction\r\n(O’Keefe, 1993; Jensen, 1996). Another function tied to gamma band activity\r\nsynchronized with thalamo-cortical activity is conscious auditory perception (Crone,\r\n2001, Joliot, 1994; Llinas, 1998).</p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1655298142),(30,14,'8) Basic Neuroanatomy of ascending sensory pathways','<p><br></p><p></p>\r\n<p></p>',1,'<p>\r\n</p>\r\n<div>\r\n    <div>\r\n        <div>\r\n            <div>\r\n                <h3>Ascending Tracts</h3>\r\n                <p>The&nbsp;<strong>ascending tracts</strong>&nbsp;refer to the neural pathways by which sensory information from the peripheral nerves is transmitted to the cerebral cortex. In some texts, ascending tracts are also known as somatosensory\r\n                    pathways or systems.</p>\r\n                <p>Functionally, the ascending tracts can be divided into the type of information they transmit – conscious or unconscious:</p>\r\n                <ul data-spx-slot=\"1\">\r\n                    <li><strong>Conscious tracts</strong>&nbsp;– comprised of the dorsal column-medial lemniscal pathway and the anterolateral system.</li>\r\n                    <li><strong>Unconscious tracts</strong>&nbsp;– comprised of the spinocerebellar tracts.</li>\r\n                </ul>\r\n                <p>In this article, we shall look at the anatomy of the ascending tracts, and consider their clinical implications.</p>\r\n            </div>\r\n        </div>\r\n    </div>\r\n</div>\r\n<div>\r\n    <div>\r\n        <div>\r\n            <div>\r\n                <h2><span id=\"The_Dorsal_Column-Medial_Lemniscal_Pathway\">The Dorsal Column-Medial Lemniscal Pathway</span></h2>\r\n                <p>The&nbsp;<strong>dorsal column-medial lemniscal</strong>&nbsp;pathway (DCML) carries the sensory modalities of fine touch (tactile sensation), vibration&nbsp;and&nbsp;proprioception.</p>\r\n                <p data-spx-slot=\"1\">Its name arises from the two major structures that comprise the DCML. In the spinal cord, information travels via the dorsal (posterior) columns. In the brainstem, it is transmitted through the&nbsp;<strong>medial lemniscus</strong>.</p>\r\n                <p>Here is a video for this pathway:</p>\r\n            </div>\r\n        </div>\r\n    </div>\r\n</div>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/xRJypyXi7dU\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><br><br>\r\n<h2><span id=\"The_Anterolateral_System\">The Anterolateral System</span></h2>\r\n<p>The anterolateral system consists of two separate tracts:</p>\r\n<ul data-spx-slot=\"1\">\r\n    <li><strong>Anterior spinothalamic tract</strong>&nbsp;– carries the sensory modalities of crude touch and pressure.</li>\r\n    <li><strong>Lateral spinothalamic tract</strong>&nbsp;– carries the sensory modalities of pain and temperature.</li>\r\n</ul>\r\n<p>Here is a video on this system:</p><br>\r\n<p></p>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/gcOqv0uzyAQ\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><br>\r\n<h2><span id=\"The_Spinocerebellar_Tracts_8211_Unconscious_Sensation\">The Spinocerebellar Tracts – Unconscious Sensation</span></h2>\r\n<p>The DCML and the anterolateral tracts transmit conscious sensations, such as pain, touch and temperature. The tracts that carry&nbsp;<strong>unconscious proprioceptive</strong>&nbsp;information are collectively known as the<strong>&nbsp;spinocerebellar tracts</strong>.\r\n    Although we cannot physically acknowledge these signals, they help our brain co-ordinate and refine motor movements.</p>\r\n<p data-spx-slot=\"1\">They transmit information from the muscles to the cerebellum.</p>Here is a video on this final tract:<br><br>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/Re8O8qfp2DY\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1653945278),(31,15,'1) Basic Metrics and Terminology of Electronics','',1,'<h3><b>How is an EEG Recorded?</b></h3><p><img src=\"@@PLUGINFILE@@/Differential%20amplification%20.png\" alt=\"Differential amplification\" width=\"450\" height=\"128\" role=\"presentation\" class=\"atto_image_button_middle\"></p><p><span style=\"font-size: 1rem;\">An EEG is recorded using a differential amplifier and electrodes. A differential amplifier is a type of electronic amplifier that amplifies the difference between two input voltages but suppresses any voltage common to the two inputs. In EEG recordings and neurofeedback, a differential amplifier is used to produce each channel or trace of activity.&nbsp;</span></p><p><span style=\"font-size: 1rem;\">There are many different brands of amplifiers in the fields of neurotherapy and neurology and the decision of what kind of amplifier to buy is one of the first major decisions a newcomer to these fields usually makes. Some amplifiers are noisier than others, some are higher quality than others, like any other product. Some amplifiers are used for neurofeedback alone and some amplifiers are used for EEG and QEEG collection, as well as neurofeedback. It behooves the new neurotherapy practitioner to do research to determine which amplifier and neurotherapy modality best suits them. This course is intended to help clarify that process.&nbsp;</span></p><p></p><h3><b>Differential Amplifiers</b></h3><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Neurofield%20Amp.png\" alt=\"Neurofield Amp\" width=\"350\" height=\"207\" class=\"img-responsive atto_image_button_left\"></span><p></p><p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Brainmaster%20amp.png\" alt=\"Brainmaster amp\" width=\"300\" height=\"207\" class=\"img-responsive atto_image_button_middle\"></span></p><p></p><p><b><span><u><img src=\"@@PLUGINFILE@@/Deymed%20amp.png\" alt=\"Deymed amp\" width=\"300\" height=\"332\" class=\"img-responsive atto_image_button_middle\"><br></u></span></b></p><p><b style=\"font-size: 1rem;\"><span><b style=\"font-size: 1rem;\"><span><b style=\"font-size: 1rem;\"><span><b style=\"font-size: 1rem;\"><span>Differential amplifiers&nbsp;</span></b><span style=\"font-size: 1rem; font-weight: 400;\">measure the voltage difference between the two signals at each of its inputs--that of the active vs. the reference electrode, each pair using a third electrode, the <b>ground electrode</b> to literally \"ground\" the recording.&nbsp;Basically, a grounding electrode establishes a direct connection to the earth or ground.</span><span style=\"font-size: 1rem; font-weight: 400;\">&nbsp;</span></span></b></span></b></span></b><br></p><p>EEG amplifiers&nbsp;<span style=\"font-size: 1rem;\">amplify separately (1) the voltage between one recording site and the ground electrode and (2) the voltage between a second recording site and the ground electrode. Then the electronics subtract one from the other (producing the difference between the two). The subtraction process removes other signals (e.g., 60 Hz line noise) that is present and common to both recording electrodes. The subtraction process itself is imperfect, so that some of the contaminants remain. Removing the contaminants and the EEG activity common to both channels is called<u>&nbsp;</u></span><span xmlns:xlink=\"http://www.w3.org/1999/xlink\" style=\"font-size: 1rem;\"><b style=\"\"><u>common mode rejection</u>&nbsp; or common mode rejection ratio (CMRR)</b></span><span style=\"font-size: 1rem;\">. The higher the CMRR, the better the amplifier system excludes unwanted contaminants. A high quality amplifier will display a very clean EEG signal without the use of filtering.&nbsp;</span><span style=\"font-size: 1rem;\">The resulting signal is amplified and then displayed as a channel of EEG activity.</span></p><p></p><p>The amplifier records the difference between a scalp electrode and a reference electrode. Different montages have different reference electrodes. The image below is an example of a bi-polar montage, such as the type used in many forms of single channel neurofeedback (methods like the Othmer method). in EEG assessment, bi-polar montages are very god for spotting local differences between neighboring channels.</p><p><img src=\"@@PLUGINFILE@@/Differential%20amplification%202.png\" alt=\"Differential amplification 2\" width=\"500\" height=\"465\" class=\"img-responsive atto_image_button_middle\"></p><h3><span style=\"font-size: 1.715rem;\">Analog vs. Digital</span><br></h3><p>Up until the 1990s, many people in neurology practices were using analog EEG recording systems. These were large systems that were the mainstay of neurological practices that cranked out EEG on paper, with ink pens scrawling back and forth.&nbsp; Paper record-keeping for patients\' EEGs was the big downside to analog EEG; modernity has led the fields of neurotherapy and neurology to digital EEG processing.</p><p><img src=\"@@PLUGINFILE@@/analog%20EEG.jfif\" alt=\"Analog EEG\" width=\"350\" height=\"283\" class=\"img-responsive atto_image_button_left\">Digital EEG came about in the 90s and has many advantages over analog EEG.&nbsp;Digital recording takes advantage of modern microprocessor costs and general flexibility. Digital copies of EEG are easy to save and share. More specifically, digital EEG allows review with different montages, filters, vertical scaling (gain or sensitivity), and horizontal scaling (e.g., time resolution or compression). It has replaced warehousing or microfilming paper records and allows for electronic exchange of EEGs. Finally, digital EEG makes possible the routine application of a variety of complex signal-processing tasks, such as frequency analysis, automated seizure detection, statistical quantitative analysis, and dipole source localization. Because of digital EEG, we have quantitative EEG and the amazing field of computational neuroscience.&nbsp;</p><h3><span style=\"font-size: 1.715rem;\"><br></span></h3><h3><span style=\"font-size: 1.715rem;\"><br></span></h3><h3><span style=\"font-size: 1.715rem;\">Impedance</span><br></h3><p>Impedance is a measure of the impediment to the flow of current, measured in ohms or kilo ohms (kohm). Larger numbers mean higher resistance to current flow. The higher the impedance of the electrode, the smaller the amplitude of the EEG signal. In EEG studies, should be at lest 100 ohms or less and no more than 5 kohm. In neurofeedback, often 15kohm is permissible.</p><p>Checking impedance is a fundamental part of working with EEG and you will undoubtedly become familiar with checking impedances in your neurotherapy career. To get good impedance means getting good connectivity, which allows for a clean recording.&nbsp;</p><h3>What is Recorded in EEG?</h3><p>Synchronous brainwaves from the brain are recorded in EEG, which are seen due to volume conduction.&nbsp;<strong>Volume conduction </strong>can be defined as the transmission of electric or magnetic fields from an electric primary current source through biological tissue towards measurement sensors.&nbsp;Volume conductor models are a basis for&nbsp;source analysis&nbsp;in&nbsp;Electroencephalography (EEG)&nbsp;and&nbsp;Magnetoencephalography (MEG).&nbsp;<img src=\"@@PLUGINFILE@@/Volume%20Conduction.gif\" alt=\"Volume Conduction\" width=\"386\" height=\"302\" class=\"img-responsive atto_image_button_right\"><br></p><p><span>The activity that is measured in EEG&nbsp;is the result of movements of ions, the so-called&nbsp;<span style=\"\">impressed currents</span>, within the&nbsp;cortex&nbsp;sheet of the human brain. The&nbsp;<span style=\"\">current dipole</span>&nbsp;is generally used as the&nbsp;\'\'atomic structure\'\'&nbsp;of the impressed current.&nbsp;</span></p><p>The current <b>dipole</b> causes ohmi<span>c&nbsp;<span style=\"\">return currents</span>&nbsp;to </span>flow through the surrounding medium. The EEG&nbsp;measures the potential differences of the return currents at the scalp surface. The reconstruction of the impressed primary current distribution from measured surface fields is called the<span><span style=\"\"><u style=\"\"><b>&nbsp;</b><span style=\"\">inverse problem</span><b>.</b></u></span></span> Its solution requires the simulation of the field distribution for a current dipole in the corresponding volume conductor using the quasi-static Maxwell equations, the so-called&nbsp;<span><u>forward problem</u></span>. All inverse methods (e.g., dipole fit and scan methods as seen in Independent Components Analysis, current density reconstructions such as LORETA) are based on the solutions of the forward problem and are thus influenced by the degree of realism in the modeling of the volume conductor.</p><h3>Alternating Current vs. Direct Current</h3><p>Both AC and DC describe types of current flow in a circuit. In&nbsp;<b><span>direct</span>&nbsp;current (DC)</b>, the electric charge (current) only flows in one direction. Electric charge in alternating current (AC), on the other hand, changes direction periodically. All brainwaves are alternating current brainwaves, the brain does not make DC.<br></p><p>AC can come in a number of forms, as long as the voltage and current are alternating. If we hook up an oscilloscope to a circuit with AC and plot its voltage over time, we might see a number of different waveforms. The most common type of AC is the sine wave. The AC in most homes and offices have an oscillating voltage that produces a sine wave.<br></p><p>Direct current is seen in High Voltage Direct Current (HVDC) transmission lines, these are the power lines that often traverse large stretches of land. The reason for this is there is little energy loss when DC is used, and the electricity can literally move at the speed of <img src=\"@@PLUGINFILE@@/HVDC.JPG?time=1636045837032\" alt=\"HVDC\" width=\"300\" height=\"206\" class=\"img-responsive atto_image_button_left\">light.&nbsp;<span style=\"font-size: 1rem;\">In the field of neurotherapy and neurology, there are DC coupled amplifiers and AC coupled amplifiers.&nbsp;An electronic amplifier takes in a weak signal and makes it stronger. To do this, you need active components, such as vacuum tubes, transistors or integrated circuits, and a power source.&nbsp;A steady DC voltage that gets mixed with an AC signal is called an offset. DC amplifiers amplify the whole signal, both AC and DC parts. This creates noise and other problems for music, so sound engineers usually use AC amplifiers.&nbsp;A DC amplifier accepts all parts of a signal, AC and DC. Engineers call this DC coupling or direct coupling.&nbsp;An amplifier with reactive components in the signal path, such as transformers or capacitors, blocks DC and permits only AC to pass through. Amplifiers with these components are called AC-coupled.</span></p><p>DC amplifiers are used in science, medicine and engineering whenever people deal with DC and slow-moving signals. Sound engineers may use DC amplifiers when they need excellent low-frequency response.&nbsp;Home stereos make up the biggest use of AC amplifiers. Radio and television engineers use very-high-frequency AC amplifiers. The AC coupling conveniently rejects noisy DC signals.<br></p><h3>tDCS and tACS</h3><p><img src=\"@@PLUGINFILE@@/Stimulation%20Modalities.png\" alt=\"Stimulation Modalities\" width=\"800\" height=\"415\" class=\"atto_image_button_middle\"></p><p>Transcranial Direct Current Stimulation and Transcranial Alternating Current Stimulation are two forms of neuromodulation that allow clinicians to stimulate the individuals brain or body. This is a form of neurotherapy and a very effective one, at that. Many neurotherapy practitioners incorporate these stimulation modalities into their practices. The Neurofield Genesis is a stimulation device that allows for all of the above forms of simulation in clinical practice (as well as pink noise and brown noise). This topic will be covered in greater depth in chapter 9. In this image, you see many forms of alternating current (continuous sine wave, triangle wave, square wave, random noise, and pulsed waves. DC is direct current and, thus, does not have a frequency.&nbsp;</p><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',17,1654208223),(32,23,'Ethics and Legalities of Practice','',1,'<div><div><div><div id=\"page-content\"><div><div><div id=\"region-main-box\"><section id=\"region-main\"><div role=\"main\"><h3><a name=\"_Toc31009226\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">PREAMBLE</a></h3><div><div><p>This module covers all ethical and professional considerations for neurotherapy clinicians and technicians. The practice of neurotherapy is both an art and a science. It will vary in terms of approach, modality, method of delivery, and services provided. This chapter covers a code of ethics that neurotherapist need adhere to. When working with patients, may situations can arise; if a situation is not covered in this chapter on ethics, it does NOT mean that ethics do not apply. While the specific wording behind these standards is important, it is the spirit and intent of these standards which must be applied to situations. Violation of these standards by any BCN Certified Practitioner or neurotherapist ought to be brought to the attention of the BCIA, at jcrawford@bcia.org,&nbsp;<strong>(720) 502-5829.</strong></p><p>Neurotherapy members are encouraged to apply for membership to either the AAPB (Association of Applied Psychophysiology and Biofeedback) or ISNR (international Society for Neurofeedback and Regulation) for belonging to a larger board and for inclusion in a <img src=\"@@PLUGINFILE@@/ISNR.jfif\" alt=\"ISNR\" width=\"297\" height=\"170\" class=\"img-responsive atto_image_button_left\">group of colleagues and professionals engaging in the same business. The professional standards adhered to by the professional organizations of neurofeedback professionals all maintain the highest ethics, values of competence, promotion of intellectual freedom, respect, integrity, honesty, fairness, and trustworthiness.</p><p><img src=\"@@PLUGINFILE@@/AAPB.png\" alt=\"AAPB\" width=\"288\" height=\"175\" class=\"img-responsive atto_image_button_right\"></p><p>Because the trade organizations supporting and advocating for neurofeedback professionals are committed to the protection of human rights, they strive to maintain respect amongst other professional communities, fostered by professionalism, integrity and dignity.&nbsp; Clinicians must hold themselves accountable for their clients welfare as it pertains to the their neurotherapy regimens, and they mist limit their services only to those areas in which they have expertise and are competent.</p><p>The ISNR\'s Guidelines for the practice of Neurofeedback as as follows:</p><p></p><div><div><div><div><h2>ISNR\'s Guidelines For Practice</h2></div></div></div></div><div><div><div><div><h2><i>Purpose</i></h2><div><div><p><i>These guidelines are intended to provide a reference to both practitioners and the public with regard to basic methods for delivery of neurofeedback, also known as EEG Biofeedback. These guidelines are an extension of the Code of Ethical Principles and Professional Conduct of the International Society for Neurofeedback and Research (ISNR) which can be found on the ISNR.org website.</i></p></div></div></div></div></div></div><div><div><div><div><h2><i>The Practice of Neurofeedback</i></h2><div><div><p><i>Neurofeedback developed as a multidisciplinary treatment modality, and is now practiced by a wide variety of providers who may or may not be licensed healthcare professionals who treat mental or other illnesses. Its range of practice includes assessment and treatment for conditions diagnosed by licensed healthcare providers, training for optimal performance (e.g., among athletes, executives, students, performing artists, and other healthy individuals), and both clinical and applied scientific research.</i></p><p><i>In general, neurofeedback involves placing sensors on the scalp of the individual, and connecting the sensors to an amplifier and computer. Through these connections, the electrical activity of the brain is recorded, and then presented back to the individual on the computer screen in the form of a video game or soundtrack that changes depending on what state the brain is in. This is the “feedback” aspect of neurofeedback that enables the individual to change their brain function and keep the game or sound on more. The means by which this signal is displayed and controlled is the responsibility of the neurofeedback practitioner and should be done in accord with the guidelines below.</i></p></div></div></div></div></div></div><div><div><div><div><h2><i>Training and Credentials for Neurofeedback Practitioners</i></h2><div><div><p><i>Membership in ISNR and certification by the Biofeedback Certification International Alliance (BCIA) are voluntary and help demonstrate to the public that a neurofeedback provider is able to provide ethical and competent training. When training objectives include the treatment of a diagnosed mental or other health condition and the delivery of a regulated assessment or intervention, it helps demonstrate to the public that the provider is able to deliver ethical and competent neurofeedback training when the provider is licensed by a government-recognized health profession board, and the provider’s scope of practice with their professional board includes assessment and intervention for that diagnosed condition. Regulations regarding licensure and scope of practice are determined and enforced by various governmental agencies, depending on state, country, or province. Consumers should ascertain that the practitioner has appropriate credentials, training, experience, and licensure to treat their problem, or is supervised by someone who does.</i></p></div></div></div></div></div></div><div><div><div><div><h2><i>Guidelines</i></h2><div><div><p><i>The following guidelines are applicable to neurofeedback practitioners regardless of client background or training objective.</i></p><p><i>ISNR members:</i></p><ul><li><p><i>Follow the ethical principles of the International Society for Neurofeedback and Research and any other professional organization to which s/he might belong.</i></p></li><li><p><i>Accurately represent their training and any professional qualifications and/or licenses they have achieved, and disclose relevant limitations.</i></p></li><li><p><i>Provide neurofeedback training only for those problems or goals for which they are competent, as demonstrated by their training, experience, licensure, or supervision.</i></p></li><li><p><i>Provide neurofeedback training for the treatment of diagnosed mental or other health conditions only if they are regulated healthcare practitioners whose scope of practice includes the diagnosis and treatment of the specific client population, and who are further trained or supervised in the application of neurofeedback for those clients.</i></p></li><li><p><i>When an unlicensed neurofeedback provider is assessing a client and the severity or complexity of the problem suggests that a diagnosable mental health problem or medical illness may be related to the goal being addressed by neurofeedback, then it is prudent for the provider to discuss this possibility with the client, review the limits of their practice, encourage the client to consult with their family physician or licensed healthcare providers, and document the discussion.</i></p></li><li><p><i>Maintain their competency through continuing education.</i></p></li><li><p><i>Regularly seek consultation and supervision for cases in order to assure themselves and the client that training is in keeping with current knowledge and practice.</i></p></li><li><p><i>Document their client’s consent to the specifics of training, including where and how the client will be touched, acknowledgment of training benefits, risks, and costs.</i></p></li><li><p><i>Accurately represent the degree of scientific support reported in peer- reviewed publications for assessment and training methods for the various problems to which neurofeedback training may be applied.</i></p></li><li><p><i>If technicians are used, document the client understanding of the technician’s qualifications, role, and degree of supervision.</i></p></li><li><p><i>Document the client’s consent for their data to be used for research and/or educational purposes, if applicable.</i></p></li><li><p><i>Document their client’s acknowledgement of the limits of confidentiality.</i></p></li><li><p><i>Document their client’s acknowledgment that training will not necessarily achieve agreed upon goals, either completely or at all.</i></p></li><li><p><i>Further document the client’s acknowledgment that unexpected changes in the client’s experience or behavior may occur during&nbsp;the course of training which may or may not be related to the training itself, and that in those cases it is important for the client to inform the neurofeedback provider so that the training methods can be either adjusted or discontinued, if necessary, and the unexpected changes can be appropriately addressed.</i></p></li><li><p><i>Provide training regardless of race, creed, color, nationality, gender, sexual orientation, religion, or social affiliation.</i></p></li><li><p><i>Collaborate with their clients to develop measurable training goals, a clear plan for training, and methods for measuring progress toward those goals. This collaboration includes regular review of progress with the client with the objective of asking for their decision regarding whether the benefit of continuing training merits the cost.</i></p></li><li><p><i>Carry out effective practices for maintaining good hygiene, applying electrodes and establishing an adequate electrical connection, and maintaining software and hardware in good and up-to-date condition.</i></p></li><li><p><i>Use hardware and software that is safe, accurate, and effective for the purpose to which it is applied. Equipment which meets the IEEE (Institute of Electrical and Electronics Engineers) standards or has been FDA registered is recommended for clinical use.</i></p></li><li><p><i>Carefully assess and document the benefits, risks, and the abilities of the person who may conduct remote or home training, before such training is begun. In general, home training should be discouraged for conditions with a clinical diagnosis. Where it is chosen, careful attention must be given to the training and supervision of the person who will be responsible for performing the neurofeedback sessions at the home. Additional full disclosure and informed consent of potential problems, how and when to report them, and methods to resolve them should be discussed, and the client’s understanding of these documented with their signature. Steps to prevent or limit the use of neurofeedback software and hardware beyond their intended purpose should be documented. The issue of performing services outside of one’s&nbsp;geographic region of license or certification must be taken into consideration.</i></p></li><li><p><i>Plan and carry out neurofeedback training that is based on scientifically validated principles and methods.</i></p></li><li><p><i>Plan and carry out an organized course of neurofeedback that is based on an initial assessment that is adequate for the presenting problem and goal, including a pre-training EEG assessment.</i></p></li><li><p><i>Provide therapeutic support, coaching, and direct supervision during client neurofeedback training that is sufficient to achieve the agreed- upon goals of the client’s training. Document the client’s understanding of the degree to which the individual who is responsible for training will be present during training.</i></p></li></ul></div></div></div></div></div></div><br><p></p><h3>Education Necessary for BCIA - Certification</h3><p></p><p><strong>To qualify for the BCN,</strong>&nbsp;you must demonstrate a Bachelor’s level degree in a health care related field. Approved health care fields include: psychotherapy, psychology, nursing, (including 2-year registered nurses with license; not including LVNs or LPNs), physical therapy, occupational therapy, rehabilitation, social work, counseling, chiropractic, exercise physiology, recreational therapy, speech pathology, physician’s assistant (proof of certification or license needed), and sports medicine.</p><p><strong>The following fields require a master’s degree:</strong>&nbsp;music therapy and counseling education (M.Ed. in counseling). Appropriately credentialed doctors of medicine are also accepted. Degrees in health care fields other than those listed above must be submitted to the Certification Review Committee. BCIA will consider requests for special review for the demonstration of equivalency for most of our requirements, including prerequisite education. For answers to eligibility questions, please contact:&nbsp;<a href=\"mailto:info@bcia.org\" target=\"_blank\" rel=\"noopener\">info@bcia.org</a>.</p><p>The BCIA\'s Professional Standards and Ethical Principles of Biofeedback can be found <a href=\"https://bcia.memberclicks.net/assets/docs/ProfessionalStandardsAndEthicalPrinciplesofBiofeedback.pdf\">here</a>.</p><p></p><h3><a name=\"_Toc31009227\">RESPONSIBILITY TO PATIENT WELFARE</a></h3><p>The goal of the neurotherapist is to advance the patient’s well being and maintain their best interests at all times.</p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Licensure</span></p><p>Anyone practicing neurofeedback ought to be under the supervision of a licensed health-care provider, unless they themselves are licensed. Approved health care licenses include RN, Psychologist, PsyD, Psychotherapist (LMFT, LPCC), MD, OD, Chiropractic Doctor, OT, LCSW, PT, and others. If you are unsure if your license will allow you to practice neurofeedback without a supervisor, contact: info@bcia.org.&nbsp;</p><p>If you choose to practice neurofeedback without a healthcare license, you cannot legally treat any medical pathology or psychopathology. If someone comes to you for the treatment of any diagnosis (i.e. depression, anxiety, ADHD, etc., you must refer out). It is mandatory that you disclose to your clients, before beginning any work with them, that you are unlicensed and cannot legally treat any medical or psychological disorder. This disclosure ought be made in written format, where the client signs their acknowledgement. Many people who are unlicensed practice Peak Performance neurofeedback, or neurofeedback on healthy individuals.</p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Equal Access Health Care</span><br></p><p>A principle of equal access to health care demands that every person who&nbsp;<b>shares the same type and degree of health need</b>&nbsp;must be given an equally effective chance of receiving appropriate treatment of equal quality so long as that treatment is available to anyone. This means that regardless of sex, race, gender, weight, income bracket, etc., all are afforded the same level of health care.&nbsp;<br></p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Scope of Practice</span><br></p><p>Neurotherapy services should be limited to the practice standards and guidelines of one\'s license or the license of their supervisor. If a neurotherapist has sufficient training in a modality of treatment (demonstrating certification or courses attended for the treatment of a condition or modality of treatment) and familiarity with a client population, they may practice neurofeedback as long as the treatment of the condition is within the limit of their license. For instance, the use of alpha/theta neurofeedback is helpful in peak performance, meditation enhancement, and stress regulation. For these demographics, a BCN-certified neurotherapist can work with&nbsp; individuals using alpha-theta neurofeedback.&nbsp;</p><p><a name=\"_Toc31009228\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Non Discrimination</a><br></p><p>Neurotherapists will not discriminate or deny services to anyone based upon religion, gender identity,&nbsp; sexual orientation, ethic or national origin, race, socioeconomic status, or disability. Within reason, neurotherapists make accommodations to treat all individuals within their scope of practice. If a neurotherapist believes someone is outside of their scope of practice (e.g. an infant), they will do their best to find a suitable referral for those seeking help.</p><p><a name=\"_Toc31009229\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Dual Relationships</a><br></p><p><img src=\"@@PLUGINFILE@@/Dual%20Relationships.jpg\" alt=\"Dual Relationships\" width=\"400\" height=\"262\" class=\"atto_image_button_right\"><span style=\"font-size: 1rem;\">A dual relationship is one that occurs outside of the neurotherapy clinic as a separate and distinct relationship during or after the termination of the neurotherapeutic relationship. Neurotherapists avoid dual relationships with patients that are able to impair professional judgment, as they are aware of their influential position in the patient-therapist dynamic. Not all dual relationships are unethical and some dual relationships cannot be avoided.</span></p><p><a name=\"_Toc31009230\">Unethical dual relationships</a>&nbsp;are those wherein a neurotherapist borrows money from a patient, hires a patient, engages in business ventures with a patent, or enters a close personal relationship with a patient (this applies to patient’s spouses, partners and family members, as well). Sexual contact, intimacy or intercourse with a patient <u>during the therapeutic relationship or two years following the relationship</u> is unethical and strictly prohibited. If a neurotherapist engages in intimacy with a former patient or their spouse or partner, or immediate family member, within two years of the termination of the patient-therapist relationship, the neurotherapist risks the revocation of their quantitative EEG diplomacy and/or their board certification in neurotherapy. This type of conduct is considered harmful and potentially exploitative to the patient.&nbsp;</p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Treatment Disruption, Abandonment or Termination&nbsp;</span><br></p><p>It is a neurotherapists professional and clinical responsibility to maintain practices and procedures that assure undisrupted care. This may include providing contact information in case an emergency situation arises while the neurotherapist is away. It is important that a neurotherapist uses clinical judgment when terminating a relationship, as termination must be done in an appropriate manner and based upon sound reason (e.g. the patient is not benefitting from treatment, continuing treatment is no longer beneficial or appropriate, the neurotherapist can no longer provide treatment due to extenuating circumstances, or in order to avoid an ethical conflict or problem). It is unethical to abandon&nbsp; to neglect a patient in treatment; if a neurotherapist is unable to continue providing treatment, they must attempt to provide their patient an alternative health care professional for their accommodation.</p><p><a name=\"_Toc31009231\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Hygiene</a><br></p><p><img src=\"@@PLUGINFILE@@/hygiene.jpg\" alt=\"hygiene\" width=\"200\" height=\"201\" class=\"img-responsive atto_image_button_left\">It is imperative that the neurotherapist maintains a clean and hygienic office for the protection of both clients and staff. This includes all equipment, sensors, pastes and gels used, preventing for cross contamination or any human byproduct (i.e. sweat, saliva, blood, etc.). In a post-pandemic world, this is of paramount importance.&nbsp;</p><p><br></p><h3><a name=\"_Toc31009232\"><br></a></h3><h3><a name=\"_Toc31009232\" style=\"color: rgb(55, 71, 79); font-size: 1.715rem; background-color: rgb(255, 255, 255);\"><br></a></h3><h3><a name=\"_Toc31009232\" style=\"color: rgb(55, 71, 79); font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Financial Concerns</a><br></h3><p>It is unethical for a neurotherapist to maintain a client relationship solely for financial gain, nor is it ethical to terminate a patient relationship for non-payment of fees, unless the termination is handled in a clinically appropriate manner. All services billed by the practitioner must be for clinical services provided directly by the clinician or by their technician.&nbsp;</p><p><a name=\"_Toc31009233\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">At Home Training</a><br></p><p>Neurotherapists recommending and enacting at home training are responsible for the patient’s (or patient’s care-takers) education and application of all neurofeedback modalities and their use. Since at home systems involve the neurotherapist not being present, the neurotherapist must take extra precautions to meet their responsibility to their patients.</p><p>Before implementing at home system use, a neurotherapist must consider the competence and capability of a patient or patient’s caretaker to administer treatments from an at home setting, and must be present via an online screen share for the initial training sessions to ensure the equipment and the set-up is appropriate. When at home training occurs, a neurotherapist must inform patients of the risk of at home training, consequences, limitations, and appropriate emergency responses, should a situation emerge. It is the neuerotherapist’s responsibility to ensure the patient signs all appropriate paperwork regarding at home training, its risks, consequences, and potential adverse effects before engaging in at home use.</p><p><a name=\"_Toc31009234\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Intake</a><br></p><p>During the initial intake, a neurotherapist will get written informed consent from their patients and clients when providing clinical<img src=\"@@PLUGINFILE@@/Intake%20Form.jfif\" alt=\"Intake Form\" width=\"299\" height=\"168\" class=\"img-responsive atto_image_button_right\"> services, including a form indicating the patient is aware of the QEEG procedure (if being done) as well as the neurotherapy procedures at hand. During this initial session, the neurotherapist is to give the client enough information about the neurotherapy process so the client adequately understands what their involvement entails.</p><p><br></p><h3><a name=\"_Toc31009235\" style=\"color: rgb(55, 71, 79); font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Disclosures and Informed Consent</a><br></h3><p>A neurotherapist ought to provide clear information about the neurotherapy modalities used in easy to understand language so the patient can make an educated decision about partaking in neurotherapy. It is of paramount importance that the neurotherapist informs their patients of potential risks and benefits of therapy and any common side effects that occur from the treatment modalities they utilize. This ought to be done in written form at the beginning of neurotherapy under an \"informed consent\" form the client signs. This ought to be signed by the patient before they begin neuro-work with the neurotherapist. On the same form, i<span style=\"font-size: 1rem;\">t is strongly recommended that the neurotherapist informs their patient of their background, theoretical and professional orientation, education, and training.</span></p><p><a name=\"_Toc31009236\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Non-Neurotherapist Roles</a><br></p><p>When a neurotherapist acts in a professional role other than the role of a neurotherapy provider (be it psychologist, psychotherapist, nurse, nutritionist, acupuncturist, chiropractor) they are acting solely within that role and may clarify, when necessary, which role they are acting in in order to prevent confusion.</p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Supervisor, Supervisee, Educator and Student Responsibilities</span><br></p>Neurotherapists maintain professional roles and boundaries when in the role of student or supervisor/educator. The supervisor/educator takes seriously their impact on their students and supervisees and, thus, do not exploit the trust and dependency of their supervisees. A neurotherapist does not engage in romantic or sexual relationships with supervisees/students (over whom they exercise professional authority).&nbsp;&nbsp;Other unethical acts include: borrowing money from students, engaging in a close personal relationship with a supervisee, engaging in a businesses venture with a supervisee, barter with supervisees, or engaging in any of the aforementioned with the student’s spouse. It is mandatory that a supervisor maintain their professional skills with recurring courses and trainings.</div><div><h3><br></h3><h3>Competence of Supervisee</h3><p><img src=\"@@PLUGINFILE@@/Teacher%20Student.jpg\" alt=\"Teacher and student\" width=\"300\" height=\"264\" class=\"img-responsive atto_image_button_left\">Neurotherapists make sure their supervisees are addressed and taught at the level of their competence and are not providing services before they are clinically capable. It is the responsibility of both the supervisor and supervisee to ensure the supervisee understands and can apply the material and neurofeedback techniques appropriately. The appropriate consultation and supervision in neurofeedback mandates that the supervisee passes all client cases by the mentor while earning their certification, in order to accurately assess the patient\'s EEG and and QEEG, in order to appropriately apply neurotherapy modalities for optimal success. The supervisor shall oversee the supervisee until they have earned their BCIA accreditation.&nbsp;</p><p>It is strongly recommended that the student continue to learn through mentorship with various individuals. The field of neurotherapy is diverse and there are many perspectives, softwares, hardwares, and applications. Typically, a neurotherapy professional builds a practice that is an amalgam of approaches and techniques. It is paramount to stay atop the latest trends and findings of the field in order to keep one\'s practice and neurotherapy applications relevant.&nbsp;</p><p><a name=\"_Toc31009237\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\"><br></a></p><p><a name=\"_Toc31009237\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Consultation with Outside Parties and Referrals</a><br></p><p>It is important that neurotherapists have access to professional communities of other clinicians doing similar work in the cases that they need to consult, collaborate with, and refer patients out to other professionals, physicians, and community resources. In cases where neurotherapy is not leading to desired results, neurotherapists ought to offer treatment alternatives that are appropriate for the patient’s symptoms. It is of paramount importance that neurotherapists do not violate HIPAA in these interactions, it is well-advised that neurotherapists provide patients with a form to sign, allowing them to disclose their case information to mentors, if they see fit.</p><p><a name=\"_Toc31009238\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Treatment Decisions and Case Notes</a><br></p><p>All mental health care practitioners keep notes of their patient sessions, including the patients subjective state, their demeanor and reported changes or challenges since the last neurotherapy session, as well as the protocol given at the time of the appointment in as much detail as is necessary. This latter form of note keeping may be kept in electronic format, but it is paramount that the neurotherapist maintains a backup copy of the treatments undertaken in the case of computer failure. This will involve the monitoring of medication and medical condition. It is not within the scope of the neurotherapist to alter the medication regimen of a patient, unless they have an MD and the consent of the prescribing physician to do so. If the neurotherapists does not have an MD, it is recommended that they connect with any prescribing physician to inform them of the treatment plan if the neurotherapy treatment&nbsp; is going to alter the patient\'s reception of the medication.</p><p><a name=\"_Toc31009239\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Confidentiality &amp; Privacy</a></p><p>A neurotherapist is held to the same levels of confidentiality as other mental health care practitioners. It is paramount that they disclose to clients and other interested parties at the outset of services the nature of confidentiality and possible limitations of the clients’ right to confidentiality. They ought to review with clients the circumstances where confidential information may be requested and where disclosure of confidential information may be legally required (most often this would be if the patient is using health<img src=\"@@PLUGINFILE@@/confidential.jpeg\" alt=\"confidential\" width=\"300\" height=\"168\" class=\"img-responsive atto_image_button_right\"> insurance and their health insurance company requests records).</p><p>When consulting with colleagues or referral sources, a neurotherapist does not share confidential information that could reasonably lead to the identification of a client, with whom they have a confidential relationship, unless they have obtained the prior written consent of the client. Information may be shared only to the extent necessary to achieve the purposes of the consultation.</p><p>It is paramount that neurotherapists do not disclose client confidences, except by written authorization or waiver, or where mandated or permitted by law. Verbal authorization will not be sufficient except in emergency situations, unless prohibited by law. When providing couple, family or group treatment, the neurotherapist does not disclose information outside the treatment context without a written authorization from each individual competent to execute a waiver. In the context of couple, family or group treatment, the neurotherapist may not reveal any individual’s confidences to others in the client unit without the prior written permission of that individual.<br></p><p>All information exchanged by the patient is confidential with these exceptions:</p><p></p><ol><li>If the patient is suicidal, the neurotherapist has the obligation of staying with the patient until they can ensure their safety. The therapist may reach out to an emergency contact and ensure the patient is in the care of a close friend, spouse, or relative. If the patient seems unstable, it is the professional obligation of the neurotherapist to see that the patient is taken to the hospital, even if by an involuntary hold (a 5150 code). This may involve the police or calling 911 if the patient is resistant</li><li>If the patient is abusing or knows of someone abusing an elderly person or a child (in which case it is the neurotherapists duty to reach out to the proper authorities (e.g. child protective services or the police)</li><li>If the patient is homicidal or threatening acting against another violently, in which case it is the neurotherapists duty to make sure all endangered parties are informed, by contacting the police</li></ol><p></p><p><br></p><p></p><h3>HIPAA Compliance</h3><p><img src=\"@@PLUGINFILE@@/HIPAA.png\" alt=\"HIPAA\" width=\"338\" height=\"149\"></p><p>HIPAA stands for&nbsp;&nbsp;Health Insurance Portability and Accountability Act. This Act was established for the protection of patients\' confidential information. Neurotherapists, like all health professionals, are expected to adhere to the principles of HIPAA. More information on HIPAA can be found here:&nbsp;https://www.hhs.gov/hipaa/for-professionals/index.html</p><p><br></p><p>Here are some of the basic coverages of the Act:</p><p></p><span style=\"font-size: 1rem;\">1) Creation and implementation of policies, procedures, and standards of conduct</span><br><span style=\"font-size: 1rem;\">2) Enabling technical protections: including encryption of patient data and password protection</span><br><span style=\"font-size: 1rem;\">3) Exercising privacy and confidentiality practices everywhere (i.e. using aliases instead of patient names)</span><br><span style=\"font-size: 1rem;\">4) Display privacy notices in office and on website</span><br><span style=\"font-size: 1rem;\">5) Exercise caution in the use and communication of Protected Health Information (PHI), PHI includes:<br></span><span style=\"font-size: 1rem;\">Identifying information, such as</span><ul><li>Names,&nbsp;</li><li>DOB,&nbsp;</li><li>Pictures,&nbsp;</li><li>Patient numbers,&nbsp;</li><li>Payment information,&nbsp;</li><li>Emails,&nbsp;</li><li>Social security numbers,&nbsp;</li><li>Biometric identities</li><li>Website links and other URLs</li><li>Telephone numbers</li><li>Vehicle Identifiers</li></ul><p></p><h3><span>Client Access to Records&nbsp;</span></h3><p><span>Neurotherapists must provide clients with reasonable access to records concerning the clients. Neurotherapists can limit client’s access to their records only in exceptional circumstances when they are concerned, based on compelling evidence, that such access could cause serious harm to the client.&nbsp; The client’s request and the rationale for withholding some or all of the record should be documented in the client’s file.&nbsp;</span></p><p><a name=\"_Toc31009240\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Limits of Neurotherapist’s Role and Contact</a><br></p><p>A neurotherapists will act solely within the provision of their role as a neurotherapist and within the role of their professional license, if applicable. A chiropractor is free to do chiropractic work, an acupuncturist is free to do acupuncture, a psychotherapist is free to do psychotherapy, etc., but no neurotherapist is allowed to reach beyond the bounds of the professional license with any neurotherapy client. For example, it would be unethical for someone without a license in mental health care to conduct psychotherapy with a patient while doing neurotherapy. The therapist will also purchase liability insurance that covers the extent of their neurotherapeutic work, including all forms of neurostimulation and neurofeedback.</p><p><a name=\"_Toc31009241\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Competence</a><br></p><p>A neurotherapist is expected to practice within the limits of their professional competence, based upon their experience, their education, and their training.&nbsp; It is also the therapist’s role to inform their patients about particular procedures and possible negative effects. A clinician who received the QEEG-D designation ought to have the competence of an intermediate practitioner and it is advised that they pursue their BCIA (Biofeedback Certification International Alliance) certificate before pursuing the QEEG-D or QEEG-T.</p><p>If a professional is serving in the role of a biofeedback or neurofeedback technician or assistant, they will engage in the practice only under the supervision of a qualified professional.&nbsp; Misrepresentation of one’s credentials, training, experience, degrees, or specialty is a violation of ethics and a violation of law in certain circumstances.</p><p><a name=\"_Toc31009242\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Treatment Alternatives and Referring Out</a><br></p><p>Sometimes a client will seek neurotherapy who would be much better suited by another form of treatment. Sometimes a patient will seek neurotherapy who has a condition that is more severe than the neurotherapist can address or is foreign to the neurotherapist. In other situations a patient may come to a neurotherapist without knowing what is wrong with them. In these situations it is the ethical duty of the neurotherapist to consider the client’s best interests and either refer to an appropriate specialist for a more suitable treatment or appropriate assessment and diagnosis. In cases where the neurotherapist does not know who to refer out to, it is best to receive consultation with a supervisor or other professional who is licensed and can give educated advice as to how to proceed.</p><p><a name=\"_Toc31009243\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Complaints</a><br></p><p>If a neurotherapist receives a filed complaint from a client, the board to which the complaint must first be presented is to the clinician’s professional licensure board. The professional boards for the practice of neurotherapy, including the International Quantitative EEG Certification Board, The Biofeedback Certification International Alliance (BCIA) Board of Directors, and the Association of Applied Biofeedback and Psychophysiology (AAPB) will be the secondary board to determine whether or not the member failed to comply with either ethical and/or legal requisites. If the neurotherapist does not have a license, these credentialing boards are the first to be notified.&nbsp;</p><p>If a neurotherapy employee or the licensed clinician receives a consumer complaint, or has been&nbsp; accused of unethical behavior, it is paramount to consult with other licensed individuals as to the best course of action for the given complaint. If it is appropriate, attempts to resolve the client\'s complaint with the client (i.e. refund of money or explanation of behavior) may be the best course of action. In cases where a complaint is formalized, or further contact with the patient would be damaging to them, consultation with the trade organization responsible for advocacy and support of the license (or, if only a board certified neurotherapist, contact with ISNR, AAPB, or BCIA) in order to determine the best course of action.</p><p><a name=\"_Toc31009244\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Core Professional Values of Neurofeedback Professionals</a><br></p><p>&nbsp;<span style=\"font-size: 1rem;\">These core professional values are borrowed from the AAPB Code of Ethics:</span></p><p></p><ul><li>Enhancing human development and improvement through the life span</li><li>Honoring diversity and embracing a multicultural approach in support of the worth, dignity, and uniqueness of people within their social and cultural context</li><li>Promoting social justice</li><li>Safeguarding the integrity of the provider/client relationship</li><li>Practicing in a competent and ethical manner</li></ul><p></p></div></div></div></section></div></div></div></div></div></div></div><footer><div><br>\r\n\r\n</div></footer>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1654219450),(33,15,'4) Signal Processing and Amplification Specs','',1,'<h3>Nyquist Principle</h3>\r\n<h3>\r\n</h3>\r\n<h5>The Nyquist principle states that in order to measure a signal you need to measure it at twice the speed of its fastest frequency. Here is&nbsp; a video that covers this principle clearly, and in good detail. Please watch until 13:31.</h5>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/FcXZ28BX-xE\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n<h3>Fast Fourier Transform (FFT)</h3>\r\n<p>The Fast Fourier Transform (FFT) is a way to decompose (and reconstruct) complex waveforms into their disparate frequencies, as well as the amplitudes of those frequencies. This is the matehematical process through which raw EEG is converted into quantitative\r\n    EEG brain maps. Here is a video by Arnaud DeLorme on the FFT process in EEG:</p><p>&nbsp;\r\n    <iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/wB417SAbdak?start=180\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe></p>\r\n<p></p><br>\r\n<h3>Gain, Notch Filters, and Bandpass&nbsp;</h3>\r\n<p>This final video is of Neurofield\'s EEG software, displaying the features of:</p>\r\n<p><b><u>Gain</u></b> - t<span style=\"font-size: 1rem;\">he sensitivity&nbsp;of the recording, measured in microvolts per millimeter. Gain is manipulated to either increase or reduce the display height of waveforms.&nbsp;</span></p>\r\n<p></p>\r\n<p><span><span style=\"\"><b style=\"\"><u>Notch Filters</u>&nbsp;- </b>these filters can be useful in deleting&nbsp;<span style=\"\">fixed-frequency noise sources</span>&nbsp;such as that from electrical line frequency (50 or 60 Hz) noise.&nbsp;</span>\r\n    </span>\r\n</p>\r\n<p><span><span style=\"\"><b style=\"text-decoration-line: underline;\">Bandpass:&nbsp;</b>&nbsp;A band-pass filter or bandpass filter is a device that passes frequencies within a certain range and rejects frequencies outside that range</span></span>\r\n</p>\r\n<p><br></p><p>\r\n</p><iframe src=\"https://drive.google.com/file/d/1kaqrZSfJmnhQNL_FJ2FSHASiWoduhciT/preview\" width=\"640\" height=\"480\" allow=\"autoplay\"></iframe>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',5,1653945736),(34,16,'An Overview of the Template for Developing Guidelines for NFB','',1,'<h3><b>The Panels</b></h3><p>In 2002, a taskforce assembled between the AAPB and ISNR trade organizations developed guidelines for assessing the efficacy of neurofeedback and biofeedback interventions. The article is made available&nbsp; within this chapter. At the outset of this article, the establishment of panels of competent professionals from the psychophysiological community (and adjunctive fields) is detailed. In their evaluation of the neurotherapy treatment modality, each panel will have discretion over \"their process and method, determining\r\nthe target condition, patient population, interventions to be included and/or excluded, provider type, and service settings.\"</p><p>The \"Template\" notes that neurofeedback assessments ought to use quantitative EEG (or similar measures) to identify abnormal patterns of cortical activity. Understanding how the EEG creates the QEEG lends the practitioner a heightened level of clinical assessment in understanding the waveforms that cause the quantitative and normative version of the data.&nbsp;</p><h4><b>Efficacy: Having the Desired Effect</b></h4><p>the fundamental requirements to determine efficacy include:</p><p><ul><li><span style=\"font-size: 1rem;\">Basic\r\nknowledge of clinical experimental design and analysis methods as well as ethical standards for human research</span></li><li><span style=\"font-size: 1rem;\">A fundamental level of training\r\nand education, possession of a foundation of relevant knowledge, and effective clinical assessment skills</span></li></ul></p><h4><b>Scientific Considerations</b></h4><p>Each experiment / assessment must specify&nbsp;</p><p><ol><li>The independent variables (e.g., sensor placement, bandwidths\r\nand frequencies, reinforcement contingencies)</li><li>The dependent variables (e.g., physiological\r\nevent being measured, response to treatment).</li><li>The “condition of interest” (COI), clearly identified and operationally defined</li><li>Guidelines specific to the modality under review</li><li>The modality\'s amenability to replicability and empirical analysis</li><li>Expected outcomes in identified variables</li><li>Identification of important variables</li><li>Outcome measures</li></ol></p><h4><b>Specificity</b></h4><p><span>1) Determination as to whether a particular treatment component is necessary to the treatment\r\noutcome,</span></p><p><span>2) Whether “Placebo” nonspecificity can be ruled out as\r\nthe dominant effect</span></p><h4><b>Clinical Utility</b></h4><p><span>Panels must determine the following:</span></p><p><span>1. Efficacy (having the desired effect) refers to the determination of treatment effect\r\nderived from a systematic evaluation obtained in a controlled clinical trial.&nbsp;</span></p><p><span>2. Clinical utility refers to the practical value of an intervention, or the extent to\r\nwhich it is practical and possible to translate the findings from efficacy studies<br></span></p><h4><span><b>HIERARCHY OF EVIDENCE: CLINICAL TRIALS AND EFFICACY STUDIES</b></span></h4><p><span><b>There is a generally accepted hierarchy\r\nof “scientific power” for each clinical trial design.<br></b></span></p><p><span><b></b></span></p><p></p><ol><li><b style=\"font-size: 1rem;\">Anecdotal Evidence</b><span style=\"font-size: 1rem;\">: This is a narrative\r\nreport about a particular treatment that worked. This is not considered scientifically\r\nrigorous.</span></li><li><b style=\"font-size: 1rem;\">Uncontrolled Case Study</b><span style=\"font-size: 1rem;\"> This will specify\r\nthe dependent and independent variables and, ideally, will include quantitative\r\npre-post measures, as well as follow-up measures. This is not considered scientifically\r\nstrong.</span></li><li><b style=\"font-size: 1rem;\">Historical Control</b><span style=\"font-size: 1rem;\">: An example of an\r\neffective historical control might be a disorder or disease that is known to be\r\nso universally lethal (Ebola virus, hemorrhagic fever) or debilitating (e.g.,\r\nAlzheimer’s Disease) that any intervention that increases survival rate or\r\nprolongs quality of life is regarded as efficacious.</span></li><li><b style=\"font-size: 1rem;\">Observational Studies</b><span style=\"font-size: 1rem;\">: These include retrospective\r\nor prospective studies that are case-controlled but not randomized or blinded,</span></li><li><b style=\"font-size: 1rem;\">Waitlist or “intention to treat” controls</b></li><li><b style=\"font-size: 1rem;\">Within-subject and intrasubject replication\r\ndesigns</b><span style=\"font-size: 1rem;\"> (i.e the A-B-A design)</span></li><li><b style=\"font-size: 1rem;\">Single blind, random assignment control\r\ndesign, either sham or active</b><span style=\"font-size: 1rem;\"> (behavioral, psychological, or\r\npharmacological) </span><b style=\"font-size: 1rem;\">treatment</b><span style=\"font-size: 1rem;\"> controls. This design “blinds” the subject to\r\nthe particular treatment condition to which they have been assigned, thus\r\ncontrolling for some of the nonspecific subject variables that may operate in\r\nthe study (expectancy, acquiescent response bias, etc.). It does not control\r\nfor experimenter bias.</span></li><li><b style=\"font-size: 1rem;\">Double blind control studies, sham or active\r\ncontrols, random assignment. </b><span style=\"font-size: 1rem;\">This design “blinds” both the subject and the\r\nexperimenter to the treatment condition, thus controlling for both subject\r\nvariables and experimenter bias.</span></li><li><b style=\"font-size: 1rem;\">Treatment Equivalence or Treatment\r\nSuperiority Designs</b><span style=\"font-size: 1rem;\">: This design compares the investigational treatment to\r\na known and accepted standard treatment.</span></li><li><b style=\"font-size: 1rem;\">Other Designs</b><span style=\"font-size: 1rem;\">: Other more sophisticated\r\nclinical trial designs</span></li></ol><p></p><p><!--[if !supportLists]--><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n\r\n\r\n<p><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n<p><b></b></p>\r\n\r\n<p><b>Criteria for Levels of Evidence of Efficacy</b></p>\r\n\r\n<p>Level 1: Supported only by anecdotal reports and/or case\r\nstudies in nonpeer reviewed venues. Not empirically supported.</p>\r\n\r\n<p>Level 2: Possibly Efficacious</p>\r\n\r\n<p>Level 3: Probably Efficacious</p>\r\n\r\n<p>Level 4: Efficacious</p>\r\n\r\n<p>Level 5: Efficacious and Specific</p>\r\n\r\n<p><b>Ethical Standard for Research</b></p>\r\n\r\n<p>Finally, the panels will examine the research reports in\r\nlight of published ethical standards governing human subject research (i.e.\r\nDeclaration of Helsinki, published by the World Medical Association (2000), and\r\nthe Belmont Report (1979), published by the Department of Health and Human\r\nServices).<b></b></p><h3><b></b></h3>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',3,1653946292),(35,18,'Standardized Clinical EEG Assessments','',1,'<h4><b>Minimum Technical Requirements for Performing Clinical\r\nElectroencephalography</b></h4><p>According to the <b>American Clinical Neurophysiological Society</b>, to find the distribution of EEG activity, it is necessary to record simultaneously\r\nfrom as many regions of the scalp as possible. When too few channels are used\r\nsimultaneously, the chances of interpretive errors increase, and, conversely, when more\r\nchannels are utilized, the likelihood of such errors decreases. This is particularly true for\r\ntransient activity.\r\nSixteen channels of simultaneous recording are now considered the minimum number\r\nrequired to show the areas producing most normal and abnormal EEG patterns.\r\nAdditional channels can be used for monitoring other physiologic activities (such as ocular movement, glossokinetc movement, or respiration.&nbsp;<br></p><p>Recording electrodes should be free of inherent noise and drift.&nbsp;To decrease noise, electrodes must be kept clean, with appropriate precautions taken\r\nafter recording from patients with contagious diseases.<br></p><p>All 21 electrodes and placements recommended by the International Federation of\r\nClinical Neurophysiology (IFCN; Jasper HH, 1958, 1983) should be used. The 10-20\r\nSystem is the only one officially recommended by the IFCN. It is the most commonly\r\nused existing system, and it should be used universally.&nbsp;An adequate number of electrodes is essential to ensure that EEG activity having a\r\nsmall area of representation on the scalp is recorded and to analyze accurately the\r\ndistribution of more diffuse activity. A smaller number of electrodes may be appropriate\r\nfor special circumstances, but is not considered comprehensive.</p><p>A grounding electrode always should be used. The ground electrode on the patient must\r\nbe connected only to the appropriate jack of the input jackbox, and never to the\r\nequipment chassis or other earth ground.<br></p><p>Interelectrode impedances should be checked as a routine prerecording procedure.\r\nOrdinarily, electrode impedance should not exceed 15000 Ohms (15 KOhms.)<br></p><p>For standard recordings, the low-frequency filter should be no higher than 1 Hz (—\r\n3 dB) corresponding to a time constant of at least 0.16 s. The high-frequency filter should\r\nbe no lower than 70 Hz (-3 dB). Note, however, that to display frequencies as high as 70\r\nHz, a computer monitor would need a horizontal resolution of at least 1400 pixels in the\r\ndata display area.&nbsp;A low-frequency filter setting higher than 1 Hz should not be used routinely to\r\nattenuate slow-wave artifacts in the record. Vital information may be lost when\r\npathologic activity in the delta range is present. Similarly, a setting lower than 70 Hz for\r\nthe high-frequency filters can distort or attenuate spikes and other pathologic discharges\r\ninto unrecognizable forms and can cause muscle artifact to resemble spikes. Production\r\nof a record with lost or inaccurate information is poor medical practice.\r\nIt must be emphasized, however, that judicious use of the low- or high-frequency\r\nfilters—with appropriate annotation on the record—can emphasize or clarify certain\r\ntypes of patterns in the record. These filter controls, therefore, should be used in analysis.&nbsp;<br></p><p>The baseline record should contain at least 20 min of technically satisfactory\r\nrecording (10 minutes eyes open and 10 minutes eyes closed is standard in the USA). Longer recordings are often more informative. Although the possibility of\r\nreformatting digital EEG allows the entire recording to be performed in a single montage,\r\nthis is not acceptable practice. Observing only one montage may prevent recognition of\r\npoor connections in electrodes that happen not to be included, and also prevent\r\nappreciation of subtle abnormalities that require special technical maneuvers (such as\r\nplacement of additional electrodes.)\r\nThe EEG is a short sample in time from the patient’s life. Within reasonable limits, the\r\nlonger the recording, the better the chance of recording an abnormality or abnormalities\r\ndemonstrating the variability of these. Experience in many centers shows that a very\r\nminimum of 20 min of artifact-free recording is necessary to assess baseline waking EEG\r\nactivity.&nbsp;<br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1643756066),(36,18,' How to recognize common normal and abnormal patterns in the EEG ','',1,'<p></p>\r\n<h3>Recognizing Normal &amp; Abnormal EEG Patterns</h3>\r\n\r\n<p>Brainwaves are characterized by their speed (frequency), size (amplitude) and shape (morphology). Frequency is the power or speed of the electrical emissions, measured in hertz (Hz). Amplitude is the power of the brain\'s electricity, measured in microvolts.\r\n    Pure microvolts is called magnitude and microvolts squared is called amplitude. Here are some other and important definitions. In EEG analysis and brain region analysis, it is helpful to think of the frequency as the adjective (i.e. theta = foggy,\r\n    groggy, fuzzy, trance-like, day-dreamy, “not all here,”) and the region that is affected as the noun.</p>\r\n<h3><br><a name=\"_Toc29328765\"><img src=\"@@PLUGINFILE@@/Waveform%20%281%29.png\" alt=\"\" width=\"500\" height=\"190\" role=\"presentation\" class=\"atto_image_button_middle\"></a>\r\n    </h3><h3><a name=\"_Toc29328765\">Important Definitio</a><a name=\"_Toc29328765\" style=\"color: rgb(55, 71, 79);  background-color: rgb(255, 255, 255);\">ns&nbsp;</a></h3>\r\n\r\n<h5><a name=\"_Toc29328765\"><b style=\"color: rgb(82, 96, 105);  \">Action\r\nPotentials: </b><span style=\"color: rgb(82, 96, 105);  \">The exchange of potassium (K+), Chloride (Cl-), Calcium (Ca</span><sup style=\"color: rgb(82, 96, 105);  \">2</sup><span style=\"color: rgb(82, 96, 105);  \">+)\r\nand Sodium (Na+) along the dendrite of a neuron, which produces a small battery\r\nthat maintains a voltage of -60 millivolts.</span></a></h5>\r\n<p><b>Amplitude:\r\n</b>The height of the brainwave and power of the electricity, measured in microvolts squared.<br><b>Asymmetry:\r\n</b>The absence or violation of balance between two hemispheres or quadrants.<br><b>Connectome: </b>The complete description of the structural connectivity (the physical wiring) of an organism’s nervous system.<br><b>Coherence: </b>The stability of phase\r\n    relationship between any two areas of the brain. Two areas are said to be coherent if they have constant respective relative phase. Coherence in excess is hypercoherence; coherence in deficiency is hypocoherence.<br><b>Frequency</b>: Cycles per second.\r\n    The standard unit of frequency is “Hertz,” which is abbreviated as Hz. 4 Hz is equal to four cycles per second.&nbsp;\r\n    <a href=\"#_ftn1\" name=\"_ftnref1\" title=\"\">\r\n        <!--[if !supportFootnotes]-->[1]<br>\r\n        <!--[endif]-->\r\n    </a><b>Frequency\r\nBand: </b>A range of wave frequencies, typically grouped as follows: delta (0-4 Hz), theta (4-8 Hz), alpha (8-12 Hz), low beta (12-15 Hz), mid beta (15-25Hz), high beta (25-40Hz), gamma (40+ Hz).<br><b>Lateralized</b>: Occurring only over one hemisphere<br><b>Bilateral:</b>    Occurring on both sides of the EEG; occurring over both hemispheres<br><b>Diffuse</b>: Widespread, occurring over a large area of one or both hemispheres<br><b>Dominant Frequency</b> (Aka Background Rhythm): The frequency of EEG activity that occupies\r\n    the greater part of the recording<br><b>Focal:</b> In a clearly delineated area of the brain as in a focal temporal spike or focal slowing<br><b>Harmonic:</b> A wave or frequency that is an integral multiple of a given frequency.<br><b>Homologous</b>:\r\n    Two areas at the same region of the brain, mirrored, sharing common function (i.e. C# is the homologue to C4)<br><b>Magnitude:&nbsp;<b>&nbsp;</b>The height of the brainwave and power of the electricity, measured in microvolts.<br></b><b>Multifocal</b>:\r\n    Having several independent foci as in multifocal paroxysmal spike discharges<br><b>Sub-harmonic:</b> A frequency that is below the fundamental frequency, which divides evenly into the fundamental frequency.<br><b>Synchrony:\r\n</b>A balance that occurs if waves of similar frequency occur simultaneously in different areas of the head. Waves that occur in different channels without a constant time relationship to each other are called asynchronous.<br></p>\r\n<p><img src=\"@@PLUGINFILE@@/Brainwaves.png\" alt=\"Brainwaves\" width=\"800\" height=\"458\" class=\"atto_image_button_middle\"></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<p>\r\n    <a href=\"#_ftn1\" name=\"_ftnref1\" title=\"\">\r\n        <!--[endif]-->\r\n    </a>\r\n</p>\r\n<p><a name=\"_Toc29328767\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Delta</a><br></p>\r\n\r\n<h3><a name=\"_Toc29328768\" style=\"color: rgb(55, 71, 79);  background-color: rgb(255, 255, 255);\">Healthy Delta</a><br></h3>\r\n\r\n<p><b><u>Delta rhythm</u></b> is a brainwave that is most commonly seen in deep dreamless sleep (NREM 4) in healthy adults and children. It is also a dominant brainwave in infants, since the earliest stages of life are times of, one, a lot of sleep, and\r\n    two, neurogenesis and angiogenesis. Young brains form, develop and grow with the production of delta. Although usually thought of as being associated with sleep and parts of the brain being “off line,” taking up nourishment, delta activity is always\r\n    present in normal EEG’s of any age.&nbsp; It is generated cortically and inhibited by afferent stimulation of the cortex.&nbsp;</p>\r\n\r\n<p>There is a substantial QEEG literature relating delta power to higher order mental functions in normal awake humans.&nbsp; Increased delta activity has been observed in normal subjects performing calculations, taking reaction time tests, and thinking\r\n    abstract thoughts.&nbsp; Delta is thought to have a functional role in allocating attention to internal mental representations, by suppressing extraneous cortical inputs and facilitating internal concentration. Anterior lead voltage in awake subjects\r\n    is 20%-30% delta.&nbsp; &nbsp;</p>\r\n\r\n<div>\r\n    <!--[if !supportFootnotes]--><img src=\"@@PLUGINFILE@@/Delta.png\" alt=\"\" width=\"400\" height=\"300\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><h3><br></h3>\r\n    <h3><a name=\"_Toc29328769\" style=\"color: rgb(55, 71, 79);  background-color: rgb(255, 255, 255);\">Pathological\r\nHigh Amplitude Delta</a><br></h3>\r\n\r\n    <p>When delta is pathological, it represents cognitive impairment or of brain damage. Delta excesses often correlated with damage to the white matter (the white matter axons are exclusively excitatory). Focal&nbsp;delta activity should always be considered\r\n        abnormal, possibly indicating a lesion, and should result in referral of the patient to a neurologist for further evaluation.&nbsp; Focal delta can also reflect white mater abnormalities, as we see in ASD.&nbsp; Generalized background slowing\r\n        indicates diffuse cerebral dysfunction, which, similar to focal slowing, is also not specific as to cause. Delta can indicate the effects of sedative centrally acting medications, neurodegenerative disorders, a widespread neurodevelopmental disorder,\r\n        hydrocephalus, metabolic or toxic encephalopathy, CNS infectious disorders such as meningoencephalitis, traumatic brain injury, hypoxia, or anoxia. The delta band may be composed of delta rhythm activity (usually over 75 µV and rather rhythmic),\r\n        slow cortical potentials (DC shifts) at .5 Hz and below, and also artifact (e.g., eye movement, glossokinetic artifact, electrodermal or sweat artifact).&nbsp; </p>\r\n    <p><img src=\"@@PLUGINFILE@@/PATHOLOGICAL%20DELTA.png\" alt=\"\" width=\"800\" height=\"397\" role=\"presentation\" class=\"atto_image_button_middle\"><br></p>\r\n    <h4><span>Focal Delta in a patient taking Lithium and Zyprexa, on the Autistic Spectrum</span><br></h4>\r\n    <p><br></p>\r\n    <p><img src=\"@@PLUGINFILE@@/Focal%20Delta.png\" alt=\"Focal Delta\" width=\"400\" height=\"557\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n    <h4><span>Figure of Slow Transient, Reflecting Hypersomnia and Word Finding Issues</span><br></h4>\r\n    <p><br></p>\r\n    <p><img src=\"@@PLUGINFILE@@/DElta%202.png\" alt=\"\" width=\"400\" height=\"722\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n    <h4>Figure of Focal Delta in a 12 year old girl with complications from an anoxic head injury\r\n    </h4>\r\n    <p><br></p><img src=\"@@PLUGINFILE@@/Delta%203.png\" alt=\"Focal Delta\" width=\"800\" height=\"503\" class=\"atto_image_button_middle\">\r\n    <p>An excess of delta activity may be seen in the records of individuals with learning disabilities, Alzheimer’s disease, demyelination, toxic or metabolic disturbances, edema, and with aging there is frequently an increase of delta waves, especially\r\n        in the left hemisphere.&nbsp; Pathological delta patterns, known as FIRDA (Frontal Intermittent Rhythmic Delta Activity) and OIRDA (Occipital Intermittent Rhythmic Delta Activity) are abnormal and pathological delta patterns. FIRDA is a transient,\r\n        rhythmic slow wave pattern over the anterior EEG leads, that indicates cerebral lesions, circulation infarcts, stroke victims, and various metabolic disturbances.</p>\r\n    <h4>FIRDA Pattern in an elderly woman with metabolic encephalopathy\r\n    </h4>\r\n    <p><img src=\"@@PLUGINFILE@@/FIRDA.png\" alt=\"\" width=\"800\" height=\"585\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><br></p>\r\n    <p><img src=\"@@PLUGINFILE@@/Delta%205.png\" alt=\"\" width=\"800\" height=\"450\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"></p>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\"><br></a></h3>\r\n    <h3><a name=\"_Toc29328770\" style=\"color: rgb(55, 71, 79);  background-color: rgb(255, 255, 255);\"><br></a></h3>\r\n    <p><a name=\"_Toc29328770\" style=\"color: rgb(55, 71, 79);  background-color: rgb(255, 255, 255);\"><br></a></p>\r\n    <h3><a name=\"_Toc29328770\" style=\"color: rgb(55, 71, 79);  background-color: rgb(255, 255, 255);\">Pathological\r\nLow Amplitude Delta</a><br></h3>\r\n\r\n    <p>Decreased delta power in quantitative EEGs has been found to be associated sometimes with complicated depression, chronic migraine, closed posterior head/neck injury, alcoholism, and a subgroup of patients who display lack of control over repetitive\r\n        thoughts and behaviors and minor motor symptoms (Gerez-Malo &amp; Tell-Valdes, 1996).&nbsp;Low voltage delta can also indicate an old injury or a series of injuries (such is the case with professional athletes (soccer, rugby, and football players)\r\n        who take many blows to the head.</p>\r\n    <h4>Figure of a football player who sustained many concussions and blows to the head. He experiences short term memory impairment</h4>\r\n    <p><img src=\"@@PLUGINFILE@@/Low%20Voltage%20Delta.png\" alt=\"\" width=\"580\" height=\"756\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></p>\r\n    <h3><a name=\"_Toc29328771\">Pathological\r\nDelta: Concussion and Mild Traumatic Brain Injury</a></h3>\r\n\r\n    <p><a name=\"_Hlk25008071\">Often in a concussion, the </a><span lang=\"EN-CA\">initial impact will lead the brain to\r\nrelease the excitatory neurotransmitter glutamate at the areas of damage, which\r\ncauses a rapid depolarization of the local neurons. After this, the axonal\r\nsodium/potassium pump goes into overdrive to rebalance ion/voltage imbalance,\r\nmore ATP (energy) is required,</span> there is a <span lang=\"EN-CA\">jump in glucose metabolism, and </span>e<span lang=\"EN-CA\">xtracellular swelling starts, reducing blood flow.\r\nThen the increase in metabolism with reduced blood flow causes an energy crisis\r\nin the cell. Cell is unable to carry out regular activity due to lack of energy\r\nand</span> o<span lang=\"EN-CA\">ften entire cell groups will go dormant to\r\npreserve themselves. </span><span lang=\"EN-CA\">This is one cause of a low voltage EEG. </span></p>\r\n\r\n    <p>It is very likely that, after a career of having hard knocks to the skull, a client’s brain will form scar tissue at the sites of the accident (after initially experiencing a state of inflammation). If the inflammation is not able to properly heal\r\n        the brain—which is its’ function—then the brain will ultimately learn to handle the inflammation by altering cellular structures to form tougher tissues, which would consequentially prevent blood perfusion at the sites of the injury and prevent\r\n        the slower brainwaves of delta and theta from being read from the surface. Among the symptoms that are commonly reported in patients with TBI and mild TBI include impairment in attention, memory, psychomotor speed, and executive functions.</p>\r\n\r\n    <p>Some of the symptoms the client may experience as a result of his head injury include: </p>\r\n\r\n    <p></p>\r\n    <ul>\r\n        <li>Difficulty figuring out how to do new things</li>\r\n        <li>Disorganization</li>\r\n        <li>Difficulty completing activities in a reasonable amount of time</li>\r\n        <li>Slower learning than is normal</li>\r\n        <li>Becoming easily angered or frustrated</li>\r\n        <li>Difficulty with word finding</li>\r\n        <li>Extreme sensitivity to light and/or sounds</li>\r\n        <li>Difficulty with concentration or focus</li>\r\n        <li>Easily distracted</li>\r\n        <li>Spacing out</li>\r\n        <li>Headaches</li>\r\n        <li>Forgetfulness</li>\r\n        <li>Impulsivity, impatience, risk taking, rudeness, social impropriety</li>\r\n        <li>Fatigue</li>\r\n        <li>Difficulty with balance, dizziness, clumsiness and even incontinence\r\n        </li>\r\n        <li>Problems reading</li>\r\n        <li>Confusion with puzzles, directions, and telling left from right</li>\r\n        <li>Difficulty understanding others</li>\r\n        <li>Difficulty switching from one task to another, especially when unexpected.</li>\r\n        <li>Getting lost easily</li>\r\n        <li>Feeling fidgety</li>\r\n        <li>Emotional difficulties (depression, fear, nightmares)</li>\r\n    </ul>\r\n\r\n    <p><a name=\"_Hlk530947264\">Groups\r\nwith a delta deficit include cocaine addicts, ADD, subtypes of OCD, and\r\nschizophrenia—all of whom have problems with frontal cortical regulation of\r\nattention or impulsive behavior, as well as the processing of extraneous\r\nstimuli.</a>&nbsp; There is evidence suggesting a significant functional relationship of the delta rhythm to the mesotelencephalic dopamine (DA) projection.&nbsp; </p>\r\n    <h3><img src=\"@@PLUGINFILE@@/Mesotelencephalic%20System.png\" alt=\"\" width=\"520\" height=\"478\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></h3>\r\n    <h3>The Mesotelencaphalic Dopamine System</h3>\r\n\r\n    <p>The estimated location of the major site for delta generation in midline and the anterior frontal cortex corresponds with the location of the main cortical terminal field of the mesotelencephalic DA projection.&nbsp; </p>\r\n\r\n    <h3><a name=\"_Hlk28339132\"></a><a name=\"_Toc29328772\">Psychodynamic Delta</a>\r\n    </h3>\r\n\r\n\r\n\r\n    <p>The basis of my conceptualization of EEG, which has formed from the works of many seminal authors and scholars, is as follows: Delta (1-4Hz) is the collective unconscious, a low frequency, high amplitude brainwave that is connected with psi-phenomena,\r\n        pre-cognitive abilities, connection with nature, and deep emotional intelligence (Wise, 1995, 2002). Delta is the rhythm of the heart.</p>\r\n\r\n    <p>Delta arises out of the cosmic unconscious; Wise (1995, 2002) believed that delta was pronounced in healers, seers, or traumatized individuals. That is, the traumatized child may rely more heavily on premonition or gut instinct, to prevent being abused.\r\n        Those with higher amplitude delta, according to Wise, may be hypervigilant or even have extra-sensory perception. Delta is the deep primal intuition, instinctual action, empathy and radar, allowing us to glean information that might not be available\r\n        via consciousness (Wise, 1995, 2002).</p>\r\n\r\n    <h2><a name=\"_Toc29328773\">Theta</a></h2>\r\n\r\n    <p>Theta is a frequency of 4-8Hz that emanates from the thalamus to the cortex and back again, it is a thalamo-cortical frequency and arrives in states of trance, deep meditation, drowsiness, under hypnosis and at the top of sleep cycle for healthy adults\r\n        (REM sleep) during dream state. Theta also arrives in non rapid eye movement sleep (NREM 2 and NREM 3) at the midline and is part of what is called a “K-complex.” &nbsp;</p>\r\n\r\n    <p>Otherwise, healthy theta is seen in children under 9 years of age and is linked up to the visual gestalt in infants. Theta is similar to delta in that it is indicative of neurogenesis in the infant and child. From an empirical perspective, theta is\r\n        one of the main rhythms of the hippocampus, where it is linked to memory encoding, spatial memory, and cognitive processes (Gorochowski, 2009; Stam, 2006). This has been found in many studies using rats. However, from intracranially implanted\r\n        electrodes in seizure patients, Cantero&nbsp;<i>et al.</i>&nbsp;(<a href=\"https://en.wikipedia.org/wiki/Theta_wave#refCantero2003\">2003</a>) found that oscillations in the 4–7&nbsp;Hz frequency range could be recorded from both the hippocampus\r\n        and neocortex in humans, whereas previously it was not known if humans created hippocampal theta, as rats do. The hippocampal oscillations were associated with REM sleep and the transition from sleep to waking, and came in brief bursts, usually\r\n        less than a second long. Cortical theta oscillations, arising from the thalamus and other subcortical structures, were observed during the transition from sleep and during quiet wakefulness; however, the authors were unable to find any correlation\r\n        between hippocampal and cortical theta waves, and concluded that the two processes are probably controlled by independent mechanisms, however they are likely related. Cortical theta is generated from the thalamus and the nucleus accumbens in the\r\n        forebrain. Frontal midline theta, as seen in brief bursts on memory retrieval tasks as the nucleus accumbens provides acetylcholine to the temporal lobe\'s limbic structures via the diagonal band of Broca, which is connected to the amygdala/hippocampus\r\n        complex, allowing rhythmicity (Gunkelman, 2014).&nbsp; Memory uses theta as a carrier wave, upon which other, faster frequencies can ride; the nesting of faster, gamma waves upon theta waves promotes short term memory (DeRidder, 2014; Klimesh,\r\n        Sauseng, &amp; Hanslmeyer, 2007). According to Gorochowski (2009), theta modulates gamma, which allows for the construction (and reconstruction) of a low-frequency-modulating-phase.</p>\r\n    <h4>Figure of Diffuse Theta</h4>\r\n    <p><img src=\"@@PLUGINFILE@@/Theta.png\" alt=\"\" width=\"500\" height=\"759\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></p>\r\n    <div id=\"ftn1\">\r\n        <p><b><a name=\"_Toc29328774\" style=\"color: rgb(55, 71, 79);background-color: rgb(255, 255, 255);\">Healthy Theta</a><br></b></p>\r\n    </div>\r\n</div>\r\n\r\n<p>Theta rhythm is a normal finding during drowsiness in the adult EEG. Theta, may be seen at the onset of sleep as the alpha rhythm slows with drowsiness. Theta is also the brainwave state of dreams. As earlier mentioned, the slow waves that occur here\r\n    correspond to rapid eye movement (REM), which is thought to be healing, developing, and rejuvenating (Crick &amp; Michison, 1983; Evans, 1983; Ornstein, 1986; Oswald, 1980; Shaffery, Oksenberg, Marks, Speciale, Mihailoff, &amp; Roffwarg, 1998; Siegel,\r\n    2010). In 1953, the hypnogogic brainwave state was discovered, consisting of a period of several minutes where the mind is overtaken with image fragments or short dramas. At that time, this hypnogogic state was dubbed “theta” and was seen in asynchronous\r\n    oscillations of 5-8 hertz (i.e., 5 to 8 waveforms over the course of 1 second) occurring over the cortex of the brain. Rhythmic or “synchronous” theta was found to be present in the awake raw EEG, increasing as subjects got drowsy or started daydreaming\r\n    (Ulrich, 2013, pp. 38-39). </p>\r\n\r\n<p>From an empirical brainwave perspective, the brain wave patterns of the dreamer have been identified as asynchronous theta and REM sleep state, which is activated endogenously in the dreaming state. Their function, according to Winson (2002) is to further\r\n    process the memory contents of the past while the individual is asleep. The hippocampus is foundational for its generation in sleep, which allows for the mapping of the sensorimotor, temporal, and environmental space (Bland &amp; Oddie, 2001). This\r\n    mapping may be linked to the storage of procedural memory, since the right parietal cortical areas (housing the right hippocampus and the medial temporal lobe diencephalon) are activated in spatial and mental imagery exercises (Schore, 2003; Solms\r\n    &amp; Turnbull, 2002). This is the same area as that which becomes activated both in dreaming and in the infant’s breast-feeding (Winson, 2002).</p>\r\n\r\n<p>Theta generation has been linked to the replenishing of important neuronal proteins, for cell and synaptic growth, as well as the production of growth hormones, neurochemicals, neurotransmitters, and neuromodulators (Shaffery et al., 1998). Furthermore,\r\n    REM sleep has been linked to the development of the hippocampi—the seat of learning and memory (Lewin &amp; Glaubman, 1975; Shaffery et al., 1998).<a name=\"_Hlk517070865\"> Theta is a rejuvenating brainwave, responsible for\r\nneurogenesis and healing. It is these slow waves that the infant and child spend\r\nmuch of their time in, as these are essential to the building of networks, as\r\nwell as feelings of safe, calm, and protectedness.</a></p>\r\n<h4>Pathological Theta</h4>\r\n<p><img src=\"@@PLUGINFILE@@/Pathological%20Theta.png\" alt=\"\" width=\"624\" height=\"334\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></p>\r\n<p>Unhealthy theta can mean many different things in EEG. From a clinical perspective, theta can indicate concussion or head trauma, as well as attention deficit disorder, distractibility, foggy thinking, inability to sequence tasks, forgetfulness, or daydreamy-ness.\r\n    One with excess theta might be accused of being a “space-cadet.” &nbsp;Having too much theta with eyes open would cause one to feel unable to focus on the task at hand for a long period of time. Any \"theta band\" activity may be slowed thalamo-cortical\r\n    alpha or limbically generated rhythmic slow activity (theta), as stated in Steriade\'s 1990 IFCN position paper.</p>\r\n<h4>Figure of Post Concussive Syndrome in a 17-year old Soccer Athlete, excessive occipital theta (Z-score summary map)</h4>\r\n<p><img src=\"@@PLUGINFILE@@/Theta%203.png\" alt=\"\" width=\"770\" height=\"1021\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n<p></p>\r\n<h4>Excessive Theta at the right posterior temporal lobe (Eyes Closed)</h4>\r\n<p><img src=\"@@PLUGINFILE@@/Raw%20Theta.png\" alt=\"\" width=\"496\" height=\"766\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></p>\r\n<h5>\r\n    <p>When there is a lack of blood flow and oxygen to the area, there is often a consequential slowing of alpha at the area, sometimes into the theta range. As an area degrades, sometimes the alpha slows considerably below the normal alpha band (i.e. less\r\n        than 8hz). A slowed alpha can represent a compromise of blood flow, and consequentially oxygen, to an area, which will lead to ischemia. The dip in alpha frequency will indicate how severe the ischemia is (Classen and Foreman, 2012). Theta will\r\n        arise with grey matter damage, which can be resultant of a trauma (such as a blow to the head), a vascular anomaly, an aneurism or structural anomaly (like the jarring of the cerebro-cervical juncture in a car accident).\r\n        <br></p>\r\n</h5>\r\n<p></p>\r\n<p></p>\r\n<p><img src=\"@@PLUGINFILE@@/Theta%20and%20Dementia.png\" alt=\"\" width=\"800\" height=\"633\" role=\"presentation\" style=\"font-size: 1rem;\" class=\"atto_image_button_middle\"></p><p><a name=\"_Toc29328776\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Psychodynamic Theta</a><br></p>\r\n\r\n<p>From Wise’s perspective (1995, 2002), theta is the subconscious, akin to Jung’s personal unconscious. It is the individual’s repressed materials, the abuses, the traumas, the trials, the tribulations, and the terrors. Theta is also the reverie, the deep\r\n    longings and wishes, all those things that we push down, to be forgotten in our subconscious. Theta gives these deeply repressed memories life at the top of the sleep cycle in the form of dreams. Wise (1995, 2002) notes that theta can also be a repository\r\n    for suppressed creativity and inspiration; she felt that theta was particularly strong during peak experiences, spiritual insights, and high-functioning brain states (such as deep meditation). She thought that theta brainwave states—which occur predominantly\r\n    when we dream—were affiliated with the subconscious (a match for Jung’s personal unconscious): underlying interpretations and meanings that we are not privy to, but which we create—those that reside under the threshold of our awareness.&nbsp; The\r\n    personal unconscious is the place where we bury our shadows and from which our behaviors unconsciously emerge.&nbsp; </p>\r\n\r\n<h3><a name=\"_Toc29328777\">Lambda</a></h3>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Lambda.png\" alt=\"\" width=\"624\" height=\"421\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></p><p>Lambda is a triangular shaped wave at the occipital\r\n    leads that represents visual tracking. It’s a visual, event related potential that has to do with visual searching—it is like an “aha” when you see something. Lambda is called lambdoid or lambdotal if your eyes are closed.&nbsp; You can see repeated\r\n    sharp transients in the back of the head in an adult that is reading or watching a movie. If a person is put on a task reading and you see theta or higher frequency delta in the back of the head, do not interpret it as a problem, because it might\r\n    be a lambda wave form showing up. Lambda waves are found mostly in patients 6 months to 10 years. </p><br><img src=\"@@PLUGINFILE@@/Lambda%202.png\" alt=\"\" width=\"624\" height=\"425\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><b>ALPHA</b></h3>\r\n\r\n<p>According to the International Federation of Societies for Electroencephalography and Clinical Neurophysiology, the alpha rhythm is defined as: &nbsp;&nbsp;&nbsp; </p>\r\n\r\n<p></p>\r\n<ul>\r\n    <li>A rhythm with a frequency of 8-14Hz in adults</li>\r\n    <li>Present in the posterior part of the head while the eyes are closed and the subject is in a state of relaxed wakefulness. </li>\r\n</ul>\r\n<!--[if !supportLists]-->\r\n<p></p>\r\n\r\n\r\n\r\n<p>Alpha is responsible as the idling state of the brain. The generation of alpha is cortico-cortical processes (Stam, 2006, p. 49), as well as a cortico-thalamic process (DeRidder, 2014; Gunkelman, 2014). That means that alpha is generated from the cortex,\r\n    as well as the thalamus. Although you are relaxed when in a predominantly alpha state, you are in the process of taking packets of data with each alpha wavelet (DeRidder, 2014).&nbsp; </p>\r\n\r\n<p>Alpha can be recognized and differentiated from theta and beta by its sinusoidal rhythm. </p>\r\n\r\n<p>The alpha rhythm attenuates (“blocks”) with the opening of the eyes, with drowsiness, concentration, stimulation or visual fixation. </p>\r\n\r\n<p>Alpha rhythm is usually between 40 – 60 microvolts. About 6% of the healthy adult population has alpha rhythm above 60 microvolts. 30% of adults have alpha rhythm less than 20 microvolts.</p>\r\n\r\n<h3><a name=\"_Toc29328779\">Healthy Alpha</a></h3>\r\n\r\n<p>Alpha is a relaxed and focused space, responsible for the state of flow, being in the zone, and creating. Alpha is the most obvious waveform in the raw EEG, typically showing itself as large amplitude, synchronous waveforms, usually emanating from the\r\n    occipital regions of the head, regions known as O1, Oz, and O2. Alpha reflects perceptual anticipation of forthcoming stimuli (DeRidder, 2014). High amplitude alpha indicates an internally oriented state (i.e., more difficult to perceive an external\r\n    trigger), and low amplitude alpha indicates an externally oriented state (i.e., easy to perceive external stimulus) (DeRidder, 2014). Typically, when an individual closes their eyes, the body is signaled to relax and alpha appears in the EEG; when\r\n    one opens one’s eyes, alpha attenuates. If alpha remains in the EEG for a while after the eyes open, there is a likelihood the individual suffers from brain fog, inability to stay focused, difficulty sequencing thoughts, and difficulty planning; if\r\n    alpha is imperceptible with closed eyes, the individual typically suffers from a trauma, such as PTSD (Swingle, 2010).</p>\r\n\r\n<p><a name=\"_Hlk52257450\"></a><a name=\"_Hlk15366181\">Alpha\r\nhas been noted as the brainwave that is responsible for daydreaming,\r\nfantasizing, visualization (relaxed, detached awareness), seen heavily in pot\r\nsmokers, dreamers, poets, and individuals who work in flow states (such as\r\nenergy healers).</a></p>\r\n\r\n<p>Alpha peak frequency is synonymous with posterior dominant rhythm (PDR) and is the subject’s “idling rate”; everyone has their own dominant alpha frequency, which typically falls between 9 Hz and 11 Hz. Average alpha peak frequency is 10 to 10.5 Hz. An\r\n    11Hz alpha peak frequency indicates a mind that is capable of processing data quickly, or quicker than most. Put simply, the brain has the capability to crunch 11 packets of data per second (the thalamus is gating at 11hz),an apt analogy is that of\r\n    a camera with a fast shutter speed. The speed indicates the capability of the photographer to get a clear, high quality shot. A fast alpha peak frequency is a sign of a facile mind that has the capability to process data quickly. In the case of ruminations\r\n    or obsessions, this asset can work towards unwanted focus or preoccupation, although it is not the cause of the symptoms, but rather a facilitator of fast processing.</p>\r\n\r\n<h3><a name=\"_Toc29328780\">Dual Alpha Peak</a></h3>\r\n\r\n<p>When someone has two separate alpha peak frequencies you see fusiform alpha. Fusiform alpha will have an arciform morphology; this is indicative of a “beat frequency”—created when there are two alpha rhythms present at the same time.<img src=\"@@PLUGINFILE@@/dual%20alpha%20peak.png\" alt=\"Dual alpha peak\" width=\"514\" height=\"468\" class=\"img-responsive atto_image_button_middle\"> </p>\r\n\r\n<p><b><u>Fusiform alpha is a beat frequency\r\nthat is the blending of two separate frequencies</u></b>. This mixing of frequencies will give you an interesting morphology that looks monomorphic, or one shape. Two alpha peaks has been observed within my own clinic as a marker of depression or tendencies\r\n    of low mood and affective disorders.</p>\r\n<p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Figure of Fusiform Alpha</span><br></p><img src=\"@@PLUGINFILE@@/Fusiform%20Alpha.png\" alt=\"\" width=\"400\" height=\"805\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"><br><br>\r\n<p>Alpha rhythm often comes on when someone closes their eyes; the clinicians should be able to get a reliable alpha reading in 20-30 seconds. Fast alpha (above 11 hz) correlates with good semantic and declarative memory performance). It is not linearly\r\n    related to IQ, but is a component of it. </p>\r\n\r\n<p>The quickening of someone’s alpha has been thought of as brain brightening. This enhances memory and semantics. Alpha is your sampling rate. If we see 10 peaks per second, you have 10 hz alpha. You have a higher resolution if you have faster alpha. You\r\n    have crisper, sharper peceptions if you have fast alpha. The alpha rhythm is considered to be made up of two separate functional components.&nbsp; Low alpha band (8-10 Hz): associated with general or global attention, and high alpha band (10-13 Hz):\r\n    reflecting directed or task specific attention.&nbsp; </p>\r\n\r\n<p>Both Sterman et al. (1996) and Klimesch et al. (1993) found that individuals with good (versus poor) memories have stronger desynchronization in the lower alpha band during the encoding and retrieval of memory.&nbsp; Crawford et al. (1995) found more\r\n    lower band alpha power in subjects whose attention was more distractible.&nbsp; When sleep deprivation occurs, it has been found to mostly affect low alpha (and theta), negatively influencing general attention (Sterman, 1999) so that excitation is\r\n    blunted and the frequent return to an inattentive idling state (Hammond, 2018).&nbsp;</p>\r\n\r\n<h3><a name=\"_Toc29328781\">Alpha Slowing</a></h3>\r\n\r\n<p>When there is a lack of blood flow and oxygen to the area, there is often a consequential slowing of alpha at the area. As the area degrades, sometimes the alpha slows considerably below the band. But this depends on how severe the ischemia is (Classen\r\n    and Foreman, 2012). If the slowing is in the theta range, if can be due to a trauma, a vascular anomaly, an aneurism or structural anomaly.</p><img src=\"@@PLUGINFILE@@/Slow%20Alpha.png\" alt=\"\" width=\"800\" height=\"449\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<p><a name=\"_Hlk15366419\">The\r\nmean adult frequency was found to be 10.5Hz, and is slightly higher in females\r\nthan in males (Brazier and Finesinger, 1944; Petersen &amp; Eeg-Olofsson, 1971).&nbsp;\r\nAlpha stabilizes at its final peak by the ages of 10 (Niedermeyer, 1999b),\r\nalthough earlier studies have tracked its stability as high as the age 15\r\n(Peterson &amp; Eeg-Olofsson, 1971)</a>.&nbsp; Mean alpha below 9 Hz is significantly low, and a mean frequency below 8 Hz “is always abnormal, usually suggestive of a diffuse encephalopathy” (Markand, 1990, p. 181) (e.g., with systemic metabolic disorders\r\n    like renal or hepatic disorders, hypothyroidism, hypoglycemia, or with cerebral insults).&nbsp; A general rule (Hughes, 1994) is that anyone from age 8 through centenarians should have an alpha background rhythm of at least 8 Hz.&nbsp;Wu and Liu (1995)\r\n    only found 1% of healthy adults to have a dominant rhythm of 8 Hz. Occasionally a sub-harmonic to alpha is found at ½ the individual’s alpha frequency, and occasionally a fast alpha variant will walk into your clinic, at 13+ Hz. You will know it is\r\n    alpha, because this 14-15 Hz rhythm will block to eye opening, and it is only found in about 3.6% of the population (Brazier &amp; Finesinger, 1944).&nbsp;Above average mean alpha levels may suggest hypervigilance, high intelligence (Gasser, Von Lucadou-Muller\r\n    Verleger, &amp; Bacher, 1983) good memory (Klimesch, Doppelmayr, Schimke, &amp; Pachinger, 1996), and a fast processing rate.&nbsp; Worst case, these are the individuals who can spin into delusional thinking and flights of fancy, where their grip\r\n    on reality is loose. </p>\r\n\r\n<p>The alpha rhythm may also increase with increased body temperature (Gundel, 1984) or hyperthyroidism.&nbsp; The 10-14 Hz range seemed to be important during intellectual activity.&nbsp; Alpha frequency is positively correlated to cognitive performance,\r\n    speed of information processing, and is significantly higher in individuals with good memory performance (Klimesch, 1999).</p>\r\n\r\n<h3><a name=\"_Toc29328785\">Alpha Amplitude</a></h3>\r\n\r\n<p>The highest amplitude of alpha is found in the occipital area and is generally below 50 microvolts (µV).&nbsp; Amplitudes of 20-60 µV have been found in 66% of people, while amplitudes below 20 µV are found in 28%, and above 60 µV in 6% (Simonova et al.,\r\n    1967).&nbsp; Children have higher amplitudes than adults (50-60 µV) and 9% of children (ages 1-15) have amplitudes of 100 µV or higher (Petersen &amp; Eeg-Olofsson, 1971).&nbsp; </p>\r\n\r\n<p>An inverse relationship exists between the frequency of alpha and alpha amplitude (Brazier &amp; Finesinger, 1944).&nbsp; About 7%-9% of adults have a “low-voltage record,” consisting of amplitudes under 20 µV (Markand, 1990), which may or may not display\r\n    alpha activity.</p>\r\n\r\n<p>Klimesch (1999) has found that upper band alpha power (10-12Hz) decreases during semantic processing (i.e. talking)&nbsp; and theta power increases during episodic memory retrieval. Klimesch (1999) also found that a low theta/alpha ratio during resting\r\n    state predicts good cognitive and memory performance, while , while under task, a large increase in theta power (synchronization) and a significant decrease in alpha power (desynchronization) is associated with good cognitive/memory performance.&nbsp;\r\n    In relation to theta activity, it should be noted that Klimesch finds that theta synchronization occurs in a narrow frequency band in the range of the peak theta frequency, whereas there is a second<span><span><b>, </b>inefficient form of theta\r\nsynchronization associated with large, but irregular activity.&nbsp; Klimesch\r\n(1999) concluded:</span></span>\r\n</p>\r\n\r\n<p><span><span>Large scale alpha\r\nsynchronization blocks information processing because very large populations of\r\nneurons oscillate with the same phase and frequency.&nbsp; In contrast, alpha\r\ndesynchronization reflects actual cognitive processes because different\r\nneuronal networks start to oscillate at different frequencies and with\r\ndifferent phases (p. 190).</span></span>\r\n</p>\r\n\r\n<p>Synchronous, persistent alpha is expected with eyes closed—this is effectively the brain “twiddling its thumbs.“ However, when eyes are open, alpha ought to diminish. If it does not, especially if it is predominantly seen on one side, the individual ought\r\n    to consult a neurologist.</p>\r\n\r\n<h3><a name=\"_Toc29328786\">Alpha Asymmetry</a></h3>\r\n\r\n<p>About 80% of individuals have greater alpha amplitude on the right. Alpha on the right can be 2x alpha on the left and still be normal. Because alpha rhythm is usually of higher amplitude on the right side (for right-handed people), a decrease of even\r\n    35% on the right may be significant (Duffy et al., 1989).&nbsp; &nbsp;If alpha is larger on the left it should not be more than 1/5x alpha on the right. When alpha frequency is slower by 1 Hz or more (and localized in one hemisphere), it may indicate\r\n    a focal abnormality (Markand, 1990) warranting a neurological consult; a difference of 1.5 Hz or more is particularly worrisome (Duffy, et al., 1989).</p>\r\n\r\n<h3><a name=\"_Toc29328787\">Alpha\r\nPeak Frequency</a></h3>\r\n\r\n<p>Alpha is considered the predominant idling rhythm in adults, however theta is the predominant rhythm in children until ages 10 - 13, when alpha becomes the more predominant rhythm. Slow brainwave activity (&lt;8hz) continues to decline in the EEG until\r\n    the late twenties. Alpha peak frequency speeds up as be age: 6 Hz at one year of age, 8 Hz range by age 3, reaching 10 Hz by about age 10 (Niedermeyer, 1999b).&nbsp; </p>\r\n\r\n<p>Beginning in the later 50\'s, there is a gradual decrease in alpha frequency, most likely due to pathology such as diminished vascular flow to the brain.&nbsp; However, alpha rhythm will remain above 9 Hz in healthy elderly subjects who do not have systemic\r\n    or neurologic problems (Markand, 1990).&nbsp; Katz and Horowitz (1982) reported an average alpha frequency of 9.8 Hz in individuals in their 70\'s, while Hubbard et al. (1976) found a mean alpha frequency of 8.6 in 10 individuals between the ages of\r\n    100 and 105 years of age.&nbsp; Alpha frequency is lowered in dementia patients.</p>\r\n\r\n<p><a name=\"_Hlk525201212\">Alpha peak frequency is the subject’s “idling rate”; every adult\r\nhas their own dominant alpha frequency, which typically falls between 9 Hz and\r\n11 Hz. Average alpha peak frequency is about 9 to 9.5 Hz. A 10Hz alpha peak\r\nfrequency indicates a mind that is capable of processing 10 packets of data per\r\nsecond—an apt analogy is that of a camera with a fast shutter speed. The speed\r\nindicates the capability of the photographer to get a clear, high quality shot.</a> A fast alpha peak frequency is a sign of a facile mind that has the capability to process data quickly. In the case of ruminations or obsessions, this asset can work towards\r\n    unwanted focus or preoccupation, although it is not the cause of the symptoms, but rather a facilitator of fast processing.<a name=\"_Hlk515397270\"></a><a name=\"_Hlk484153329\"></a></p>\r\n<h3>Developmental Alpha</h3>\r\n<p><img src=\"@@PLUGINFILE@@/Developmental%20Alpha.png\" alt=\"\" width=\"500\" height=\"638\" role=\"presentation\" class=\"atto_image_button_middle\"></p>\r\n<p>As we age, alpha speeds up. At the age of 4 months our alpha frequency is 4Hz. By 12 months it should be 6Hz and by the time we reach the age of 3 years old it should speed up to 8 Hz. Usuall its approximately 9 Hz by 9 years of age and by the time we\r\n    reach ten years old it should be maturing to approximately 10 Hz. In practice it has been noted that boys often take longer than girls to have their alpha mature. Sometimes boys are as old as 13 when their alpha matures.&nbsp;</p>\r\n<h3><a name=\"_Toc29328788\" style=\"color: rgb(55, 71, 79); font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Alpha Blocking</a><br></h3>\r\n\r\n<p><a name=\"_Hlk52257811\"></a><a name=\"_Hlk529261354\">Alpha is thought\r\nto be the brainwave that enacts feelings of being in the “flow,” of being in\r\nthe “zone,” or of being present. During the production of alpha, we generally\r\nare fixed on one task, meditation, or sight. We are typically not dealing with\r\nthoughts that would otherwise busy the mind (i.e. monkey mind type of\r\nthoughts). When someone closes their eyes and does not produce alpha it is\r\nconsidered alpha blocking, which can indicate an inability to relax and calm\r\ndown. It should be noted that 10% of the healthy adult population will not\r\ndisplay alpha with eyes closed. When alpha blocking occurs with eyes closed, it\r\ncan also indicate hypervigilance, a sign of trauma—the individual “white\r\nknuckling”” or displaying an inability to relax. When people’s alpha amplitude decrease\r\nwith eyes closed this is more likely the case. </a><a name=\"_Toc525053829\">In cases like these,\r\nthe ability to calm, to self sooth, the quiet otherwise troublesome thoughts,\r\nmight not come as easily as it would to one’s peers</a>. </p>\r\n\r\n\r\n\r\n<h3><a name=\"_Toc29328789\">Temporal\r\nLobe Alpha</a></h3>\r\n\r\n<p><a name=\"_Hlk39003886\"></a><a name=\"_Hlk523168276\"></a><a name=\"_Hlk526143762\"></a><a name=\"_Hlk525136443\">The\r\nappearance of alpha at the temporal leads is most easily seen in a Laplacian\r\nmontage. “Excess Temporal Lobe Alpha” (TLA) classification is used when\r\nevidence exists that the temporal lobe generates abnormal amounts of alpha. TLA\r\nsuggests frontal lobe disengagement which results in temporal lobe idling and suggests\r\nan affective perceptual problem, prosodic comprehension difficulty, and even a\r\ndeficit in spatial reasoning</a>. </p>\r\n\r\n<p>It is important to accurately determine the source of the alpha and to rule out alpha contamination from posterior regions. Alpha contamination occurs when occipital and parietal alpha spreads into EEG sensors placed in the temporal lobe region, creating\r\n    the illusion of temporal lobe and frontal lobe alpha (due to ear reference contamination) (Hammond &amp; Gunkelman, 2001). </p>\r\n<p>Figure of Temporal Lobe Alpha</p>\r\n<p><img src=\"@@PLUGINFILE@@/Temporal%20Lobe%20Alpha.png\" alt=\"\" width=\"800\" height=\"827\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n<h3><a name=\"_Toc29328790\">Trauma Marker Alpha</a></h3>\r\n\r\n<p>With eyes open, when we see the appearance of alpha gating at T6, which has been found to be a common finding in soldiers who have even been in active combat. TLA suggests frontal lobe disengagement which results in temporal lobe idling. At the location\r\n    of T6 this excessive gating is often seen in individuals dealing with trauma or anxiety.&nbsp; </p>\r\n<p><img src=\"@@PLUGINFILE@@/Temporal%20Lobe%20ALpha%202.png\" alt=\"\" width=\"624\" height=\"399\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><a name=\"_Toc29328791\">Anteriorized\r\nAlpha</a></h3>\r\n\r\n<p>Anteriorized alpha can indicate a number of things. It can&nbsp; mean there is a heightened degree of vigilance or an affect-regulatory issue (this would be reflected in depressive and motivational issues). However, frontal alpha in the EEG may reflect\r\n    drowsiness, as well. Lastly, frontal alpha can indicate that the individual consumes cannabis regularly.</p>\r\n<p><img src=\"@@PLUGINFILE@@/Anteriorized%20alpha.png\" alt=\"\" width=\"500\" height=\"835\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><a name=\"_Toc29328793\">Mu</a></h3>\r\n\r\n<p><a name=\"_Hlk39004292\">Mu rhythm &nbsp;is a\r\nmonomorphic “wicket rhythm” and is often a tick faster than the individual’s\r\nalpha peak frequency (i.e. if one’s alpha peak is at 10Hz, they would present\r\nmu at 11+ hz typically). Mu always presents in C3 and C4, over the sensory\r\nmotor cortex, when the mirror neurons are not engaged. Mu is an indication of frontal\r\nlobe disengagement.</a></p>\r\n\r\n<p>As a baby, mirror neurons enable us to mimic our parents, and “motherese” (a parent’s repeating the “goo -goo” and “gaa-gaa” of babies) enables us to learn speech sounds. We learn all these things by mimicking. Burgoon (1985): 60% of human communication\r\n    is non-verbal and mu is a sign that non-verbal communication is not being seen or perceived by the brain.</p>\r\n\r\n<p>Mimicking and mirroring speech is controlled by the brain’s frontal central loop and central-temporal loop (The temporals allow for the perceptual comprehension of the mimicry). The right-hand side of the sensory motor strip of the brain (C4) is responsible\r\n    for mimicking impressions and the emotional tone of speech, as well as integrate empathy, and emotion. Mirror neurons on the left (C3) lay down language. Oxytocin is for social bonding and oxytocin attenuates mu.&nbsp; Oxytocin is a hormone produced\r\n    in the hypothalamus and released by the pituitary, which plays a role in social bonding, sexual reproduction, childbirth, and the period after childbirth. &nbsp;When we are creating oxytocin, we cannot create mu. </p>\r\n\r\n\r\n\r\n<p>If you suspect mu and you ask your patient to wiggle their fingers, the presence of mu will disappear. <b>&nbsp;</b>It is noteworthy that Mu is present in 70% of the autistic population, whereas only 15% of the fully normal population has mu and 50% of\r\n    the ADHD population have it, as well as 50% of Affective Disorders.<b></b></p><img src=\"@@PLUGINFILE@@/mu%20rhythm%20.png\" alt=\"\" width=\"549\" height=\"769\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h4>Figure of qEEG of Mu Rhythm</h4><br><img src=\"@@PLUGINFILE@@/QEEG%20of%20Mu.png\" alt=\"\" width=\"624\" height=\"521\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h4>Figure of Raw qEEG representation of mu (red box) and harmonic of mu (green box)</h4>\r\n<p><img src=\"@@PLUGINFILE@@/mu%20in%20raw.png\" alt=\"\" width=\"571\" height=\"661\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h2><a name=\"_Toc29328794\">Beta (1, 2, 3)</a></h2>\r\n\r\n<p><a name=\"_Hlk52258251\"></a><a name=\"_Hlk529253653\"></a><a name=\"_Hlk535906617\"></a><a name=\"_Hlk525201352\">Beta occurs from local groups of pyramidal\r\nneurons synchronize; beta &nbsp;is a\r\ncortico-cortical frequency (which means its origin is the bark of the brain,\r\nthe cortex). Beta ranges from Beta 1 (12-15Hz) Beta 2 (15-18Hz), Beta\r\n3(18-25Hz), and High Beta (25-30 Hz)</a> (some cap beta as high as 40Hz). <a name=\"_Hlk521998265\">Beta </a>predominantly occurs in the frontocentral areas of the brain, usually with an amplitude of 30µV or less and is symmetrical This is the brainwave\r\n    of our normal waking consciousness and encompasses all executive functioning, such as making plans, acting, and problem-solving. Beta II is at work much of the time that we are processing details, comprehending, and making meaning. Beta III is shown\r\n    during periods of high focus and engagement. When pathological, beta often appears in high amplitude, often indicating stress, anxiety, fear, and worry. It is beta that allows us to determine what makes us up, who we are, what we believe in (and do\r\n    not believe in), and all other components of our identity. It might be argued that the other frequencies inform our ego state (and they do), but our primary mode of thought is in beta. Individuals with too much high amplitude beta are often those\r\n    suffering from neurological conditions. Wise (1995) noted that “excessive amounts of beta can lead to great psychological discomfort” (p. 3).</p>\r\n\r\n\r\n\r\n<p>Beta is active thought, active thinking. This signature suggests a brain that is having difficulty calming down—there are indications of an hyperaroused or hyperalert state. Of particular interest is the right frontotemporal&nbsp; cortex; it appears this\r\n    is the origin of the high amplitude fast wave activity.&nbsp; This area contains most of the dopamine sensitive neurons in the human cortex, which are associated with reward, attention, planning, motivation, and short term memory. It is bordered from\r\n    behind with the pre-central gyrus, containing the primary motor cortex, an area responsible for voluntary body movements.</p>\r\n\r\n\r\n\r\n<p>&nbsp;</p>\r\n\r\n<h4>Figure of anxiety as seen in the EEG via high amplitude beta (raw data)</h4><img src=\"@@PLUGINFILE@@/beta%20anxiety.png\" alt=\"\" width=\"624\" height=\"561\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h4>Figure of qEEG for High Amplitude Beta signifying anxiety</h4><img src=\"@@PLUGINFILE@@/QEEG%20of%20beta.png\" alt=\"QEEG of Beta\" width=\"624\" height=\"827\" class=\"img-responsive atto_image_button_middle\"><br><br><br>\r\n<h3><a name=\"_Toc16242804\"></a><a name=\"_Toc29328795\">Spindling Beta</a></h3>\r\n\r\n<p>&nbsp;<b style=\"font-size: 1rem;\"><u>Spindling beta</u></b><span style=\"font-size: 1rem;\"> is associated with:</span></p>\r\n\r\n<p></p><ul><li>cortical irritability</li><li>toxic encephalopathy</li><li>epilepsy</li><li>pre-epileptic auras</li><li>benzo toxicity</li><li>10% of ADD &amp; ADHD</li><li>Affective disorders</li><li>Bipolar disorders</li></ul>\r\n    <!--[if !supportLists]--><p></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<p>Very often beta of this morphology and frequency acts as a stabilizing rhythm, or as a compensatory frequency for a less stable EEG. Beta Spindles arrive in EEG as sleep spindles, as a stabilizing rhythm, to prevent one from awakening. &nbsp;Spindling\r\n    beta represents a nonspecific indicator of cortical dysfunction or encephalopathy when <u>determined <b><i>not</i></b>\r\nto be a medication effect</u>. Beta spindles often correlate with an overall anxious demeanor characterized by frequent and intense ruminative thinking. Spindling beta is hyper synchronous and is indicative of central nervous system hyperarousal. Spindling\r\n    beta is also associated with cortical irritability, toxic encephalopathy, epilepsy, pre-epileptic auras, and benzodiazepine toxicity. It also indicates a wakefulness drive, making maintaining sleep more difficult (either difficulty falling asleep\r\n    or staying asleep). This waveform is kindled easily and is common in bi-polar, anxiety, insomnia, as well as impulsivity. </p>\r\n\r\n<h4>Figure of Benzodiazepine-induced Spindling beta (raw data)</h4><br><img src=\"@@PLUGINFILE@@/Spindling%20Beta%202.png\" alt=\"\" width=\"624\" height=\"556\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h4>Figure of qEEG for high amplitude spindling beta (Benzodiazepine use)</h4>\r\n<p><img src=\"@@PLUGINFILE@@/Qeeg%20of%20spinding%20beta%20.png\" alt=\"\" width=\"624\" height=\"808\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h2><a name=\"_Toc29328796\">Gamma</a></h2>\r\n\r\n<p><span style=\"\">Of all the brainwaves, gamma (40+ Hz)\r\nis the least understood. This is largely because of the, until recent,\r\ntechnological limitations of equipment to pick up these very fast, very tiny,\r\n30+ Hz brainwaves. Complicating the process is the fact that gamma is easily\r\nconfused with muscle artifact from the head and jaw. Gamma is seen in the EEG\r\nwhen the participant is presented with unpredicted stimuli (Arnal et al.,\r\n2011). &nbsp;It is the “aha!” or “Eureka!” of\r\nthe EEG. It arrives in bursts when we recognize something novel.</span></p>\r\n\r\n<p>Gamma travels in envelopes, which surround the oscillation, making it appear with a spindle shape, and it has the ability to arise in any structure of the brain, because interneurons connected by GABA <sub>A </sub>receptors are ubiquitous throughout the\r\n    brain (Buzsaki, 2006, p. 75). Of most interest, gamma has been implicated to be the binding rhythm of consciousness (Buzsaki, 2006, Gold, 1999; Hughes, 2008). It is not generated via a local neurophysiological generator, but is rather an emergent\r\n    property of networks (Gunkelman, 2015) and is related to subjective awareness (Gunkelman, 2014). &nbsp;Gamma is healthy when it is nested in other frequencies, which is a phenomenon known as phase-amplitude cross frequency coupling, where the phase\r\n    of one frequency (e.g., theta) changes the amplitude of another frequency (e.g., gamma). As the theta goes electro-negative, gamma is active, but when theta goes positive, gamma attenuates (Gunkelman, 2015). Gamma has also been tied to deep meditative\r\n    states. Lutz, Greischar, Rawlings, Richard, and Davidson (2004) found that long-term meditators produce self-induced high amplitude gamma when meditating.</p>\r\n\r\n<p>Gamma-frequency oscillations are typically short-lasting, transient events (Buzsaki, 2006, p. 76). One of the markers of pathological gamma is persistence; healthy gamma ought to occur in bursts or “chirps” (DeRidder, 2014). Low-frequency oscillations\r\n    (such as those of delta and theta) have been reported to coordinate long-range communication, while gamma oscillations (40-150) coordinate local communication (Buzsaki &amp; Draguhn, 2004; von Stein et al., 2000). Local communication is between very\r\n    close neuronal pools. At times brainwaves come into harmony (e.g., 45 Hz gamma laid over a background of 9 Hz alpha is a harmonic, since 45 divides into 9), and other patterns that represent certain states of being and of mind.</p>\r\n<h4>Figure of Gamma Activity</h4>\r\n<p><img src=\"@@PLUGINFILE@@/Gamma.png\" alt=\"\" width=\"1000\" height=\"719\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n\r\n<p>&nbsp;</p><br>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',20,1655387770),(37,18,'Developmental EEG','',1,'<p></p><h2><a name=\"_Toc29328798\">Pre-natal</a></h2>\r\n\r\n<p>At the point of conception, the strategy of the\r\nnervous system is coded in the genes, and the brain follows a pre-defined\r\nblueprint. The initial connectome of the brain, which comes into being very\r\nearly in development, is largely a product of genes and randomness.</p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Developmental%20EEG.png\" alt=\"\" width=\"800\" height=\"674\" role=\"presentation\" class=\"atto_image_button_middle\"></p><p><br></p><p>At 4 weeks, the first brain\r\ncells, the neurons, are establishing at 500,000 per minute. These cells will\r\nnever turn over, unlike the skin. Neurons born in fetal life function all the\r\nway into old age. Within the first 13 weeks of life the reptilian structures of\r\nthe brain are fully formed (the brainstem, spinal cord, cerebellum, and pons).\r\nThe first stage of wiring is when fundamental networks form via an odyssey of\r\nthe neurons, which grab onto glia, to form long fibrous white mater tracks that\r\nbuild the resting state networks in the brain. These are the gross networks of\r\nthe brain. <a name=\"_Hlk28771800\">Low frequency oscillations (i.e., delta and\r\ntheta) help to coordinate long-range communications that run on these networks,\r\nbetween lobes of the brain (von Stein, Chiang, &amp; Konig, 2000). </a>Similar to a musical\r\ninstrument, the longer the string, the lower the pitch (Kung, 2013). These long connections are\r\narchitecturally fundamental for the brain’s development.</p><p><br></p><h4><img src=\"@@PLUGINFILE@@/Fetal%20Development.png\" alt=\"\" width=\"800\" height=\"841\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></h4><h4><span style=\"font-size: 1rem; color: rgb(82, 96, 105); font-family: &quot;Open Sans&quot;, sans-serif;\">By 24 weeks, the\r\nvital organs of the fetus are well formed, the lungs are prepared to fill with\r\nair and the brain has billions of neurons, building 2 million connections every\r\nsecond, until the brain has become a network of trillions of criss-crossing\r\nwires with more connections than stars in the sky. In this second phase of\r\ndevelopment, connections that will remain as integral are made, as are less\r\nimportant connections. When a connection is built and strengthened, it is\r\nreinforced and made to stay, while the less important connections atrophy and\r\nare lost—this is called pruning. Disruption here, within the earliest steps of\r\ndevelopment, during the creation and migration of neurons, is expected to cause\r\nabnormalities that are easy to see, such as microcephaly and lissencephaly, if\r\nthe fetus survives.</span></h4><h3><span style=\"font-size: 1rem; color: rgb(82, 96, 105); font-family: &quot;Open Sans&quot;, sans-serif;\">Lissencephaly,\r\nwhere the brain does not form gyri and sulci, but is smooth, occurs between 12\r\n– 24 weeks of life.</span></h3><p><img src=\"@@PLUGINFILE@@/Lissencephaly.png\" alt=\"Lissencephaly\" width=\"461\" height=\"307\" class=\"img-responsive atto_image_button_middle\"></p><p>Microcephaly, where the head does not grow to its normal size in utero<br></p><p><img src=\"@@PLUGINFILE@@/Microcephaly.png\" alt=\"\" width=\"500\" height=\"288\" role=\"presentation\" class=\"atto_image_button_middle\"><br></p><p><a name=\"_Toc29328799\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Premature Babies</a><br></p>\r\n\r\n<p><span style=\"font-size: 1rem;\">When babies are born before they\r\nare fully developed they lack calcification level in the skull and, for that\r\nreason, their EEG appears of a larger amplitude than a new born baby.</span></p>\r\n\r\n<p>While a burst suppression pattern\r\nsuggests a person is about to die, a premature baby will show a burst\r\nsuppression pattern, which is a normal pattern for a brain that is not ready to\r\nbe out of the womb. This pattern consists of long periods of generalized\r\nattenuated or “flat” activity interrupted by high amplitude\r\nbursts of mixed frequencies and waveforms. The periods of quiescence between\r\nbursts can be as short as 6 seconds or as long as 25 to 30 seconds.</p><h4>Figure of a chart of EEG patterning that occurs in early life</h4><p><img src=\"@@PLUGINFILE@@/Chart%20of%20Developmental%20EEG.png\" alt=\"\" width=\"800\" height=\"309\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p></p><p>&nbsp;</p>\r\n\r\n<h3><a name=\"_Toc29328800\">Birth</a></h3>\r\n\r\n<p>By the time a baby is born, the creation of\r\nneurons is virtually complete. Neurons continue to grow dendritic branches well\r\nafter birth. At birth, a baby’s brain is less than 1 pound of gelatinous\r\ntissue. This is the foundation of the unconscious processes. During this time,\r\nas well, delta is prominent because the white matter is not yet myelinated. Consequentially,\r\ninfants spend a great\r\ndeal of time in&nbsp;<a href=\"https://en.wikipedia.org/wiki/Slow-wave_sleep\" title=\"Slow-wave sleep\">slow-wave\r\nsleep</a>, and thus have delta\r\nwave activity as their predominant wave form. Analysis of the&nbsp;<a href=\"https://en.wikipedia.org/wiki/Wakefulness\" title=\"Wakefulness\">waking</a>&nbsp;EEG of a&nbsp;<a href=\"https://en.wikipedia.org/wiki/Newborn\" title=\"Newborn\">newborn</a>&nbsp;infant indicates that delta\r\nwave activity is predominant in that age, and still appears in a waking EEG of\r\nfive-year-olds.<a href=\"https://en.wikipedia.org/wiki/Delta_wave#cite_note-isbn0-632-05361-5-14\"><sup>[14]</sup></a><sup></sup></p>\r\n\r\n<p>The neonatal weeks are\r\ncrucial for the neurophysiological effects of nursing on the somato-sensory\r\nprojection areas of the mouth and the relevant associative cortical areas.\r\nChugani et al. (1987) have shown in PET recordings that during the first weeks\r\nof life there is an increase in blood flow in those brain structures (brain\r\nstem, cerebellum, striatum and the sensory areas of the cortex) that\r\nparticipate in nursing responses. At six months, the <i>theta </i>rhythm\r\nprevailed in both hemispheres, but had a right hemisphere posterior maximum.\r\nPaul et al. (1996) have shown in infants from the age of 2 to 26 weeks that\r\nfeeding is connected with an amplitude increase and a growing degree of\r\nsynchronization in the EEG, with an exception of the age of 10 weeks,\r\nwhen no significant EEG changes were recorded. This newly acquired\r\nneurophysiological organization between subcortical and cortical structures can\r\ngive rise to a synchronized activity in wide brain areas (Scher, 1989). The\r\nspecial kind of <i>θ</i>-activity\r\nwhose activation we were able to recognize during feeding in 6 month-old\r\ninfants has been termed hedonic <i>θ</i>-activity\r\nby Maulsby (1971).</p>\r\n\r\n<h3><a name=\"_Toc29328801\">Vision</a></h3>\r\n\r\n<p>New synapses are\r\ncreated at a staggering rate in the infant brain. IN BA 17 alone, over ½\r\nmillion per second are developed between 2 and 4 months of age. In fetu development\r\nalso destroys connections (107). Initially the baby sees as though they were looking\r\nat a faded photograph through a tube. This prevents excess stimuli. </p>\r\n\r\n<h3><a name=\"_Toc29328802\">Breastfeeding</a></h3>\r\n\r\n<p>Because the\r\nprimary source of activity of the EEG is in the cortical neural processes, the\r\nchange in the EEG pattern in newborn infants during the feeding processes may\r\nbe indicative of a shaping of a primitive protomental image, i.e. a sensory\r\nmemory formation at the cortical level, that starts after birth and runs in\r\nparallel to the deep automatic brain functions regulating the reflexive and\r\nautonomous neural events of the nursing exchanges. This may be important, since\r\nthe participation of the cortex in the effects of newborn feeding has not been\r\nrecognized before and its plausible implications for the bodily self experience\r\n(the nascent body ego) is so far unknown, in contrast to the relatively\r\nwell-known role of the brain stem and the diencephalic structures that regulate\r\nthe sucking reflex, the homeostasis of vital biological func- tions and the\r\nbasic affective processes (Damasio, 1996, 2000; Lehtonen, 2006; Watt, 2003).</p>\r\n\r\n<p>In another study\r\npenetrating the same developmental phenomena, Paul et al. (1996) have shown in\r\ninfants from the age of 2 to 26 weeks that feeding is connected with an\r\namplitude increase and a growing degree of synchronization in the EEG, with an\r\nexception of the age of 10 weeks, when no significant EEG changes were\r\nrecorded. These observations are quite in line with our findings. Chugani et\r\nal. (1987) have shown in PET recordings that during the first weeks of life\r\nthere is an increase in blood flow in those brain structures (brain stem,\r\ncerebellum, striatum and the sensory areas of the cortex) that participate in\r\nnursing responses. These references, though short and selected, illuminate\r\nthe wide scope of physiological phenomena that are connected with nursing and\r\nthe multiple changes in the psychophysiological state of the offspring that occur\r\nin infant care.</p>\r\n\r\n<h3><a name=\"_Toc29328803\">Auditory Perception</a></h3>\r\n\r\n<p>Long\r\nbefore the infant can comprehend language or speak a single word, it has a\r\nrepertoire of signals to communicate its internal states. Experimental studies suggest the infant is\r\nendowed immediately after birth with a readiness to differentiate the mother’s\r\nvoice from a non-mother voice (Fifer and Moon, 1994). During\r\nthis fundamental period, the child’s innate neoverbal abilities are hugely\r\ninfluenced by social and emotional factors. Developments occur due to dialogic\r\n“face engagements where the emotionally-attuned mother shares in and\r\narticulates the child’s emotional state.&nbsp;\r\nIn these experiences, the infant reads the\r\nmother’s face for positive emotions, appraisals of relevant and interesting\r\ninteractions and events. &nbsp;</p>\r\n\r\n<p>By Approximately one year of\r\nage comes the emergence of single word speech. At this stage, the infant\r\nincreasingly attends to both the visual and auditory stimulation of his\r\ncaretakers’ faces. The visual information received from faces is utilized in\r\nspeech perception (Green &amp; Kuhl, 1989).</p>\r\n\r\n<h3><a name=\"_Toc29328804\">Hypnagogic Hypersynchrony</a></h3>\r\n\r\n<p>Hypnagogic Hypersynchrony (HH) is\r\nthe pattern seen in infants and children during the transition from drowsiness\r\nto sleep. It consists of high amplitude, paroxysmal, bilateral, rhythmic bursts\r\nof 3 to 5 Hz waves. Unlike, POSTS, which live in the occipital leads, HH is a\r\ndiffuse pattern, tending towards anterior dominance. It may emerge as early as\r\n4 months but is seen in the majority of infants between 6 to 8 months old. HH\r\nmay be continuous from ages 8 to 12 months but as the child ages a more\r\nparoxysmal type of HH is seen. The pattern begins to dissolve by age 2 years\r\nand is usually gone by age 12 years. Since this is only a transition pattern,\r\nit will disappear once N2 sleep is reached. At three months, the distinctive\r\npattern of hypnagogic hypersynchrony emerges replacing the high amplitude 2 to\r\n3 Hz rhythm seen during drowsiness. This high amplitude bisynchronous rhythmic\r\n3 to 6 Hz activity can be paroxysmal or continuous for several minutes either\r\nat the beginning or end of the sleep cycle.</p>\r\n\r\n<p>After 3 months of age, all NREM and REM sleep stages show maturation as\r\nwell as development of new patterns. REM now only occupies 25% of the total\r\nsleep time. During NREM sleep, patterns reach mature formations. Sleep spindles\r\nare fully developed, synchronous, and symmetrical by 2 years. The amplitude and\r\nincidence of V-waves and K-complexes decrease at 3 to 4 years until the adult\r\nwaveform is attained.</p>\r\n\r\n<h4>Figure of Hypnogogic Hypersynchrony</h4><img src=\"@@PLUGINFILE@@/Hypnogogic%20Hypersynchrony.png\" alt=\"\" width=\"604\" height=\"385\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\"><br></a></h2><h2><a name=\"_Toc29328805\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Pediatric EEG (Age 1 to Adolescence)</a><br></h2>\r\n\r\n<p>A child has\r\nhundreds of trillions of connections in the brain, twice as many as the adult.\r\nExperience determines which of these connections to take away and which of them\r\nto leave. This pruning process is what learning is, on a neurodevelopmental\r\nlevel. As the child grows into a adult, the brain becomes more and more complex.</p>\r\n\r\n<p>As the baby grows into an adult,\r\ntheir processing rate also speeds up, from 4Hz at 4 months of age, 6Hz at 12\r\nmonths of age, and finally 8Hz by 3 years of age. B the time the child reaches\r\n10 (some say even 15) years of age, their alpha peak frequency (also called\r\nposterior dominant rhythm) has sped up to 10Hz, roughly, where it will stay\r\nuntil they reach their later 50s.</p>\r\n\r\n<h3><a name=\"_Toc29328806\">Language and Auditory\r\nPerception</a></h3>\r\n\r\n<p>While 13-month-old\r\nbabies listen and understand with both cerebral hemispheres, but by 20 months\r\nthe language center of the brain has begun to shift to the left hemisphere,\r\nwhere the majority of adult process primary auditory information (Wernicke’s\r\nand Broca’s areas). The brain will begin to specialize in languages that it\r\nknows best, and this language will trigger the left hemisphere. Foreign\r\nlanguages will still access the right hemisphere (one of the reasons\r\nintroducing multiple languages to your child is beneficial to their\r\nneurological development).</p>\r\n\r\n<h2><a name=\"_Toc29328807\"></a><a name=\"_Toc16242767\">Posterior Slow Waves of Youth</a> (PSWY)</h2>\r\n\r\n<p>Posterior slow waves of youth are\r\nphysiologically high-voltage theta or delta waves most commonly seen in\r\nchildren aged 8–14 years, but uncommon in children under 2 years. PSWYs &nbsp;occur in 15% of healthy individuals aged 16–20\r\nyears but are rare in adults above 21 years of age. These are slow theta and\r\ndelta waves that are intermixed with alpha waves. They attenuate with eyes\r\nopening and they occur as sporadic single waves or as bursts of\r\ntransient waves interspersed by one or several seconds or regular background\r\nactivity. PSOY are usually bisynchronous but can have shifting symmetry (Stern\r\n2005).</p><h4>Posterior\r\nSlow Waves of Youth in a 2 <sup>1/2</sup> year old male</h4><p><img src=\"@@PLUGINFILE@@/PSWY.png\" alt=\"PSWY\" width=\"800\" height=\"773\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p></p><h3><a name=\"_Toc29328808\">POSTS</a></h3>\r\n\r\n<p>Appearing in\r\nchildren, Positive Occipital Sharp Transients of Sleep (POSTS) are surface\r\npositive monophasic or diphasic waves are occipital in origin and synchronized,\r\nalthough they can be asymmetric between posterior electrode arrays. POSTS\r\nappear around age 5 years as the occipital delta of sleep begins to decrease\r\n(Yamada and Meng 2010). Transient and sharp in nature, they are high amplitude\r\n4 to 5 Hz runs, lasting 1 to 2 seconds, and repeating every 4 to 6 seconds.\r\nThey are seen during late N1 sleep stage and disappear with deep sleep.</p>\r\n\r\n<h4>Figure of Positive Occipital Sharp Transients in a child drifting into\r\nNREM2 sleep</h4><img src=\"@@PLUGINFILE@@/POSTS.png\" alt=\"\" width=\"800\" height=\"642\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br><p></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><h3><a name=\"_Toc29328809\">OIRDA</a></h3>\r\n\r\n<p><a name=\"_Hlk505064545\">OIRDA\r\nstands for occipital intermittent delta activity. OIRDA is a delta pattern that\r\noften spreads from the occipital leads to the posterior temporal regions on\r\nboth the right and the left hemispheres. This pattern is usually seen in\r\nchildren, however the clinical significance of it is not yet agreed upon within\r\nthe neurological community. While OIRDA has been linked to epileptic disorders,\r\nit has also been linked to encephalopathy. There are some cases of OIRDA\r\nreported that have not demonstrated pathological significance. </a></p>\r\n\r\n\r\n\r\n<p>&nbsp;<img src=\"@@PLUGINFILE@@/OIRDA.png\" alt=\"\" width=\"624\" height=\"465\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><h2><a name=\"_Toc29328810\">Adolescence</a></h2>\r\n\r\n<p>The teenage brain is the final\r\nfrontier of immense neural development The focus of brain development at this\r\npoint is the pre-frontal cortex. This region, “the fourth brain,” allows us to\r\nmake future plans, and is involved in personal responsibility, morality, and self-control.\r\nThis maturation process shapes personality, behavior and identity.&nbsp; During this time girls are dealing with the\r\nflux of estrogen and progesterone, and for boys the production of testosterone\r\nincreases. This all occurs in the limbic system, generated by the hypothalamus,\r\nwhich can lead to emotional lability and moodiness. </p>\r\n\r\n<p>Adolescents create\r\nmelatonin on a different schedule than adults, which makes them stay up at\r\nnight about two hours later. This s one of the reasons teenager sleep until\r\nnoon on weekends (when they’re not in school). In addition, teenage brains need\r\nmore sleep than adults (9-10 bours compared to 8).</p>\r\n\r\n<p><a name=\"_Toc29328811\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Adult</a></p>\r\n\r\n<p>Stem cells in a\r\nnew brain are prolific, but in an adult brain, few neurons are produced and\r\nmost stem cells remain inactive. It is from age 25 until about 55 (or later\r\n50s) that we are at the seeming apex of our development as humans. Our sleep\r\ncycles remain constant, our hormones are also reliable, and we are relatively\r\nstable (barring insult). Inless otherwise mentioned herein, when EEG is\r\nreferenced, in general, it is referenced in view of the normal, healthy adult\r\nbran. </p>\r\n\r\n<h2><a name=\"_Toc29328812\">Senior</a></h2>\r\n\r\n<p>One of the\r\nfundamental components of how we age has to do with the maintenance of physical\r\nexercise. In addition, mental activity and heredity play big roles in our\r\nageing process, but when we exercise, we create more brain-derived neurotrophic\r\nfactor (BDNF) which fertilizes brain cells and propels the growth of new neurons.\r\nStudies have found that rodents who exercise produce two times as much BDNF as\r\ntheir ore sedentary counterparts. The brains of elderly people who exercise are\r\nin far better shape, on average, than those who don’t.</p>\r\n\r\n<p>Similar to the body, in a\r\nmetaphorical sense, the brain is like a muscle. The more that you exercise it\r\nwith information and novelty, the better it gets. Suddenly, at seventy, you\r\nrealize the declines of your twilight years have aggregated and that you are\r\nnot cognitively what you used to be. The more unfamiliar the information, the\r\nmore trouble you are going to have as an elderly person. A perfect example is\r\nthe difficulty many baby boomers have with computers, if they did not adopt use\r\nof the new hardware (and software) and maintain abreast of the changes as they\r\naged.</p>\r\n\r\n<p>When we learn\r\nsomething new, neurons in the hippocampus send messages across the gaps that\r\nconnect the terminal buttons, strengthening networks associated with learning. Essential\r\nto the strength of the connections are calcium molecules, which go into a\r\nneuron and make the connection more reliable. Calcium travels through NMDA\r\nreceptors, which are inextricably linked to cognitive decline in age. NMDA\r\nreceptors are glutamate receptor and ion channel proteins found in nerve\r\ncells. These receptors are very important for controlling synaptic plasticity\r\nand memory function.</p>\r\n\r\n<p>While we may see\r\nthe diseases and pathologies related to age wreak havoc on the body, they area\r\nalso wreaking havoc on the brain. As we age, our processing rate slows down\r\nfrom its peak (typically 9 -11 Hz) to a slowed version. We become less able to\r\nretain new information and the areas of the brain most recently developed for\r\nevolution are the most vulnerable. This is notably the temporal lobes and the\r\npre-frontal cortex (in combination responsible for auditory processing, memory\r\nand executive functioning).</p><br><p></p><p></p><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',15,1654216981),(38,18,'Intake Assessment','',1,'<p><b>Intake Assessment</b></p><p><span>The first meeting the clinician has with a client may start with the moment they answer the phone or respond to an email from the inquiring patient or client (if you are a licensed clinician, the term \'patient\' is correct for the population you treat; if you are not a license clinician, \'client\' is the more appropriate term). While this first meeting may seem inconsequential, it sets the stage for the future initial consultation, or intake session. It is important to gather all basic information at this stage, including the patients contact information (email and / or phone), their name, and whether they desire to use insurance or cash pay.&nbsp;</span></p><p>There are many online systems that make this type of management possible, and allows for a growing practice. A few systems are:&nbsp;<span style=\"font-size: 1rem;\">Jane, Practice Fusion, Care Cloud, Centricity and Medisoft (2022). Before you start an independent practice, research which system best suits your needs.&nbsp;</span></p><p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/patient%20and%20therapist.jpeg\" alt=\"therapist\" width=\"500\" height=\"334\" class=\"atto_image_button_middle\"></span></p><p><span style=\"font-size: 1rem;\">One of the most important pieces for any clinician or neurotherapist to keep at the forefront of their mind is their capacity to treat the patient </span><u style=\"font-size: 1rem;\">according to their clinical license or lack thereof.&nbsp;</u><span style=\"font-size: 1rem;\">&nbsp;If the neurotherapist does not have a clinical license, their role is limited to stress reduction and peak performance. They are not allowed to treat psychopathologies (like mood disorders, psychological disorders, or physical issues). If you do not have a clinical license (as an LMFT, LSCW, Chiropractor, RN, psychologist, MD, etc.) it is paramount that you refer out any patient presenting with a legitimate mental (or physical) health condition.&nbsp;</span><br></p><p><b>Initial Consultation</b></p><p><span>The initial consultation is the first&nbsp; in-person meeting between a neurotherapist and their patient. During this meeting, much about the patient should be covered, including their medical history, any medications they are taking, education to date, their family history, emergency contact info, drug and alcohol use (recreational and other), job, relationship (married, single, etc.), if they have&nbsp; children, significant life events their history of developmental trauma (i.e. was their any abuse or neglect or tumultuous home environment while under age 18) and most importantly, the reason they are seeking your help at the moment.&nbsp; All of this information ought to be written down (usually by the patient) in their intake forms, but also discussed in person with the clinician.&nbsp;</span></p><p><span><b>Forms</b></span></p><p><img src=\"@@PLUGINFILE@@/Intake%20form.png\" alt=\"INtake form\" width=\"500\" height=\"620\" class=\"img-responsive atto_image_button_middle\"></p><p>Of most important forms is that wherein the patient consents to HIPAA. This stands for The Health Insurance Portability and Accountability Act of 1996, and is<span>&nbsp;<span style=\"\">a federal law that required the creation of national standards to protect sensitive patient health information from being disclosed without the patient\'s consent or knowledge</span>. Some other important forms are: insurance consent forms, fee consent forms, QEEG consent forms, and an informed consent form for the types of neurotherapy done at the location.&nbsp;</span></p><p><span><b>Additional Forms</b></span></p><p><span><span>There are times when additional forms are necessary. Some other forms clinicians may want to consider incorporating into their practice (depending upon individual patient need) are:</span></span></p><p></p><ul><li><span><span><u>Assessment of progress</u> (where a patient ranks their assessment of their improvement throughout the course of treatment)</span></span></li><li><span><span><u>Release of information</u> form (in case the parents of the 18+ year old patient want information, or the patient wants you to share information with another physician / health care practitioner)</span></span></li><li><span><span><u>GAD 7</u> (depression assessment), good for ongoing assessment</span></span></li><li><span><span><u>PHQ - 9 </u>(anxiety assessment), good for ongoing assessment</span></span></li><li><span><span><u>Insurance forms </u>(if the patient is paying insurance, its wise to have them sign something acknowledging financial responsibility should their insurance fall through)</span></span></li><li><u style=\"font-size: 1rem;\">Credit Card Information form</u><span style=\"font-size: 1rem;\"> (in case you want to have their card on file to bill for ongoing sessions</span></li><li><u style=\"font-size: 1rem;\">Suicide Prevention Contract</u><span style=\"font-size: 1rem;\"> (this is to be used only if the patient is presenting with suicidal ideation or desirousness.&nbsp; These contracts usually cover steps to take in case suicide feels dangerously close, including hotlines to call, therapists number and other emergency plans)</span></li><li><u style=\"font-size: 1rem;\">Protocol Progress Sheets</u><span style=\"font-size: 1rem;\"> (this is an in-house form for the patient\'s folder, documenting their progress with each protocol used)</span></li><li><u style=\"font-size: 1rem;\">Seizure Checklist</u></li><li><u style=\"font-size: 1rem;\">Sleep Inventory</u></li></ul><p></p><p><b>Pre and Post Treatment Assessment</b></p><p><span>Most clinicians in the neurotherapy realm take assessments of their patients\' brain data. This is usually in the form of EEG, which is quantified for ease of interpretation and analysis. Here are some before and after images--often the quantitative data can be quite compelling.&nbsp;</span></p><p><span><img src=\"@@PLUGINFILE@@/bipolar%20befre%20and%20after.png\" alt=\"bipola berofre and after\" width=\"700\" height=\"372\" class=\"img-responsive atto_image_button_left\"><br></span></p><p><span><img src=\"@@PLUGINFILE@@/Acute%20Stress%20Disorder%20before%20and%20after.png\" alt=\"acute stress disorder\" width=\"700\" height=\"495\" class=\"img-responsive atto_image_button_left\"><br></span></p><p><span><img src=\"@@PLUGINFILE@@/Vascular%20Dementia.png\" alt=\"Vascular Dementia\" width=\"700\" height=\"554\" class=\"img-responsive atto_image_button_left\"><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span>Some clinicians use Event Related Potentials (ERPs) to determine reaction times. This is a more advanced form of computational neuroanalysis and those who subscribe to is say they cannot imagine working without them.</span></p><p><span><img src=\"@@PLUGINFILE@@/ERP%20before%20and%20after%20%281%29.png\" alt=\"ERP before and after\" width=\"600\" height=\"572\" class=\"img-responsive atto_image_button_left\"><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span><br></span></p><p><span>The final type of before and after assessments taken are of cognitive exams--some are the more well-known and formal examinations (like the MMPI, the&nbsp;WAIS-IV, and the WISC-IV, though these are administered less commonly and what is more popular in clinic are the automated tests, such as Cambridge Brain Sciences psychological exams and CNS Vital Signs.</span></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',8,1655387553),(39,18,'Capping and Recording an EEG','',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/695265616?h=1eeb6f126b&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"Capping_Shane (1).mp4\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',2,1648931747),(40,18,'Video of Normal EEG','',1,'<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/17uKMFfTupY\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1648935193),(41,18,'EEG for Beginners - How to Recognize Waveforms','',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/457888913?h=562f022b36&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"Week One  - EEG and QEEG for Beginners, Fall Session\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1648935902),(42,18,'Missed and Meaningful Signatures in EEG and QEEG','<p>This video covers many important parts of EEG and QEEG analysis.&nbsp;</p><p>1) Sleep Architecture</p><p>2) Vigilance Theory</p><p>3) Signatures of Depression</p><p>4) Signatures of ADHD</p><p>5) Pathological Signatures</p><p>6) Epileptiform Content</p><p>7) Ischemias</p><p>8) TBI</p><p>9) Spindling Beta</p><p>10) Anxiety<span style=\"font-size: 1rem;\">...... and more.</span></p><p><br></p>',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/484119388?h=830670bd84&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"Week Four - EEG and QEEG For Beginners\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1648936797),(43,21,'Explanation of Z-Score Neuroanalysis and Neurofeedback','<p>Robert Thather, PhD, discusses the creation of normative \"Z-score\" neurofeeedback and the creation of his Quantitative EEG database.</p>',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/429334628?h=19c30c8de6&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"THATCHER - Z SCORE (with intro and outro)\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1648937827),(44,18,'The Phenotype Model with Jay Gunkelman','',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/589486357?h=cb70efe2cb&amp;title=0&amp;byline=0&amp;portrait=0&amp;speed=0&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479/embed\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" frameborder=\"0\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\"></iframe></div><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1648937973),(46,18,'Definition of QEEG with Jay Gunkelman','',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/429326339?h=674a4c9c71&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"JAY - DEFINITION OF QEEG (with intro and outro)\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1649004952),(47,18,'QEEG101 with Tiff Thompson','',1,'<div style=\"padding:75% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/695437529?h=32627f600c&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"EEG101.mp4\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1649005004),(48,18,'The Discovery of SMR with Barry Sterman','',1,'<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/509061030?h=38f000c233&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"STERMAN - Discovering the Sensory Motor Rythmn (SMR)\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1649023208),(49,18,'The Wisdom of Morphology by Tiff Thompson','',1,'<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/dpY2F_2nrAo\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1649024231),(50,18,'Source Localization','',1,'<p>Source localization is difficult with EEG, the more channels one has in the measurement, the more accurate the source localization is. One software tool that has allowed for greater source localization in EEG is LORETA.</p><p></p><h2><a name=\"_Toc35418102\">LORETA</a></h2><p>LORETA stands for Low Resolution Electromagnetic Tomographical Analysis and was developed and published on by Roberto Pascual-Marquis et al. in 1994. LORETA was a way to locate electric activity in the brain based upon multi-channel EEG recordings. LORETA assumed the that, among the infinite set of possibilities of source localization for EEG, the neighboring neurons were simultaneously synchronized with the source defined. The computational task that LORETA undertakes is finding the smoothest of all possible 3D tomographical distributions (a common procedure in generalized signal processing). Tomography is the term used, as it is accurate in the sense that it is used in PET, MRI, and CT scans.</p><h4><b>&nbsp;Here are a few videos showing a few ways LORETA is used in EEG Analysis</b></h4><h4>Here is a video of LORETA as used in EEGLab in MatLab by Arnaud DeLorme</h4><h2>&nbsp;<div><div><div tabindex=\"-1\" title=\"LORETA in EEGLab\" preload=\"auto\" id=\"id_videojs_624a205ed713c_2\" data-setup-lazy=\"{&quot;techOrder&quot;: [&quot;youtube&quot;], &quot;sources&quot;: [{&quot;type&quot;: &quot;video/youtube&quot;, &quot;src&quot;:&quot;https://www.youtube.com/watch?v=amttvN_Sb6A&quot;}], &quot;language&quot;: &quot;en&quot;, &quot;fluid&quot;: true}\" lang=\"en\" role=\"region\" aria-label=\"Video Player\"><div><iframe id=\"id_videojs_624a205ed713c_2_Youtube_api\" frameborder=\"0\" allowfullscreen=\"1\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" title=\"YouTube video player\" width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/amttvN_Sb6A?controls=0&amp;modestbranding=1&amp;rel=0&amp;showinfo=0&amp;loop=0&amp;fs=0&amp;hl=en&amp;enablejsapi=1&amp;origin=https%3A%2F%2Fschoolofneurotherapy.com&amp;widgetid=1\"></iframe><div></div></div><div tabindex=\"-1\" aria-disabled=\"false\"></div><div aria-live=\"off\" aria-atomic=\"true\"></div><button type=\"button\" aria-live=\"polite\" title=\"Play Video\" aria-disabled=\"false\"><span aria-hidden=\"true\"></span>Play Video</button></div></div></div>&nbsp;<br><a name=\"_Toc35418103\"></a></h2><p></p><h4>Here is a video of LORETA and ICA as used in WinEEG by Juri Kropotov</h4><p></p><p></p><div><div><div tabindex=\"-1\" title=\"Juri Kropotov and LORETA in WinEEG\" preload=\"auto\" id=\"id_videojs_624a205ed71d4_3\" data-setup-lazy=\"{&quot;techOrder&quot;: [&quot;youtube&quot;], &quot;sources&quot;: [{&quot;type&quot;: &quot;video/youtube&quot;, &quot;src&quot;:&quot;https://www.youtube.com/watch?v=CrrA771v-WY&quot;}], &quot;language&quot;: &quot;en&quot;, &quot;fluid&quot;: true}\" lang=\"en\" role=\"region\" aria-label=\"Video Player\"><div><iframe id=\"id_videojs_624a205ed71d4_3_Youtube_api\" frameborder=\"0\" allowfullscreen=\"1\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" title=\"YouTube video player\" width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/CrrA771v-WY?controls=0&amp;modestbranding=1&amp;rel=0&amp;showinfo=0&amp;loop=0&amp;fs=0&amp;hl=en&amp;enablejsapi=1&amp;origin=https%3A%2F%2Fschoolofneurotherapy.com&amp;widgetid=2\"></iframe><div></div></div><div tabindex=\"-1\" aria-disabled=\"false\"></div><div aria-live=\"off\" aria-atomic=\"true\"></div><button type=\"button\" aria-live=\"polite\" title=\"Play Video\" aria-disabled=\"false\"><span aria-hidden=\"true\"></span>Play Video</button></div></div></div><br><p></p><p></p><h4>Here is a video of LORETA as used in Neuroguide by Bob Thatcher</h4><p></p><div><div><div tabindex=\"-1\" title=\"Bob Thatcher on LORETA in Neuroguide\" preload=\"auto\" id=\"id_videojs_624a205ed7245_4\" data-setup-lazy=\"{&quot;techOrder&quot;: [&quot;youtube&quot;], &quot;sources&quot;: [{&quot;type&quot;: &quot;video/youtube&quot;, &quot;src&quot;:&quot;https://www.youtube.com/watch?v=VzQoLg-FKBQ&quot;}], &quot;language&quot;: &quot;en&quot;, &quot;fluid&quot;: true}\" lang=\"en\" role=\"region\" aria-label=\"Video Player\"><div><iframe id=\"id_videojs_624a205ed7245_4_Youtube_api\" frameborder=\"0\" allowfullscreen=\"1\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" title=\"YouTube video player\" width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/VzQoLg-FKBQ?controls=0&amp;modestbranding=1&amp;rel=0&amp;showinfo=0&amp;loop=0&amp;fs=0&amp;hl=en&amp;enablejsapi=1&amp;origin=https%3A%2F%2Fschoolofneurotherapy.com&amp;widgetid=3\"></iframe><br>\r\n\r\n</div></div></div></div><br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',2,1654223070),(51,18,'Signal Measurement, filtering methods, and other software fundamentals of digital EEG analysis','<p>This is a video made by software engineer Dr. Sahin Ozsoy covers principles such as bandpass, gain, notch-filter, and other important concepts in Signal Processing.</p>',1,'<div style=\"padding:75% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/695504393?h=7a631131a9&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"VerticalScaleandFiltering (1).mp4\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script><p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1649025736),(52,19,'Different Types of Neurofeedback','',1,'<p></p>\r\n<h3>Neurofeedback and Neuromodulation protocols</h3>\r\n<div>\r\n    <p></p>\r\n    <p>Neurofeedback is based on the success of operant conditioning, the underlying thesis of which is the Law of Effect, which states, when you reward something, you reinforce that behavior. In the case of neurofedback, the patient is rewarded for making\r\n        the appropriate (programmed) brain wave frequency or connectivity metrics, via either visual or auditory reinforcement.</p>\r\n    <p>Many neurofeedback modalities are preceded by an assessment of the brainwave activity, typically through a Quantitative EEG brainmap; there are schools of neurofeedback that do not do this, including the Othmer method and Valdeen Brown’s Neuroptimal.</p>\r\n    <p>There are many different modalities and ways to do neurofeedback. Some are single channel (one active electrode) some are two channels, some are four channels, and some use a 19-channel cap. Since neurofeedback is EEG biofeedback, using the brainwaves\r\n        as the mechanism that is measured is brainwave activity.</p>\r\n    <p>Neurofeedback is based on the success of operant conditioning, the underlying thesis of which is the Law of Effect, which states, when you reward something, you reinforce that behavior. In the case of neurofeedback, the patient is rewarded for making\r\n        the appropriate (programmed) brain wave frequency or connectivity metrics, via either visual or auditory reinforcement.</p>\r\n    <p>Many neurofeedback modalities are preceded by an assessment of the brainwave activity, typically through a Quantitative EEG brainmap; there are schools of neurofeedback that do not do this, including the Othmer method and Valdeen Brown’s Neuroptimal.</p>\r\n    <p>There are many different modalities and ways to do neurofeedback. Some are single channel (one active electrode) some are two channels, some are four channels, and some use a 19-channel cap. Since neurofeedback is EEG biofeedback, using the brainwaves\r\n        as the mechanism that is measured is brainwave activity.</p>\r\n    <p>During neurofeedback training, individual EEG electrodes or a full 19-channel cap are placed on the scalp and the EEG activity of the patient is monitored and fed back to them in real time. Based on the feedback and the practitioner’s guidance, changes\r\n        in brainwave patterns occur and are associated with positive changes in physical, emotional, and psychological states of being.</p>\r\n    <p>Often a patient will ask: “how do I make this work?” or “what do I do?” and the answer is they “will” the screen (or tone) to respond positively to them. The answer that I always use is: “get out of your own way and let your brain do its thing, do\r\n        not get too attached to doing better or doing worse, it will continue to ebb and flow.”</p>\r\n    <p>Neurofeedback is based on the principle that the brain responds to ‘information’ on a conscious and nonconscious manner, and typically without any assistance. We have the ability for complex processing. We find most tasks like breathing, eating and\r\n        digestion are ultimately performed without our focused attention.</p>\r\n    <p><a name=\"_Toc35418104\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">LENS and HPN</a><br></p>\r\n    <p></p>\r\n    <div>\r\n        <p>The LENS (<i>Low Energy Neurofeedback System)</i> technology leverages the neuroplasticity, innate within each and every individual, to help alleviate symptoms, optimize functioning, and reclaim lost neurological and physiological potential. This\r\n            unique approach targets the central nervous system and helps to restore functioning that may have been compromised as a result of brain injury including stroke and concussions, trauma, PTSD, surgical procedures, anoxic events, medications,\r\n            birth trauma, environmental influences, etc. These events often leave in their wake anxiety-depression spectrum issues, headaches, migraines, attention deficits, emotional disturbances, explosiveness, behavioral disorders, movement disorders,\r\n            pain, range of motion issues, etc. </p>\r\n        <p>There are four areas that distinguish the LENS from traditional neurofeedback: </p>\r\n        <p><span style=\"font-size: 1rem;\">1. </span><i style=\"font-size: 1rem;\">Significantly fewer sessions</i><span style=\"font-size: 1rem;\">: rather than using operant conditioning to train the brain, the LENS technology utilizes the client’s unique real-time brain wave metrics (also known as EEG) to </span>\r\n            <i style=\"font-size: 1rem;\">interrupt the maladaptive mechanisms</i><span style=\"font-size: 1rem;\"> that have been adapted by the CNS in response to head trauma and other events listed above. This produces measurable changes in brainwave activity and subsequent symptom reduction or elimination in significantly fewer sessions, with the number needed to improve/restore functioning for the majority of clients falling within the 2-15 session range.</span><br></p>\r\n        <p>2. <i>Does not require conscious effort from the client:</i> the LENS has been used successfully with babies (as young as 3 months of age)/toddlers/children, clients on the autism spectrum, those with ADD/ADHD, and even animals (including racehorses,\r\n            giraffes, gorillas and chimpanzees).</p>\r\n    </div>\r\n    <div>3. <i>Session Duration</i>: a typical LENS session lasts about 6 minutes, and this includes skin prep, sensor placement, running the software, sensor removal and post-session cleanup. For some clients, the actual duration of the LENS itself is as\r\n        little as 1 second. Due to this short session duration, the LENS works well for those who are unable to pay attention to a computer screen for long periods of time, and/or who are not able to understand instructions such as is needed with traditional\r\n        neurofeedback.\r\n        <br></div>\r\n    <div><br></div>\r\n    <div>4. <i>Address pain issues</i>: the LENS technology has been applied to other areas of the body (limbs, torso, hands, etc.) to successfully address pain, discomfort, range of motion issues, and more.</div><br>\r\n    <p></p>\r\n    <h3><a name=\"_Toc35418105\">A LENS Neurofeedback System</a></h3><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/LENS%20Neurofeedback%20System.png\" alt=\"LENS Neurofeedback System\" width=\"919\" height=\"234\"><br>\r\n    <p></p>\r\n    <p><br></p><b>High Performance Neurofeedback, </b>aka HPN Ultra Low Power Neurofeedback, was invented by Cory Snook and is thought to be another version of the LENS. HPN is a type of brainwave based biofeedback that has shown promise of clinical efficacy\r\n    in addressing the symptoms associated with Traumatic Brain Injury (TBI), Post-Concussive Syndrome, Post-Traumatic Stress Disorder (PTSD), Anxiety, Depression, “brain-fog,” and attention deficit disorders.<br><br>\r\n    <p>HPN measures and tracks the electrical activity of the brain (brainwaves) and then sends directly back to the brain a very weak, imperceptible signal containing information based on the just preceding brainwave activity. The power in the signal is\r\n        estimated to be about 3 p W (picowatts). Although the power in this signal is amazingly small, the brain appears to be able to adjust its own functioning based on this feedback.</p>\r\n    <h3><a name=\"_Toc3535268\" style=\"color: rgb(55, 71, 79); font-size: 1.715rem; background-color: rgb(255, 255, 255);\">S</a><span style=\"font-size: 1.715rem;\">low Cortical Potential Neurofeedback and Infra Slow Fluctuation  Neurofeedback</span><br></h3>\r\n    <p></p>\r\n    <p><span lang=\"DE\">Slow Cortical Potential Neurofeedback and Infra-Slow Neurofeedback involve dialing in the right slow cortical potential frequency for the client. In a colloquial sense, these neurofeedback modalities are said to coordinate electrical activity in the brain, controlling activation and deactivation of those behavioral networks.</span></p>\r\n    <p><span lang=\"DE\">Infra-slow Fluctuation (ISF) electroencephalogram (EEG) biofeedback is focused on the lowest energy the brain produces (&lt; 0.1 Hz). The intervention is performed with a Direct Current (DC) coupled neurofeedback amplifier. It is distinct from Slow Cortical Potential (SCP) training and Infra-Low Frequency (ILF) training. It shares a similar optimization process with ILF that focuses on emergent state shifts within sessions.</span></p>\r\n    <h4><a name=\"_Toc35418107\"><span lang=\"DE\">What Are Slow Cortical Potentials and what are Infra Slow Oscillations?</span></a><span lang=\"DE\"></span></h4>\r\n    <p><span lang=\"DE\">Slow Cortical Potentials are slow shifts in the EEG that last from 0.3 seconds to several seconds, infra slow oscillations are typically 0.1Hz and lower. These shifts in the EEG reflect the depolarization of large groups of pyramidal cells in the cortex. These slow shifts are caused by the burning of blood glucose, that makes up the hemodynamics of the glial cells. For two decades researchers have proposed that neurons, glial cells, and blood may be regarded as compound generators of these infra-slow bioelectrical phenomena (Hughes, Lőrincz, Parri, &amp; Crunelli, 2011; Zschocke &amp; Speckmann, 1993). Thalamocortical neurons have been observed to exhibit robust infra-slow oscillations (ISOs), in vitro, at approximately 0.005–0.1 Hz (Lőrincz, Geall, Bao, Crunelli, &amp; Hughes, 2009). After a reappraisal of in vivo and in vitro evidence, Crunelli and Hughes (2010) have proposed a three cardinal oscillator model that identifies one cortical and two thalamic sources of infra-slow frequencies. Astrocytes have recently been identified by Hughes et al. (2011) as a source of ISOs in the 0.003–0.1 frequency range. These researchers observed neurons in cat Thalamus succumbing to a cyclic inhibitory influence that they proposed was generated in the slow regime by Thalamocortical astrocytes. These cells create large electro-negative swings when they depolarize. Slow Cortical Potentials (SCP) are changes of cortical polarization lasting several hundred milliseconds to several seconds. SCPs are related to the excitability level of underlying cortical regions. Negative SCP shifts reflect higher cortical excitability while positive shifts reflect reduced excitability or even inhibition. Sheets of cortical neurons are depolarized in the creation of SCPs. It has been hypothezised that in autism spectrum cases, the threshold of depolarization is too high and in ADHD cases, the threshold of depolarization is too low. Additionally, in patients with seizure conditions, large negative potential shifts have been observed moments before a seizure. (ADHD children are taught to increase the negativity of the SCP, while autistic and seizure cases are taught to decrease the negativity of the SCP).<br><br></span>\r\n        <span lang=\"DE\"></span>\r\n    </p>\r\n    <p><span lang=\"DE\">In Europe Slow Cortical Potential (SCP) neurofeedback is taught by Ute Strehl , who uses a visual to reflect higher arousal (in electro-negative potentials, that is, going up) and lower arousal (in electro-positive potentials, going down). In clinical thresholding, it is important to verbally encourage and reward the patient, especially if they are children. SCP training is a “one size fits all protocol” with the majority of the training done at the vertex. As first developed, the client attempted to produce cortical excitation, a negative DC shift, in the case of ADHD; or cortical inhibition, a positive DC shift, in the case of Epilepsy over the course of many short trials (Birbaumer, 1999; Birbaumer et al., 1994, Kotchoubey et al.,2001 ). More recently SCP training has evolved to train in both negative and positive cortical shifts in the same session with proportions of negative and positive trials dependent on client presentation (Strehl et al., 2006). In clinical interventions, such as epilepsy or ADHD Ute Strehl always implements SCP feedback as a technique in the framework of behavior therapy which is being enumerated by the German statutory health insurance.</span></p>\r\n    <p><span lang=\"DE\">Ute Strehl and colleagues have published extensively in RCT (randomized controlled trials) studies on their work.They have used a slow-wave filter and a 500-millisecond interval moving window. This methodology is available using thought technology equipment and screens (</span>\r\n        <span lang=\"DE\"><a href=\"http://www.thoughttechnology.com/\">www.thoughttechnology.com</a></span><span lang=\"DE\">; <a href=\"https://www.neurocaregroup.com/neuroconn-technologie.html\">https://www.neurocaregroup.com/neuroconn-technologie.html</a>; <a href=\"https://www.mindmedia.com/\">https://www.mindmedia.com/</a>). An important, mandatory feature of SCP feedback is the online artifact control as eye movements and huge EMG actitivty may interfere with EEG activity.</span></p>\r\n    <p><span lang=\"DE\">In America, Infra Slow Neurofeedback is being taught by Siegfried and Sue Othmer. ISF training owes its lineage to the early Beta/SMR training of Susan Othmer and EEG Spectrum (Kaiser &amp; Othmer, 2000). That intervention was done with a single channel of EEG and an intra-hemispheric bipolar montage on the motor strip and temporal lobes. The starting frequency was in the 12–18 Hz range depending on the targeted hemisphere. The Othmers and others (Putman, Othmer, Othmer, &amp; Pollock, 2005; Stokes &amp; Lappin, 2010), modified this technique to include inter-hemispheric placements beginning on the temporal lobes. Instead of set reward bands, a 3 Hz window was shifted up or down contingent upon client response. The intervention produced immediate state shifts in the client. The trainer targeted state regulation in real time by discovering an optimum frequency through trial and error for each client. Success was defined by the immediate improvement in affect and arousal regulation in session and ultimately by generalized improvements in behavioral and state regulation in life. Over time, it became apparent that the vast majority of clients were finding an optimum clinical response at lower and lower frequencies until 2007, when the beginning frequency was established at 0–3 Hz.</span></p>\r\n    <p><span lang=\"DE\">Infra Low neurofeedback is being taught by Mark Smith. Smith has reported clinical results including increased relaxation, better sleep, profound changes in physiology, and a renewed sense of well-being in daily life. ISF neurofeedback was put to the test by using Biofeedback equipment that measured a subject’s physiological response to the training. What was found during that training was blood pressure normalized, heart rate slowed, hands became warm and dry, breathing became deeper and slower and the big muscles in the shoulders (trapezius) relaxed. All direct indications of the relaxation response.</span></p>\r\n    <h3><a name=\"_Toc3535269\">Alpha-Theta</a></h3>\r\n    <p>Alpha/theta training, in which the goal is to achieve an altered, hypnogogic state of consciousness, useful for therapeutic purposes. During alpha theta training, the participant is typically reclined or laying supine, in a comfortable room in a comfortable\r\n        position, with their eyes shut, They are listening to auditory feedback (one popular set of sounds is the sounds of ocean waves and the sound of waves upon the shore). The individual in alpha theta training is trained to increased the amplitude\r\n        of their theta frequencies so that they surpass their alpha frequencies, inducing what is considered a deep state. This increase of theta and decrease of alpha is called a cross-over and is the clinical goal of alpha-theta neurofeedback.</p>\r\n    <p> Some clinicians use Alpha-Theta neurofeedback only as polish at the end of many neurofeedback sessions, as the accessing of theta while conscious can create abreactions in individuals who are not ready to access the deeper realms where suppressions\r\n        and repressions reside. On the flip side, this can be a hugely healing protocol for individuals who need to integrate and incorporate the activation behind stress responses.</p>\r\n    <h3><a name=\"_Toc35418109\">A diagram showing the concept of an alpha theta crossover, the y-axis related to amplitude</a></h3>\r\n    <p><a name=\"_Toc35418109\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Crossover.png\" alt=\"crossover\" width=\"868\" height=\"476\"><br></a></p><br>\r\n    <p></p>\r\n    <p><span style=\"font-size: 1rem;\">Many of the great minds of our times—artists, musicians, scientists, and geniuses of all sorts—have described arriving at their discoveries and innovations often when in a deep dream-like reverie. The alpha-theta brain wave state that reflects this level of trance teeters on the borderline between consciousness and unconsciousness and is the threshold between alpha and theta—a soft, awake brain wave state. This altered state of consciousness has been called different things by different researchers. Maury (1848) called it “hypnogogia,” Green, Green, &amp; Walters (1970) called it “the reverie state,” and Budzynski (1977) dubbed it “the twilight state.”</span><br></p>\r\n    <p>Individuals will often enter this state when daydreaming, resting, meditating, engaging in “mindless” activity (i.e. running, driving long distances), or entering sleep. This state is a calm, relaxed, and unattached presence wherein people report\r\n        receiving imagery, sounds/music, or thoughts of novelty. Einstein reported coming to the notion of this theory of relativity while daydreaming, observing sunbeams and imagining what it would be like to ride on them (Boyd, 1995). Thomas Edison\r\n        used to intentionally induce this state to answer his pressing questions by falling asleep in a chair while holding a ball bearing, with a pie tin placed on the ground underneath his hand. Upon entering light sleep, he would drop the ball bearing\r\n        onto the pie tin, waking him—at which point he would scribble the ideas that arrived in his mind (Robbins, 2000, p. 191).</p>\r\n    <p>In a letter published in 1912, Mozart wrote a colleague about his experience around creativity, music, and this light stage of reverie:</p>\r\n    <p><i>            When I am . . . completely myself, entirely alone, and of good cheer—say, traveling in a carriage or walking after a good meal, or during the night when I cannot sleep, it is on such occasions that my ideas flow best and most abundantly. Whence and how they come I know not, I cannot force them. . . . All this fires my soul, and provided I am not disturbed, my subject enlarges itself, becoming methodized and defined, and the whole, though it be long, stands almost complete and finished in my mind, so I can survey it, like a fine picture or a beautiful statue, at a glance. Nor do I hear in my imagination the parts successively, but I hear them, as it were, all at once. What a delight this is, I cannot tell! All this inventing, this producing, takes place in a lively dream. (34)</i></p>\r\n    <p>This brain wave state Einstein, Mozart, Edison, and others created their masterpieces in is was likely composed of two frequencies: alpha, which is recorded on an electroencephalogram (EEG) as 9-12 oscillations per second (Hz), and theta, 5-8 oscillations\r\n        per second (Hz). Alpha theta is used for many clientele populations, including peak performance neurofeedback training. This training is a means of inducing in the performer heightened amplitudes and presence of alpha and theta brain wave states,\r\n        theorized to bring about “flow” states, or experiences of “being in the zone.” The goal of this type of neurotherapy is to increase the ratio of theta to alpha, encouraging a crossover, whereby the amplitude of theta brainwaves supersedes the\r\n        amplitude of alpha being produced. In personal neurofeedback practice as clinician, I often incorporate alpha-theta training into neurotherapy sessions once an individual has worked through their major psychological or emotional problems via psychotherapy\r\n        or other forms of neurofeedback, demonstrating self-regulation. Otherwise there is risk in accessing the unconscious memories residing in theta state and bringing them into conscious awareness while the individual is psychologically unprepared.\r\n        Alpha-theta training is like a polish, used once a subject displays evidenced psychological readiness to fine-tune their higher-level functioning skills.</p>\r\n    <p>In Egner and Gruzelier’s 2003 study on the enhancement of musicianship in music conservatoires with the aid of neurofeedback, it was discovered that individuals training alpha-theta brainwave states had a positive trend in three criteria of instrumental\r\n        competence (notably, “perceived instrumental competence, especially rhythmic accuracy”), musicality (notably “stylistic accuracy, interpretive imagination, and expressive range”), and communication (notably “emotional commitment and conviction,\r\n        ability to cope with the stress of the situation and with deportment”), whereas the study’s control group (without any neurofeedback) evidenced no improvements (p. 3). In the conservatoires’ real-life quantification, the neurofeedback recipients\r\n        also saw an average a jump of two class grades.</p>\r\n    <p>Another study testing novice singers’ singing abilities as a result of alpha-theta training found similar results in performance communication (specifically “scales of commitment, confidence, enjoyment, attention holding, and deportment”) as well\r\n        as in the technical areas of “breathing, diction, and pitch.” Lastly, the individuals subject to alpha-theta neurofeedback experienced “increased expressiveness, confidence, and stage presence,” all of which positively corresponded with their\r\n        respective alpha-theta learning indices (Leach et al., 2008). While these studies are exciting and noteworthy, they are the first of few and there remains to be a lack of science linking alpha-theta brainwave states and musical abilities.<i></i></p>\r\n    <p><b> </b><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\"><a name=\"_Toc3535270\">Amplitude</a> Training</b></p>\r\n    <p></p>\r\n    <p>Amplitude training was the first neurofeedback “protocol” to be developed, and is uptraining or downtraining the size (or amplitude) of an EEG frequency or range of frequencies. Peak to peak (P – P) and root mean squared (RMS) are measures of a frequency’s\r\n        amplitude from peak to valley. Single channel EEG feedback is usually simple amplitude training, where the individual is suppressing or enhancing frequency bands of delta, theta, alpha, beta, or hight beta. The Neurofield amplitude training is\r\n        currently the only modality that allows for the uptraining of gamma frequencies. In the use of single channel training, a clinician can use ear electrodes as references, or they can use bi-polar training, where one area of the head is trained\r\n        relative to another area of the head. Amplitude training can also be undertaken using a full 19-channel EEG cap.</p>\r\n    <h3><b><a name=\"_Toc35418111\"></a><a name=\"_Toc3535271\">Single Channel v 19-channel</a></b></h3>\r\n    <p>At one time in the history of the field, there was a debate as to whether single channel was better than full 19-channel, and vice versa. The difference is the difference in training one to four channel locations, as opposed to training with 19 active\r\n        electrodes. One is not better than the other, and the question to ask is: is it preferable to train the entire brain (based on the client’s presentation and EEG brainmap) or is it preferable to train single channels? There are many single channel\r\n        amplifiers on the market. </p>\r\n    <h3><b><a name=\"_Toc35418112\"></a><a name=\"_Toc3535272\">Z-score Neurofeedback</a></b></h3>\r\n    <div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/429334628?h=19c30c8de6&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"THATCHER - Z SCORE (with intro and outro)\"></iframe></div>\r\n    <script src=\"https://player.vimeo.com/api/player.js\"></script>\r\n    <p><br></p>\r\n    <p><a name=\"_Toc3535272\"></a></p>\r\n    <p><a name=\"_Toc3535272\">Z-score neurofeedback is used to train the individual towards the “Z of zero.” This means that the individual’s EEG is bring driven towards the normal range. Z-score neurofeedback can be used for measures of coherence, phase, and power differentials in the brain.  Providers that offer Z-score training software are Brainmaster, Neurofield, and Neuroguide.</a></p>\r\n    <p><a name=\"_Toc3535272\">Live Z-scores can be used either for live assessment or for feedback training, depending on how the system is configured and used. When used for assessment, live Z-scores can be viewed during data acquisition, and can also be recorded and reviewed. Z-score neurofeedback relies upon a database of neurotypical EEGs as a basis of relatively.  The z-scores are integrated into the feedback design and they are used to control displays, sounds, and other information for the purpose of operant conditioning and other learning paradigms.<br></a></p>\r\n    <p><a name=\"_Toc3535272\"></a></p>\r\n    <p><a name=\"_Toc3535272\">In Neuroguide, for instance, the live z-scores are monitored using a dynamic JTFA mode (joint time frequency analysis), as opposed to a fast fourier transform (FFT), which is more commonly used for QEEG results (an average of data over time). A Joint time frequency analysis allows for instant z-score feedback, providing real-time information about the state of the brain.</a></p>\r\n    <a name=\"_Toc3535272\">\r\n        <p>The rapid analysis and feedback of Z-scores is essential for timely feedback. Z-score training can be accomplished with 2 or 4 channels of EEG, or with 19 channels. However, the live feedback is not the same as those observed using the postprocessed\r\n            QEEG results.</p>\r\n    </a>\r\n    <p>When inspecting individual live Z-scores in Neuroguide, it is observed that their typical values are not the same as those observed when using postprocessed QEEG results. This is not a problem or defect in the system, it is a natural consequence of\r\n        watching a live statistic, versus a static statistic. Live Z-scores can be used to train a combination of variables including absolute and relative power, power ratios, coherence, phase, and asymmetry. When used in this manner, the EEG Biofeedback\r\n        Training Using Live Z­-Scores and a Normative Database system is no longer targeting just a single variable or attribute. Rather, the possibility arises of training the brain in a complex multi-dimensional manner, s that it learns a comprehensive\r\n        brain state. </p>\r\n    <p>With Z-score training, we can also choose to uptrain or downtrain any components we like, including combinations of components, or relationships between components. So we can train to a Z score of ­2 or ­3, or +2 or +3 or even +6 if we choose. </p>\r\n    <p>Real time Z-score neurofeedback uses instantaneous measures of the EEG data compared to a Gaussian distribution to averaged “instantaneous” time domain spectral measures from groups of normal subjects and then cross­ validates the means and standard\r\n        deviations for each subject for each instant of time.<br></p>\r\n    <h3><b>Wide Band Inhibit (aka “squash”) Neuroptimal</b></h3>\r\n    <p>Little is known about the mechanism of action in Valdeane Brown’s Neuroptimal. This program is a simple set up, where the active electrodes are placed at C3 and C4 and the references are place on the upper ear cartilage and the ground electrode is\r\n        placed on the ear lobe. The activity of the EEG is measured and displayed (using feedback visual called a “mind mirror”) . The slowest activity measured is 0.1Hz and the fastest is 64 HZ. The frequencies are squashed, overall, and this is thought\r\n        of as a squash protocol to many in the field. As stated on the Neuroptimal website: “The differences in electrical signal are measured in terms of Duration, Intensity, Frequency and Shift and is unique to Neuroptimal. This information is offered\r\n        back to the brain in real time via auditory and visual interruptions of the media.” The Neuroptimal approach involves training both sides of the brain at the same time, over the motor strip, using multiple frequencies and reinforcement tones.\r\n        There are three basic stages of training, and the system alters training frequencies at each stage. The Neuroptimal system is dedicated to reducing abnormal variability in the EEG to enhance system integration and functioning.\r\n    </p>\r\n    <p>The system is described on the website as “a unique and highly expanded Neurofeedback process that is more sophisticated than the antiquated linear approaches that only include the 2-D model of frequency and amplitude as initially founded in the field\r\n        of [NF. As a result, Neuroptimal is able to recognize the incredible natural potential of the brain and give information (or communication) that mirrors what the CNS just did. This information takes the form of mathematical interruptions in the\r\n        auditory and visual fields that offers the individual a “mirror” into their own electrical activity. Thereby reminding the individual to move away from discomfort.”</p>\r\n    <p>The Neuroptimal system is marketed to non-clinical users, noting that brain maps and other means of clinical assessment are not necessary, since the device has not been termed a medical device by the FDA, but instead as a personal wellness device.\r\n        They are explicit that the system does not diagnose, treat, mitigate, prevent, or cure any disease, disorder, or abnormal physical state.</p>\r\n    <h2><a name=\"_Toc35418114\">Mind Mirror Neurofeedback, Displaying the Amplitude on the Y-axis and the frequencies on the X-axis</a></h2><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Mind%20Mirror.jpg\" alt=\"Mind Mirror\" width=\"865\" height=\"503\"><br><br>\r\n    <h3><a name=\"_Toc35418115\"></a><a name=\"_Toc3535274\">Multi-Variate Training</a></h3>\r\n    <p>Four channel multi-variate training is a type of neurofeedback that Rob Coben invented, which measures and trains coherence between four electrodes. The protocol works when inputs from sensors are transformed into multivariate coherence values across\r\n        all possible combinations of the four locations or sensors. This information makes up the reward band. Additionally, there are three user-defined inhibit hands that encourage a decrease in EEG frequencies, as a form of amplitude training. </p>The\r\n    multivariate nature of how coherence is calculated comes close to the brain’s noise, itself, and Coben theorizes this makes it easier for the client to train, as opposed to the typical coherence model, where cross correlations between pairs of electrodes\r\n    is used (bivariate coherence). The compromise to using pairwise coherence measures include inter-electrode\r\n    <p>distance, volume conduction of the brain, and the inability to capture three-dimensional brain activity (Nnez, 1994; Nunes and Srivinasan, 2006).</p>\r\n    <p>This method has been demonstrated on the EEGer Training system (developed by Ed Hamlin). Coben and Myers (2010) have shown that four channel multi-variate training has had greater efficacy than single or dual channel coherence training; they believe\r\n        that one advantage to four-channel multi variate training is the number of electrodes used, as well as the statistical sophistication of what is actually fed back to the client.</p>\r\n    <p>Coben intends to continue to refine his model of four channel multi-variate coherence training, foreshadowing future enhancements involving functional connectivity.&nbsp;</p>\r\n    <p><a name=\"_Toc3535277\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">HEG</a><br></p>\r\n    <p>Hemoencephalography (HEG) is a method of measuring brain function by measuring the brain blood flow. <a href=\"http://www.biocompresearch.org/\">Hershel Toomim</a> first coined the term hemoencephalography in 1997. Toomim discovered that the manipulation\r\n        of brain blood flow is voluntary and can be trained using neurofeedback techniques. With the sensor giving feedback of increased blood flow, we can voluntarily increase brain blood flow at the location of the sensor. HEG trains the subject to\r\n        increase blood ﬂow to a targeted area of the brain. Neurofeedback, as we have known it so far, measures the electrical activity of the brain, EEG, as a feedback signal to be controlled by the patient. Here EEG is substituted with blood oxygenation\r\n        for the same purpose.</p>There are two kinds of HEG, pIR and nIR (near infrared), the former is up training temperature and the latter is uptraining oxygen via interaction with an infrared light. Near-infrared HEG (nirHEG): uses a spectrophotometer\r\n    to measure the oxygenated blood flow inside the skull. The bone is translucent and lets light in. The Instrument measures the amount of blood that\'s carrying oxygen. This is similar to the \"pulse-oximeter\" that is used as a finger clip in the hospital,\r\n    and that shines a red light through your skin to measure the blood oxygen level. <br>\r\n    <p>The advantage to using the nirHEG is that the elastic band on the head is easily moved to any location on the scalp to train the corresponding area of the brain. HEG is used on the frontal lobes and other areas where skin is showing. it will not work\r\n        when placed on the hair, however. Unlike traditional neurofeedback, HEG is not affected by eye blinks or facial movement which cause distortion when using EEG.</p>\r\n    <p>Neurofeedback using this new technique provides a means to exercise selected brain areas. Exercise increases blood ﬂ ow to the chosen brain module. Capillaries and dendrites grow with brain exercise (Kaiser 1997, Thompson et al. 1998, Joyce and Seiver\r\n        1997, Rossiter 1996, 1996, Kaiser 1997). An audible tone was devised that increased in pitch to signify increased blood oxygenation. To increase oxygenation one would merely attend to the highest note in each trill and will the next higher note\r\n        to sound. Application of the headband and monitoring patient progress is simple. The treatment process is divided into ten-minute segments. Usually three to four such segments constitute a treatment session.<br><u>Why is brain blood flow important?</u><br>Active\r\n        areas of the brain are marked by high oxygen density and higher than normal temperature. The blood carries the fuel for the brain: oxygen and glucose. When an area of the brain is more active, it has increased blood supply. The brain dilates the\r\n        capillaries of the area in use to bring more blood supply. With continued use, more capillaries and more synaptic connections between neurons are built in that area. When we increase blood flow, that area of the brain is able to do it\'s job better\r\n        and more efficiently.</p>\r\n    <p>Sequential processing, including using language and executing tasks in proper order, takes place in the frontal lobes. Increased blood supply helps the brain accomplish these tasks.</p>\r\n    <p>The frontal cortex is in charge of inhibiting impulses, when appropriate. If the frontal cortex is not functioning well, a person will show a lot of impulsive behaviors. Also involved in this inhibition is control of migraines. <a href=\"http://www.stopmymigraine.com/\">Jeffrey Carmen</a>        has shown that when the frontal cortex has increased blood supply, migraine headaches are well controlled. The frontal lobes are important in the function of working memory. Working memory is important for reading comprehension and carrying out\r\n        tasks.\r\n    </p>\r\n    <p></p>\r\n    <h3><a name=\"_Toc35418117\">Single Photon Emission Computerized Tomography (SPECT Scan) demonstrating blood flow pre-and post-treatment</a></h3><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/HEG%20Image.png\" alt=\"HEG Before and After Image\" width=\"679\" height=\"364\"><br>\r\n    <p></p><br>\r\n    <p></p>\r\n    <h3><b><a name=\"_Toc35418118\"></a><a name=\"_Toc3535278\">Othmer Method</a></b></h3>\r\n    <p>The Othmer method (can be found at eeginfo.com) is recommended for intractable brain based disorders of childhood, such as seizures, conduct disorder, bipolar disorder, spectrum based disorders, pervasive developmental delays, cerebral palsy, birth\r\n        trauma, and acquired birth injuries. Their device is an amplifier, and they rely exclusively on bipolar montages.</p>\r\n    <p>Building primarily on the work of Sterman, they developed a basic and reliable approach to neurofeedback that does not utilize brain mapping. Much of their early techniques involve balancing left and right hemispheres with respect to levels of arousal\r\n        (1999).\r\n    </p>\r\n    <p>The Othmers now largely proffer a new paradigm called Infra-low Frequency Training that involves training sub-delta frequencies that are actually slow shifts in dc brain potentials. This method involves training in frequency ranges of .0003 Hz or\r\n        lower. Despite considerable controversy over whether present day amplifiers are actually capable of accurately providing data on such low frequencies, the Othmers claim that they have modified their amplifiers to achieve this feat. These slow\r\n        frequencies are thought to be base frequencies of the EEG, also considered frequencies of hemodynamics—or the burning of blood glucose. A large number of clinicians have adopted this approach. It has gained recognition among clinicians for being\r\n        very effective, especially in developmentally challenged children. Mark Smith has adopted a more conservative approach with this paradigm by building on more accepted frequency ranges of .001-.003 Hz or higher that can be easily measured with\r\n        modern amplifiers.</p>\r\n    <p></p>\r\n    <h4><a name=\"_Toc35418119\">How does It Work?</a></h4>\r\n    <p>Slow cortical potentials are slow event-related direct-current shifts of the electroencephalogram. Slow cortical potential shifts in the electrical negative direction reflect the depolarization of large cortical cell assemblies, reducing their excitation\r\n        threshold. They change periodically from being electrically positive to electrically negative. They are described as a phasic tuning mechanism related to activities in the brain stem reticular process, the thalamus and the basal ganglia. These\r\n        dc shifts are reflected in the superficial cortical layers and represent synaptic activities in the apical dendrites in those layers. Negative shifts represent increased probability of firing while positive shifts represent decreased probability\r\n        or inhibition. Negative shifts are described as related to the utilization of resources for attention, memory, and other related cognitive mechanisms.</p>\r\n    <h3><a name=\"_Toc35418120\"></a><a name=\"_Toc3535279\">At Home Trainers</a></h3>\r\n    <p>There are at home trainers on the market currently, some offered through New Mind Academy (Richard Soutar’s work), others offered through a program called Myndlift, which uses a muse device to train the pre-frontal cortex of the brain. Through this\r\n        program, people are directed through at home use with the assistance of a local clinician.</p>\r\n    <h3><a name=\"_Toc35418121\">LORETA (Low Resolution Electromagnetic Tomographical Analysis)</a></h3>\r\n    <p><a href=\"https://vimeo.com/443110917\" target=\"_blank\">To see a video explanation of LORETA, click here. </a></p>When recording an EEG, 50% of the data arriving at the site of the electrode is from neurons directly underneath it, and 95% of the data\r\n    comes from within 6 centimeters distance (that’s a circle with a diameter of 2 <sup>1/3</sup> inches—big) (Nunez, 1982; 1995, Cooper et al., 1965). This is one of the reasons that EEG is limited in terms of what it can determine spatially (i.e. where\r\n    something lives in the brain). LORETA neurofeedback training is Z-score training that uses three dimensional source localization so that the location within the interior of the brain can be pinpointed with accuracies of 1cm. LORETA neurofeedback is\r\n    thought to target subcortical structures that are showing deviance in the amount of frequency generated.\r\n    <p></p>\r\n    <p></p>\r\n    <h3>LORETA Z-score</h3>\r\n  <iframe src=\"https://player.vimeo.com/video/443110917?h=bbd6d9f3ed&amp;color=13979b&amp;title=0&amp;portrait=0\" width=\"640\" height=\"360\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n    <p>LORETA Z-Score neurofeedback is thought to regulate the deep structures of the brain and improve connectivity between the brain networks through targeting the central voxel within certain regions of the brain. In each session, a cap with 19 sensors\r\n        is applied to your head. During training, your brainwaves learn to become balanced and normalized as they are rewarded.</p>\r\n    <p>The goal of LORETA is to reinforce stability of information processing in dysregulated networks and connections based on the client’s symptoms. It targets the specific areas of the brain and connections between nodes that are linked to the symptoms.\r\n        In doing so it specifically targets deep brain structures that are out of balance. Similar to traditional Neurofeedback (single channel Neurofeedback) training it provides operant conditioning (rewards) based on your brainwaves compared to the\r\n        brainwaves of a healthy population.</p>\r\n    <p>It is possible to train coherence, phase, and power from 88 Brodmann areas in LORETA Z-score neurofeedback.</p>\r\n    <p>There are a few ways to choose what regions of the brain to train using LORETA Z-score Neurofeedback. One means is using a symptom checklist, which is created from the patient’s EEG. Another method is using Neurodesigner.</p>\r\n    <h2><a name=\"_Toc35418122\">Image from NeuroGuide Z-Score LORETA Neurofeedback</a></h2><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/LORETA%20in%20Neuroguide.png\" alt=\"LORETA in Neuroguide\" width=\"762\" height=\"1640\"><br><br><br>\r\n    <p></p>\r\n    <p></p>\r\n    <h2><a name=\"_Toc35418123\"></a><a name=\"_Toc3535280\">Neuromodulation protocols</a></h2>\r\n    <p>Neuromodulation is also known as neurostimulation is different than neurofeedback, but fits under the umbrella of neurotherapy. Neurofield’s neurotherapy system is known for the blending of neurostimulation into neurofeedback training. Neuromodulation,\r\n        at the clinical level, is comprised of transcranial alternating current stimulation (tACS), transcranial direct current stimulation (tDCS), transcranial random noise stimulation (tRNS), transcranial pink noise stimulation (tAPNS) and pulsed electro-magnetic\r\n        field stimulation (PEMF).</p>\r\n    <h3><a name=\"_Toc35418124\">Three Stimulation Modalities used in Neuromodulation</a></h3>\r\n    <p><a name=\"_Toc35418124\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Three%20Stimulation%20Modalities.png\" alt=\"Three Stimulation Modalities\" width=\"904\" height=\"912\"><br></a></p>\r\n    <h3><a name=\"_Toc35418125\">Transcranial Alternating Current Stimulation (tACS)</a></h3>\r\n    <p>tACS is a form of electrical stimulation that uses two electrodes (a positive electrode called an anode and a negative electrode, the cathode) to pass current back and forth through either the brain or the body. It is called alternating current because\r\n        the side which is giving and receiving electrons (anode and cathode) continuously switches. Any frequency, or blend of frequencies, can be given with these devices. So, if a patient is in need of more delta, the clinician can stimulate them in\r\n        the delta frequencies. This technology is engineered, developed, and sold through Neurofield, Inc, (founded by Nicholas Dogris and Brad Wiitala). Clinicians use stimulation devices to help their patients heal, recover, and change the behavior\r\n        of the brain and their bodies. As opposed to neurofeedback, neurostimulation shows the brain how to behave and the brain, like a copy cat, mimics the stimulation frequency.</p>\r\n    <h3>The NeuroField System</h3>\r\n    <p><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Neurofield%20System.jpg\" alt=\"Neurofield System\" width=\"700\" height=\"426\"><br></p>In transcranial alternating current stimulation, one applies current\r\n    and encourages neural synchronization. As electrons pass through the brain (from anode to cathode) the populations of neurons they go through become more likely to fire. This increased likelihood of firing is generalized to the entire area where current\r\n    is applied. This can cause neurons which were formerly out of phase with each other to align. This happens not just during treatment, but is hypothesized to cause lasting changes to the brain. This is called Spike Timing Dependent Plasticity.\r\n    <h2><a name=\"_Toc35418126\">The Mechanism of Transcranial Alternating Current Stimulation</a></h2><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/tACS.png\" alt=\"tACS\" width=\"777\" height=\"415\"><br><br>\r\n    <h3><a name=\"_Toc35418127\">Transcranial Direct Current Stimulation (tDCS)</a></h3>\r\n    <p>tDCS is transcranial direct current stimulation. It is a form of electrical stimulation that is used to treat many conditions and pathologies, both in the brain and in the body. The technology uses a positive and a negative electrode (called the anode\r\n        and the cathode, respectively). Direct current passes a one-way current through the brain or the body. In the brain, a surge in calcium ions and in sodium ions creates a condition of neuroplasticity, which makes the brain more susceptible to neurofeedback\r\n        and pEMF conditioning. tDCS It increases the potential of the brain to change, learn and grow.</p>tDCS 1) increases blood flow at the targeted areas and, thus, leads to vaso-perfusion (which helps to heal wounds on the brain and the body and also\r\n    encourages angiogenesis and neurogenesis), 2) causes large scale network organization, 3) stimulates/excites the positive electrode site (anode) which increases glutamate and decreases GABA, and inhibits the negative electrode site (cathode) creating\r\n    more GABA at the site of stimulation, and causes calcium and sodium surges in the glial cells, which leads to flexibility in polarity shifting. TDCS does not force the brain to fire. Some of the symptoms and pathologies addressed by tDCS include migraines,\r\n    age-related cognitive decline, and other disorders where the tissues of the brain agree damaged or compromised (such as cerebro-vascular issues, stroke, and some epileptogenic profiles). tDCS protocols cause the underlying blood vessels to dilate,\r\n    which allows oxygenation of the affected areas. A recent meta-analysis showed no serios adverse effects on over 1,000 people across 33,200 sessions (Bikson et al., 2016).<br>\r\n    <h3><a name=\"_Toc35418128\">The application of transcranial direct current</a></h3><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/tDCS.png\" alt=\"tDCS\" width=\"700\" height=\"674\"><br><br><br>\r\n    <h3><a name=\"_Toc35418129\">Transcranial Random Noise Stimulation</a></h3>\r\n    <p>tRNS is a form of electrical stimulation that is used to pass noise (like the white noise of a television screen) through the brain and/or the body. One way to consider tRNS is as a “Wall of noise”. tRNS is different from tDCS because instead of giving\r\n        steady current from anode to cathode, it is giving current at randomized frequencies and milliamperes between the two sites. This means that the region of the brain between the electrodes are stimulated, increasing neuroplasticity and reducing\r\n        stuck patterns. This is one modality used to unlearn problematic fixed patterns. tRNS has also shown benefit for learning in people with developmental abnormalities. When tRNS stimulation is given during math lessons, it helps more than sham stimulation\r\n        or behavioral therapy. Issues of hyper or hypo coherence and hyper or hypo phase lag are addressed by white noise, in addition, white noise is often used at the first layer of multi-layer protocols.</p>\r\n    <h3><a name=\"_Toc35418130\">Different Forms of White Noise Stimulation</a></h3>\r\n    <p><a name=\"_Toc35418130\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Whit%20Noise%20Stim.png\" alt=\"White Noise Stim\" width=\"956\" height=\"346\"><br></a></p>\r\n    <p><br></p>\r\n    <p><a name=\"_Toc35418130\"></a></p>\r\n    <h3><a name=\"_Toc35418131\">Pink Noise Stimulation</a></h3>\r\n    <p>Pink Noise is filtered white noise. This form of stimulation affects the resting membrane potential and has the same types of de-coupling properties as white noise. It also creates increased blood perfusion. Pink noise appears to have an effect on\r\n        microstates, which are associated with the “on-off” switching of a neuron. In using pink noise, you can saturate a neuron with a filtered set of frequencies, that influence the switching of the neurons, effectively changing the ways that they\r\n        fire. tRNS is one modality that can be used to address stuck patterns, such as thalamo-cortical dysrhythmias (which are found in many hearing disorders, form of mood and affect regulation disorders, some attention deficit disorders, and some movement\r\n        disorders). Thalamo-cortical dysrhythmias are disorders where there is a persistent gamma waveform attached to a slower carrier wave (typically 8hz or less). Pink noise is typically one step in a multi-step protocol.</p>\r\n    <h3><a name=\"_Toc35418132\">The bell curve of pink noise</a></h3>\r\n    <p><a name=\"_Toc35418132\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Pink%20Noise.png\" alt=\"pink noise in NF\" width=\"686\" height=\"426\"><br></a></p>\r\n    <p><br></p>\r\n    <p><a name=\"_Toc35418130\"></a></p>\r\n    <h3><a name=\"_Toc35418133\"></a><a name=\"_Toc3535282\">pEMF (Pulsed Electro-Magnetic Frequency)</a></h3>\r\n    <p></p>\r\n    <p><a name=\"_Toc35418130\"></a></p>\r\n    <p><a name=\"_Toc35418130\">Pulsed Electromagnetic Field (pEMF) stimulation is imperceptible, yet the effects are real. pEMF creates an electromagnetic field, which allows cells and tissues in its wake to oscillate at the same frequency. The frequency and duration of the pEMF are important components of the effectiveness of the treatment. This modality is gentle compared to other stimulation technologies. You can\'t feel it because an electromagnetic field is generated through a wire coil that flows through the air and passes through your body effortlessly. One of the happy benefits of pEMF is the increase in blood flow at the site of the stimulation, which can increase angiogenesis by way of allowing more oxygen rich blood to make its way to the site.  At low intensity pEMF is safe and has numerous clinical benefits, including affecting the resting membrane potential (without the forced depolarization of the membrane), inflammation reduction, nerve healing, the healing of bones, the remediation of depression and other affective disorders, and postoperative pain.</a></p>\r\n    <p><a name=\"_Toc35418130\">Due to the low-level voltage output of pEMF, it is safe for infants, the elderly, and animals.</a></p>\r\n    <h4><a name=\"_Toc35418130\">pEMF devices are known for the ability to help reduce pain</a></h4><a name=\"_Toc35418130\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/pEMF%20for%20Pain.png\" alt=\"pEMF for Pain\" width=\"976\" height=\"618\"><br></a>\r\n    <p></p>\r\n    <p><br></p>\r\n    <p><a name=\"_Toc35418130\"></a></p>\r\n    <h3><a name=\"_Toc35418134\"></a><a name=\"_Toc3535283\">CES</a></h3>\r\n    <p><b>Cranial</b> electrotherapy <b>stimulation</b> (CES) is a form of neurostimulation that delivers a small, pulsed, alternating current via electrodes on the head. Recently, a systematic review (2018) found insufficient evidence that CES has clinically\r\n        impactful effects on <a href=\"https://en.wikipedia.org/wiki/Fibromyalgia\" title=\"Fibromyalgia\">fibromyalgia</a>, headache, neuromusculoskeletal pain, degenerative joint pain, depression, or insomnia and there is low-strength evidence suggesting\r\n        modest benefit in patients with anxiety and depression (Shekelle et al, 2018)</p>Dave Siever\'s company, Mind Alive creates cranial electric stimulators, that use photic stimulation, as well as ear clips that deliver small stimulation through the\r\n    ear lobes. <br><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/486/mod_lesson/page_contents/385/Mind%20Alive%20hardware.jpg\" alt=\"Mind Alive Hardware\" width=\"713\" height=\"246\"><br></div><br><br>\r\n<p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',8,1655391402),(53,19,'Early Protocols: SMR, Alpha-Theta, Theta/Beta with Joel Lubar','',1,'<h4>The Peniston - Kulkosky Protocol</h4>\r\n    <p>In the late 1980s, Dr. Eugene Peniston, a clinical psychologist spearheaded research with Paul Kulkosky at the Fort Lyon Colorado, Veterans Hospital, using techniques he had learned at the Menninger Clinic. The protocol guided users into a trancelike\r\n        state where alpha waves and theta waves are both elevated. Peniston found that these frequencies could be used to treat many things, including alcoholism, drug addiction, and depression.&nbsp;</p>\r\n    <p>These two ran a study of thirty men who were both veterans and alcoholics. The experiment divided the men into three groups: one group received talk therapy with AA\'s 12-step process (n=10), no treatment (n=10), and the \"Peniston Protocol\" (n=10).\r\n        In the group receiving the Peniston Protocol, the biofeedback they were doing was alpha-theta neurofeedback, seeking the \"alpha-theta crossover\" wherein the theta amplitudes surpass the alpha amplitudes. In this space the alcoholics (and consequentially\r\n        others) gained access to the realm in which their traumatic memories were quarantined. Thus deep psychological material was often plumbed, sprouting the theory that alpha-theta neurofeedback got to the very root of people\'s issues.</p>\r\n    <p>When the efficacy of the various interventions were measured (with tests including the Beck Depression Inventory, the Minnesota Multiphasic personality Inventory II, blood draws and EEGs) and the individuals given the biofeedback interventions showered\r\n        higher amplitude alpha and theta activity, a reduction in depression, and other favorable results (for instance, their blood showed less beta-endorphins than the other groups, indicating the white-knuckling associated with quitting drinking was\r\n        missed by those undergoing alpha-theta treatments). Eight of the ten alcoholics who did the biofeedback quit drinking for good (all the others were re-hospitalized for their addictions within 18 months of the study).</p>\r\n    <p>Their paper \"Alpha Theta Brain Wave Training and Beta Endorphin Levels\" was published in a journal \"Alcoholism: Clinical and Experimental Research,\" which sent a tremor of excitement throughout the biofeedback community. They published subsequent\r\n        papers on the efficacy of alpha-theta neurofeedback on PTSD from the Vietnam war.</p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">Open Focus</span></p><p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Open%20Focus%20Book.jpg\" alt=\"Open Focus Book\" width=\"204\" height=\"319\" class=\"img-responsive atto_image_button_middle\"></span></p><p><span style=\"font-size: 1rem;\">Les Fehmi\'s Open Focus was founded on the generation of alpha frequencies, and his attempt to get people to generate alpha waves. In this effort, he would ask people 28 questions around \"relaxation imagery\" to see if they produced alpha content. Questions\r\n        like: \"Can you imagine the space between your eyes?\" and \"can you imagine the space between your ears?\" provoked people into an alpha state automatically. This, Fehmi thought, was synchronous alpha providing a fdep and relaxing state. One of Fehmi\'s\r\n        devices to generate this kind of EEG was a photic stimulator, used along with Open Focus tapes. People who ascribed to this version of EEG biofeedback reported less stress.&nbsp;</span></p>\r\n    <p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">SMR Neurofeedback</span><br></p>\r\n    <p>The first studies in the field by Sterman (Sterman, Wyrwicka, &amp; Roth, 1969) found significant changes in brainwave patterns of cats during a learned suppression of a cup-press response for food; they did a follow up effort to determine if the\r\n        cats could voluntarily produce this Sensory Motor Rhythm ( SMR) pattern by making a food reward contingent on SMR production. The cats easily accomplished the task. When used in further studies investigating the effects of a highly epileptogenic\r\n        fuel compound on cats, they proved to be highly resistant to seizure. While cats not previously trained, experienced seizures and death. SMR training had somehow inoculated the cats against experiencing seizures demonstrating that training this\r\n        pattern of increased spindle density resulted in a strong and permanent effect on neural processes that did not involve placebo effect. Lubar and Shouse (1976) followed with research showing that symptoms of ADHD could be increased or decreased\r\n        using NFB. These pioneering studies led to a larger number of investigations that continued showing efficacy, while others started to focus on the physiological changes in the brain. Hershberg et al. (2004) noted that there are several neurofeedback\r\n        studies using fMRI that demonstrate the control of the brain through feedback as valid. fMRI studies in human subjects have shown that the SMR EEG pattern is clearly associated with an increase in metabolic activity in the striatum of the basal\r\n        ganglia nuclear complex (Birbaumer, 2005).</p><p><br></p><h4>Joel Lubar on Researchers known Over the Years</h4><br>\r\n<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/517282542?h=2fc3bacb18&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"LUBAR - Researchers Known Over the Years\"></iframe></div>\r\n<script src=\"https://player.vimeo.com/api/player.js\"></script>\r\n<p><br></p>\r\n<h4>Joel Lubar on ADHD and&nbsp; the Theta/Beta Ratio</h4>\r\n<p><br></p>\r\n<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/517281013?h=1a0d0e8782&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"position:absolute;top:0;left:0;width:100%;height:100%;\" title=\"LUBAR - Neurofeedback, ADD, ADHD &amp;amp; the Theta-Beta Ratio\"></iframe></div>\r\n<script src=\"https://player.vimeo.com/api/player.js\"></script>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',9,1654218195),(55,19,'Decision Tree and Protocol Development','',1,'<p>There are many ways to assess a patient and determine which neurotherapy protocol to use (and there are many different neurotherapy protocols to choose from). These two component parts of your clinical practice: 1) Assessment techniques, and 2) Applied Neurotherapeutic practices, are of foremost importance to the range of applicability your success as a neurotherapist reaches.&nbsp;</p><p>Of the assessment techniques available to you, there are some who believe no prior recording of the brain (EEG or QEEG) is necessary before treatment. This is the belief of Sue and Siegfried Othmer and EEG Info, for instance. Many other camps use abbreviated QEEGs, wherein only a few electrodes are used. In Richard Soutar\'s New Mind Academy, there is the option of collecting EEG data from a limited number of channels (12), but one can also upload data in 19 channels. In Paul Swingle\'s Quick Q (also called a clinical QEEG since their patient database referenced is of individuals from their clinic, the practitioner conducts the assessment using one active electrode and moving it to different places on the scalp.</p><p>This section shows many different means of quantitative analysis from many different providers in the neurotherapy realm. While the decision tree process and protocol development process is different for each school, fundamentally, its advised the practitioner is able to identify the source of the patient\'s symptoms through the data recorded and analyzed.&nbsp;</p><h4><b>Paul Swingle\'s Clinical QEEG Assessment Report</b></h4><p><img src=\"@@PLUGINFILE@@/Quick%20Q%20Map.png\" alt=\"Quick Q Map\" width=\"1000\" height=\"1057\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Quick%20Q%20Map%202.png\" alt=\"Quick Q Map 2\" width=\"1000\" height=\"1021\" class=\"img-responsive atto_image_button_middle\"><br></p><p><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"></b></p><h4><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><b>Protocol Guide for New Mind Academy</b></b></h4><p>The New Mind Academy uses between 12 and 19 electrodes for client assessment, but many single channel or dual channel protocols are assigned thereafter. Below is a Mini Q Report as generated by Richard Soutar\'s software.</p><p></p><p><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">New Mind Academy\'s Mini Q Report</b><br></p><p><b><img src=\"@@PLUGINFILE@@/New%20Mind%20Map%201.png\" alt=\"New Mind Map 1\" width=\"750\" height=\"1017\" class=\"img-responsive atto_image_button_left\"><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><img src=\"@@PLUGINFILE@@/New%20Mind%20Map%202.png\" alt=\"New Mind Map 2\" width=\"750\" height=\"734\" class=\"img-responsive atto_image_button_left\"><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><p><b><br></b></p><h4><br></h4><p><span style=\"font-size: 1rem;\"></span></p><h4><span><b>The Neurofield System</b></span></h4><p></p><p><span style=\"font-size: 1rem;\">Many clinicians pre</span><span style=\"font-size: 1rem;\">fer to analyze the raw EEG data and then process it through one or&nbsp; more quantitative methods. The school of neurotherapy, using the NeuroField EEG system is one where the raw EEG data is first analyzed through raw inspection (if the clinician so chooses) and then processed and analyzed quantitatively, through power analyses and Independent Components Analysis. Finally, the data can be assessed from synchrony indexes, such as power power coupling analysis and others. This is a more advanced form of computational analysis. Neurofield uses the open source software of EEGlab within its analysis. What is compelling about this level of analysis is one can use more than 19 electrodes, providing a higher resolution picture of the brain and a more approximate sourcing of important components This software also uses three Gaussian curves, as opposed to one, with an algorithm called AMMICA: adaptive mixture independent Components Analysis. Finally, this software identifies artifacts in the components with a program called IC Label, however the clinician can use their naked eye to determine if they agree--even algorithms make mistakes sometimes.</span><br></p><h4><br></h4><p><span><b><img src=\"@@PLUGINFILE@@/Neurofield%20EEG%201.png\" alt=\"Neurofield EEg 1\" width=\"1000\" height=\"511\" class=\"img-responsive atto_image_button_left\"><br></b></span></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Neurofield%20EEG2.png\" alt=\"Neurofield EEG2\" width=\"1000\" height=\"806\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Neurofield%20EEG%203.png\" alt=\"Neurofield EEG 3\" width=\"1000\" height=\"653\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Neurofield%20EEG%204.png\" alt=\"Neurofield EEG 4\" width=\"1000\" height=\"653\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Neurofield%20EEG%205.png\" alt=\"Neurofield EEG 5\" width=\"2452\" height=\"1460\" class=\"img-responsive atto_image_button_middle\"><br></p><p><img src=\"@@PLUGINFILE@@/ICs.png\" alt=\"Independent Components\" width=\"700\" height=\"426\" class=\"img-responsive atto_image_button_left\"><br></p><h3><span style=\"font-size: 1rem;\"><h4></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b><br></b></h4><h4><b>iSYNC Brain Database</b></h4></span></h3><p><span style=\"font-size: 1rem;\">Other QEEG systems also use independent components analysis, such as iSync (the South Korean databases), however there is automatic artifact rejection via a cleaning process, which some clinicians do not prefer (since real data could possible be cleaned out). This is a robust EEG analysis software, however, and worth a look.&nbsp;</span><br></p><h4><br></h4><p><b><img src=\"@@PLUGINFILE@@/Isync1.png\" alt=\"isync 1\" width=\"750\" height=\"666\" class=\"img-responsive atto_image_button_left\"><br></b></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Isync%202.png\" alt=\"isync 2\" width=\"1000\" height=\"341\" class=\"img-responsive atto_image_button_middle\"><br></p><p><br></p><p></p><h4><b>WINEEG and HBI Database</b></h4><p><span>Another EEG analysis software that looks at independent components is WinEEG, built by Juri Kropotov. Like Isync and Neurofield EEG, WinEEG takes into account independent components analysis, which is a more advanced method of computations neuroanalysis. WinEEG uses an algorithm called Infomax, which uses one gaussian curve to analyze the EEG data into individual components.&nbsp;<br></span></p><img src=\"@@PLUGINFILE@@/WinEEG1.png\" alt=\"HBI Database\" width=\"800\" height=\"449\" class=\"img-responsive atto_image_button_left\"><br><p></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/WinEEG2.png\" alt=\"WinEEG2\" width=\"800\" height=\"631\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/WinEEG4.png\" alt=\"WinEEG4\" width=\"291\" height=\"270\" class=\"img-responsive atto_image_button_left\"><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',5,1655392267),(57,19,'Applied Psychophysiology: EEG and QEEG Assessment to Link Symptoms to Findings','',1,'<p style=\"text-align: center;\"><br></p>\r\n<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/703362670?h=6557b6b8cb&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\" style=\"text-align: center; position: absolute; top: 0px; left: 0px; width:100%; height:100%;\" title=\"qeeg101.mov\"></iframe></div>\r\n<script src=\"https://player.vimeo.com/api/player.js\"></script>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1655392303),(58,18,'Normative Databases','',1,'<br><iframe src=\"https://player.vimeo.com/video/443179794?h=810cdfcb58&amp;color=13979b&amp;title=0&amp;portrait=0\" width=\"640\" height=\"360\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n<p></p>\r\n<h2><br></h2>\r\n<h4>Quantitative EEG analysis (qEEG) refers to signal processing and extraction of features from the EEG signal, in some cases there is a normative group that the individual being surveyed is compared to, and sometimes the data is digitized without a comparative\r\n    reference.\r\n</h4>\r\n<p>In the typical neurotherapy practice, 19 channel EEG is digitized, edited or adjusted to remove extra cerebral artifact, and subjected to spectral analysis using the fast Fourier transform (FFT).&nbsp;</p>\r\n<p><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/361/Fast%20Fourier%20Transform.png\" alt=\"Fast Fourier Transform\" width=\"1400\" height=\"948\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n<p><b></b></p>\r\n<h3><b>Inclusion and Exclusion Criteria for Normative Databases</b></h3>\r\n<div>\r\n    <div>\r\n        <p></p>\r\n        <p><b>Normative databases are constructed and validated based upon the scientific standards of gaussianity, cross-validation, amplifier matching and peer-reviewed publications. A clinically normal database is one where individuals are carefully screened for relevant abnormalities using other clinical tools such as psychometric assessment or MRIs.&nbsp;</b></p>\r\n        <p><b>The database should represent the mix of ages, gender, ethnicity, socioeconomic status and other demographic factors present in the overall population.&nbsp;<b>“Representative sampling”</b>&nbsp;means a demographically balanced sample of different\r\n            genders, different ethnic backgrounds, different socio-economic status and different ages.&nbsp;</b>\r\n        </p>\r\n        <p><b>Using a rigorously screened population, deviations represent the difference from “well-functioning” as compared to “average.” Poor screening procedures result in admitting individuals into a normal group who have significant clinical problems. Careful screening of the subjects that comprise a normative database is critical so that representative samples of healthy and otherwise normally functioning individuals are selected and individuals with a history of neurological problems, psychiatric problems, school failure and other deviant behaviors are excluded.&nbsp;</b></p>\r\n        <p><b>While it may be too expensive and exhaustive to require that all individuals have full MRI, PET, fMRI, complete neuropsychological evaluation, genetic analysis, blood and urine testing, etc., it would be ideal. A second-best option, then, is to get questionnaire information and objective assessments of general health, and social and intellectual functioning. It is especially important to get many children sampled in a normative database, because dramatic developmental changes occur in children and adolescents in relatively short time intervals. Where two years difference will not alter the demographics of an adult, it can signify important differences in, say, a 4-year-old and a 6-year-old.</b></p>\r\n        <p><b>It is important for a database to have a large sample size, although ultimately this criterion is less important than careful calibration, elimination of artifact, rigorous standards during data collection and rigorous standards for data analysis and approximation to a Gaussian distribution. To be considered a clinically valid normative database, there must be peer review (published), tests of reliability, tests of statistical validity, cross-validation tests, full disclosure of the inclusion and exclusion criteria, and adequate sample sizes for different age groups. Normative databases must use healthy participants who do not have any psychological or physiological pathologies.</b></p>\r\n        <p><b>Many normative databases available for clinical use contain the mean values of EEG features (absolute power, relative power, coherence measures, etc.); the “normative” quantification of theta data is the standard deviation of the features relative to the normal population (see John, Prichep, &amp; Easton, 1987). Certain databases provide magnitude, (the square root of power), while others provide amplitude (which is power measured in microvolts squared).&nbsp;&nbsp;</b></p>\r\n        <p><b>Relative power represents the percentage of power in any bands compared with the total power in the patient’s EEG (e.g., “relative theta” is the percentage of theta of the combined sum of delta, theta, alpha, and beta). One way to describe relative power is “how the client spends their time.”&nbsp;</b></p>\r\n        <p><b>Other derived measures that have been normed include hemispheric asymmetry for power (which often reflects the power differential between different sites in the brain), coherence (the stability of the phase relationship between electrode sites, and phase (the measure of time delay between activities at two sites). It should be recognized that these measures are not statistically independent, and significant deviations on more than one feature may be representing the same neurophysiological process (i.e. hypercoherence in alpha may also be represented in a global alpha amplitude deviation, due to a contaminated reference). &nbsp;</b></p>\r\n        <p><b><a href=\"https://vimeo.com/443179794\" target=\"_blank\">Click here to watch a brief in depth video of normative databases</a></b></p>\r\n        <p></p>\r\n        <h2><b><a name=\"_Toc35342982\">Asymmetry in Quantitative EEG Maps (NeuroGuide)</a></b></h2><b><br><p></p><p><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/362/Asymmetry.png\" alt=\"Asymmetry\" width=\"500\" height=\"378\"></p><h2><br></h2><p><a name=\"_Toc35342982\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/362/Coherence.png\" alt=\"Coherence in WinEEG\" width=\"291\" height=\"270\"><br></a></p><h4><a name=\"_Toc35342983\">Coherence measures in Quantitative EEG Maps (WinEEG and iSyncBrain)</a></h4><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/362/Coherence%202.png\" alt=\"Asymmetry\" width=\"427\" height=\"379\"><br><p></p><p>While some normative databases rely on a linked ears reference, the savvy clinician will reference a database that has multiple montage possibility (in the case of contaminated reference).&nbsp;Coherence measures the stability of the phase relationship between two time series, calculating the difference between two signals measured at the scalp. &nbsp;Coherence in excess is hypercoherence; coherence in deficiency is hypocoherence.&nbsp;Coherence measures do not separate phase and amplitude.&nbsp;</p><p>Unfortunately, coherence measures are also apt to be spurious and false positives are likely.&nbsp;In EEG measures, a linked ears or mastoid reference used can significantly alter the both the power and phase at each electrode site, if a high amplitude source of EEG is at one or more of the temporal electrodes. For similar reasons, any common reference coherence data must be interpreted cautiously. Even in average references, spuriously large coherences can occur from superficial dipoles at large interelectrode differences.&nbsp;&nbsp; Fein et al. (1988) argue the most diligent way to measure coherences is with reference-free recording methods, while Nunez et al (1997) agree, noting that Laplacians give the best intermediate spatial range coherence estimates.&nbsp; Finally , of import to valuation of synchrony measures offered, coherence measures do not separate phase and amplitude.<br></p><p><br></p><h4>Erroneous Coherences (Image Below)</h4><p></p><p></p><h2><a name=\"_Toc35342984\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/362/Erroneous%20Coherences.png\" alt=\"Erroneous Coherences\" width=\"700\" height=\"683\"><br></a></h2><h2><br></h2><h4><a name=\"_Toc35342984\">Phase Measures in Quantitative EEG Maps (Neuroguide)</a></h4><p><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/362/Phase.png\" alt=\"Phase\" width=\"501\" height=\"379\"></p><p></p><p></p><h4><a name=\"_Toc35342985\">Quantitative “Normative” and Non-Normative Database Validation Steps</a></h4><p>A quantitative database should represent the mix of ages, gender, ethnicity, socioeconomic status and other demographic factors present in the overall population. The method of recruitment of normal individuals also should be considered. Poor screening procedures will result in admitting individuals into a normal group who have signiﬁcant clinical problems. Regardless the method of recruitment, care must be exercised not to entice individuals to participate and falsify information because of the ﬁnancial gain. Normative databases are to be constructed and validated in respect to the basic scientific standards of gaussianity, cross-validation, amplifier matching and peer-reviewed publications.</p></b></div>\r\n</div>\r\n<h4><b>Statistical Analysis of Normative Databases</b></h4>\r\n<div>\r\n    <div>\r\n        <p></p>\r\n        <p><b>Spectral power is an often used measure in qEEG studies. The amount of power for each frequency or frequency band for a given electrode is computed and compared to the database mean value. The results are often represented as z-scores, that is the difference between the mean score of a population and the patient’s individual score divided by the standard deviation of the population. Z-scores detect and characterize potential abnormalities from the tested individual, relative to the normative population within his/her own age range. It is not strictly the number of deviations, rather the pattern of deviations that is most relevant. The use of parametric statistics assumes a normal (Gaussian) distribution of the variable(s) in question.</b></p>\r\n        <p><b>The&nbsp;Gaussian&nbsp;distribution&nbsp;is&nbsp;a&nbsp;fundamental&nbsp;distribution&nbsp;that&nbsp;is&nbsp;used&nbsp;throughout&nbsp;science,&nbsp;for&nbsp;example,&nbsp;the&nbsp;Schrodinger&nbsp;wave&nbsp;equation&nbsp;in&nbsp;Quantum&nbsp;mechanics&nbsp;uses&nbsp;the&nbsp;Gaussian&nbsp;distribution&nbsp;&nbsp;as&nbsp;basis&nbsp;functions&nbsp;(Robinett,&nbsp;1997).&nbsp;&nbsp;The&nbsp;application&nbsp;of&nbsp;the&nbsp;EEG&nbsp;to&nbsp;the&nbsp;concept&nbsp;of&nbsp;the Gaussian&nbsp;distribution&nbsp;requires&nbsp;the&nbsp;use&nbsp;of&nbsp;standard&nbsp;mathematical&nbsp;transforms&nbsp;by&nbsp;which all statistical&nbsp;distributions&nbsp;can&nbsp;be&nbsp;transformed&nbsp;to&nbsp;a&nbsp;Gaussian&nbsp;distribution&nbsp;(Box&nbsp;and&nbsp;Cox,&nbsp;1964). Quantitative EEG uses transforms that are applied to the power spectrum of the digital time series in order to approximate a normal distribution.</b></p>\r\n        <h4><b><a name=\"_Toc35342987\">Gaussian distribution</a></b></h4>\r\n        <p><b>&nbsp;<img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/363/Gaussian%20Distribution.png\" alt=\"Gaussian Distribution\" width=\"500\" height=\"364\"></b></p>\r\n        <p></p>\r\n        <p><b><br></b></p>\r\n        <p><b><br></b></p>\r\n        <p><b><br></b></p>\r\n        <p><b>Here is a video describing Gaussianity:&nbsp;</b></p>\r\n        <div>\r\n            <div>\r\n                <div tabindex=\"-1\" title=\"Gaussianity\" preload=\"auto\" id=\"id_videojs_6269e5c9d0c4d_1\" data-setup-lazy=\"{&quot;techOrder&quot;: [&quot;youtube&quot;], &quot;sources&quot;: [{&quot;type&quot;: &quot;video/youtube&quot;, &quot;src&quot;:&quot;https://www.youtube.com/watch?v=IIuXF5QRBTY&quot;}], &quot;language&quot;: &quot;en&quot;, &quot;fluid&quot;: true}\" lang=\"en\" role=\"region\" aria-label=\"Video Player\">\r\n                    <div><iframe id=\"id_videojs_6269e5c9d0c4d_1_Youtube_api\" frameborder=\"0\" allowfullscreen=\"1\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" title=\"YouTube video player\" width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/IIuXF5QRBTY?controls=0&amp;modestbranding=1&amp;rel=0&amp;showinfo=0&amp;loop=0&amp;fs=0&amp;hl=en&amp;enablejsapi=1&amp;origin=https%3A%2F%2Fschoolofneurotherapy.com&amp;widgetid=1\" data-gtm-yt-inspected-10=\"true\"></iframe>\r\n                        <div></div>\r\n                    </div>\r\n                    <div tabindex=\"-1\" aria-disabled=\"false\"></div>\r\n                    <div aria-live=\"off\" aria-atomic=\"true\"></div><b><button type=\"button\" aria-live=\"polite\" title=\"Play Video\" aria-disabled=\"false\"><span aria-hidden=\"true\"></span>Play Video</button></b></div>\r\n            </div>\r\n        </div>\r\n        <p></p>\r\n        <p></p>\r\n        <p><b>The next two figures are representations of raw, un-normed data, and Z-score data, respectively, in spectral graphs. The raw image shows the absolute power of the EEG in microvolts squared. We see that 10Hz shows up at approximately 16mV<sup>2&nbsp;</sup>. The second image shows the data in Z-scores, or how deviant from the norm these frequencies are. We can see that the purple line (representing one electrode) is 3+ standard deviations above the norm between 14 – 16 Hz, and 4+ standard deviations above the norm at 28 Hz. Both of these findings are potentially artifactual, but this cannot be determined without an analysis of the raw EEG.</b></p>\r\n        <h4><b><a name=\"_Toc35342988\">Spectral Power in Microvolts squared (y-axis) and hertz (x-axis)</a></b></h4>\r\n        <p><b>&nbsp;&nbsp;</b></p>\r\n        <p><b>&nbsp;<img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/363/Spectral%20Power.png\" alt=\"Spectral Power\" width=\"599\" height=\"553\"></b></p>\r\n        <p></p>\r\n        <p><b><br></b></p>\r\n        <p></p>\r\n        <h4><b><a name=\"_Toc35342989\">Spectral Power in Z-Scores (y-axis) and hertz (x-axis)</a></b></h4>\r\n        <p><b>&nbsp;<img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/363/Z-Score%20Spectral%20Power.png\" alt=\"Z-Score Spectral Power\" width=\"595\" height=\"541\"></b></p>\r\n        <p></p>\r\n        <p><b><br></b></p>\r\n        <p></p>\r\n        <p><b>The next figure we see is showing, one graph per electrode channel, the raw data in the EEG on a spectral display. This imagery is from WinEEG. Each peak represents a rhythm in the data, showing kurtosis, or the expected bell shape that indicates it is a frequency range.</b></p>\r\n        <p><b><br></b></p>\r\n        <h4><b><a name=\"_Toc35342990\">Spectra of Raw EEG (not norm referenced) as seen at each electrode in WinEEG</a></b></h4>\r\n        <p><b>&nbsp;<img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/363/WinEEG%20Spectra.png\" alt=\"WinEEG Spectra\" width=\"1000\" height=\"636\"></b></p>\r\n        <p></p>\r\n        <p><b><br></b></p>\r\n        <p></p>\r\n        <p><b>The figure below illustrates a common modern quantitative EEG analysis where EEG traces are viewed and examined at the same time that quantitative analyses are displayed so as to facilitate and extend analytical power.</b></p>\r\n        <p><b><br></b></p>\r\n        <p></p>\r\n        <p></p>\r\n        <h4><b><a name=\"_Toc35342991\">Raw EEG and Quantitative EEG</a></b></h4>\r\n        <p></p>\r\n        <p><b><a name=\"_Toc35342991\"><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/476/mod_lesson/page_contents/363/Raw%20vs.%20Quantitative.png\" alt=\"Raw EEG vs. Quantitative EEG\" width=\"1000\" height=\"604\"></a></b></p><b><a name=\"_Toc35342991\"><p><br></p></a></b></div>\r\n</div>\r\n<p><b>Here is a video on Fast Fourier Transform:&nbsp;</b></p>\r\n<div>\r\n    <div><b><div tabindex=\"-1\" title=\"FFT Video\" preload=\"auto\" id=\"id_videojs_6269e57b9fde2_1\" data-setup-lazy=\"{&quot;techOrder&quot;: [&quot;youtube&quot;], &quot;sources&quot;: [{&quot;type&quot;: &quot;video/youtube&quot;, &quot;src&quot;:&quot;https://www.youtube.com/watch?v=spUNpyF58BY&quot;}], &quot;language&quot;: &quot;en&quot;, &quot;fluid&quot;: true}\" lang=\"en\" role=\"region\" aria-label=\"Video Player\"><div><iframe id=\"id_videojs_6269e57b9fde2_1_Youtube_api\" frameborder=\"0\" allowfullscreen=\"1\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" title=\"YouTube video player\" width=\"640\" height=\"360\" src=\"https://www.youtube.com/embed/spUNpyF58BY?controls=0&amp;modestbranding=1&amp;rel=0&amp;showinfo=0&amp;loop=0&amp;fs=0&amp;hl=en&amp;enablejsapi=1&amp;origin=https%3A%2F%2Fschoolofneurotherapy.com&amp;widgetid=1\" data-gtm-yt-inspected-10=\"true\"></iframe><div></div></div><div tabindex=\"-1\" aria-disabled=\"false\"></div><div aria-live=\"off\" aria-atomic=\"true\"></div><button type=\"button\" aria-live=\"polite\" title=\"Play Video\" aria-disabled=\"false\"><span aria-hidden=\"true\"></span>Play Video</button></div></b></div>\r\n</div><b>&nbsp;</b>\r\n<p></p>\r\n<p>There are numerous clinical normative databases for many different medical comparisons; normative databases help to evaluate clinical disorders. &nbsp;The National Library of Medicine’s database has a comprehensive list of normative databases, that can\r\n    be found by search for “normative database: at:&nbsp;<a href=\"http://www.ncbi.nlm.nih.gov/sites/entrez\">http://www.ncbi.nlm.nih.gov/sites/entrez</a>. In using a normative database, we are comparing a single person to a population of “normal” individuals\r\n    for comparative purposes. A normative database will not only identify frequencies or metrics in which the patient is not normal, but will also identify the degree of their deviance.</p><br><br>\r\n<p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',12,1655388378),(59,20,'Frequently Asked Questions','',1,'<h4>Client Preparation for Neurofeedback</h4><p>It behooves the clinician to have a well-worked out approach to meeting clients, introducing them to the neurotherapy process, and addressing any concerns they might have. Some of the commonly asked questions are things like:</p><p><span><b>Q: What is neurofeedback?</b></span></p><p>A:&nbsp;Neurofeedback, also called EEG biofeedback, is a way of training the behavior of the brain (in terms of the amplitudes of certain brainwaves, or the connectivity dynamics of the brain). The tools used are EEG equipment (electrodes, differential amplifiers) and any kind of feedback (usually tones or video feedback). It is used for a variety of psychopathologies and physical pathologies.<br><br>Once the clinician determines how the problem manifests in the brainwave, using EEG measurement equipment, they can then encourage or discourage different behaviors from the brain by rewarding or punishing different EEG behaviors. After a certain number of sessions (typically between 20 and 40) the brain has learned to operate differently, leading to different behaviors and experiences of life.</p><p><span><b>Q; How long does it take?&nbsp;</b></span><b style=\"font-size: 1rem;\">Will it address my condition?&nbsp;</b></p><p>A: While it\'s wise to not make promises or guarantees for how long the therapy will take or whether it will address the client\'s concern, anecdotal and academic evidence are compelling and often adequate for answering these kinds of questions. Depending on the experience of the practitioner and the types of modalities used, answering the client\'s concerns with general answers is possible.&nbsp; Some modalities take longer than others. In the field of neuromodulation (i.e. tDCS, tACS, Pink noise, etc.) 25 sessions is an average amount for conditions that are more common (e.g. neuroses, such as anxiety, stress, panic, etc., or ADHD), while some modalities can take 60-80 sessions or more.&nbsp;</p><h4>Some other Frequently Asked Questions and Answers</h4><p><b>Q: Is Neurotherapy dangerous? Can it hurt me?&nbsp;</b></p><p>A; Short answer: no. Neurofeedback is an operant conditioning method, meaning we are using your brain’s own system of conditioning to create changes in the way your brain behaves. Typically, the worst outcome of a bad neurofeedback session is feeling overly wired or overly tired.<br><br>A: The long answer: it is possible. If the person administering neurofeedback is not experienced or credentialed and has not taken an appropriate assessment, such as a brain map and an intake, they are essentially flying blind. Many pathologies show up with various profiles and presentations in the EEG. It is imperative that the patient researches the competency of their clinician and ensures they have the minimal credentials in the field of neurotherapy before allowing them to do brain work.<b><br></b></p><p><b>Q: Does Neurofeedback Work?</b></p><p>Short answer: Yes. Neurofeedback, which is a means of rewarding the desired brainwave activity or inhibiting problematic brainwave activity with auditory or visual feedback works. How well it works is contingent upon the competency of the practitioner, as well as the tools they have at their disposal. Imagine going to a doctor who hadn’t updated any of his equipment in 30 years, and was practicing with old techniques and assumptions. This would be troublesome and possibly dangerous for the patient. The same goes for neurofeedback. The field of neurofeedback has been around since the 1970s, and many clinicians received their training in the early 1990s with simplistic modalities. The patient ought to expect their clinician regularly attends trainings and keep his/her equipment up to date, as well as his/her clinical perspectives.<br><br>Neurofeedback abetted by neurostimulation is a faster, and cutting-edge method wherein the clinician first shows the brain what it ought to do (i.e. make theta frequencies), then follows up later with neurofeedback, as a conditioning tool. This one-two approach is a solid and reliable way to impact change in the brain.<br></p><p><b>Q: How does neurofeedback work?</b></p><p><span>A: First, the clinician gets an assessment of the client’s brainwave patterns, through a brain map. They also assess the patient through an intake process. Then, they determine what patterns and behaviors in the brain are creating the problem. A classic example is a traditional Attention Deficit Disorder case, where there is too much theta (daydream, hypnogogia, trance-like) and not enough beta (active, conscious thinking). This client has a high theta / beta ratio. The clinician would then determine the source and location of the excess theta and would downtrain (encourage suppression) of the excessive theta brainwaves, while uptraining (encouraging greater amplitudes) of beta brainwaves. This is done using electrodes or a full 19-channel EEG cap. By programing their software for this particular patient, the clinician can reward (via visual or auditory feedback) the optimal state of low amplitude theta brainwaves and high amplitude beta brainwaves, which will lead to a permanent state where the brain knows how to produce more beta and less theta, on a consistent basis. The result, in this example, is a decrease in the attention deficit symptoms due to excess theta, allowing the individual greater focus, clarity, and presence in their functioning.<br></span></p><p><span><b>Q: Does neurofeedback last?</b></span></p><p><span><span>Short answer: yes. Neurofeedback lasts if the duration of training was long enough and if the training was frequent enough. Neurofeedback training is similar to going to the gym. You are trying to alter the functioning of your brain permanently. If you are seeking change, multiple times at the gym, per week, is recommended.<br><br>We typically train our clients anywhere from 3-5 times per week in the beginning of their training (once per week is akin to going to the gym once per week and expecting change). Once we have a few weeks of intensive work under our belts and we are seeing changes, we can begin to titrate back the training regimen to twice per week, then once per week, and eventually once per every other week, until the client’s training has completed.<br><br>After the initial course of training, the occasional neurofeedback tune-up may be desired, but is typically not necessary.<br></span></span></p><p><span><span><b>Q: How does neurostimulation work? Does it work with neurofeedback?</b></span></span></p><p><span><span>If neurotherapy is like going to the gym, then neurofeedback is like weight training and neurostimulation is like cardio vascular exercise. We often begin our clients with cardio for the first few sessions. This primes their system and has an immediate, noticeable effect for most. It is a way to show the brain what we want it to do on its own.<br><br>Once we have a few sessions of neurostimulation, we begin adding in neurofeedback. Neurofeedback is the strength training that conditions the brain. The combination of neurostimulation and neuromodulation is a complete training regimen that speeds up the progress and the duration of treatment.<br></span></span></p><p><span><span><b>Q: Is there any research to support neurofeedback?</b></span></span></p><p><span><span><span>Yes. There is a frequently updated bibliography that is maintained by the International Society for Neurofeedback Research. <a href=\"https://www.isnr.org/isnr-comprehensive-bibliography\" style=\"\">See link here.</a><br><br>One difficulty with neurofeedback research is that nearly all pathologies have different profiles. There is no thing as a one size fits all treatment approach. In addition, it takes a trained clinician to determine the appropriate treatment for each individual.<br></span></span></span></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',4,1653958506),(60,20,'Monitoring Client Progress','',1,'It is imperative to keep thorough client records of what protocols have been selected, how long they were applied, what metrics were trained, and the client\'s response. There are many ways the clinician can keep track of this. Some clinicians choose\r\nold school paper and pen in their client folder, while there are also many electronic record keeping systems available.&nbsp;<br><br>Here is one video demonstrating recording the treatment history in Neurofield.<br><br><iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/pOrbHm2Anhg\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><br><br>It is important that the\r\nclient is always attended to--whether by a technician or by the clinician themself. If the client ever seems at all drowsy, they are likely fatigued and complete with the session. Often children will fatigue faster than adults. When you see a patient\'s\r\nscores plummeting, chances are good they have completed their session; pushing&nbsp; client past their point of fatigue is not recommended. Many neurofeedback sessions are as short as 20 minutes, while others (alpha/theta, for instanace) ca go as log\r\nas 60 minutes.&nbsp;<br>Each different type of neurofeedback has different thresholding techniques, this will be best imparted by educators teaching each particular modality.&nbsp;<br><br><b>New Protocols<br></b><span>The brain creates the most complicated noise in the known universe; that said, sometimes a protocol, no matter how well thought out, will not yield the result the practitioner expected it to. If a client does not react at all or reacts negatively (i.e. they feel overly wired or overly tired), the clinician should re-evaluate their protocol, hopefully gleaning an understanding why it did not create the desired outcome so they can apply the precedent to future cases. Some clinicians choose to get a new EEG / QEEG to assess progress and to assist with the new protocol evaluation.&nbsp;<br></span><br><b>Choosing Montages for Single Channel Training</b><br>\r\n<p><span style=\"font-size: 1rem;\">The montage chosen for single channel training is important, since the reference will have an impact on the way the active electrode signal is read. Remember, one is never measuring the brain from one electrode, but always one active and one reference.\r\n    In the case of 19-channel EEG and LORETA training, average or weighted average montages are possible.&nbsp;</span><br></p>\r\n<p>Here is a short video of montages in EEG, which will discern how to determine the best montage to address the issue the clinical desires to focus on.&nbsp;</p>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/AcW97nMLGEs\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',7,1654223286),(61,20,'Pre-Training','',1,'<p>The introductory period before a client begins neurofeedback is dependent on the clinician\'s toolkit. Some clinicians will choose biofeedback modalities to stabilize and better regulate the system before entering neurotherapy. Modalities that are common\r\n    are pEMF stimulation, heart rate variability treatment, and psychotherapy. There is no \"one way\" to enter neurofeedback and what is of imperative importance is that the clinician understands the brain that they are working on before applying any treatment\r\n    modality. This is of course accomplished through a thorough EEG and QEEG assessment, followed (preferably) by a report wherein the client\'s symptoms are outlined and understood.</p>\r\n<h4>Impedance Checking Before EEG</h4>\r\n<p>When gathering the EEG, the clinician must be able to discern real data from artifactual data. This topic is covered in the earlier secion on artifacts. Most EEGs have a system of impedance checking that goes along with the amplifier.&nbsp;</p>\r\n<p>Here is a video of impedance checking in the Neurofield system.</p>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/OPof2CEqYq8\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',1,1651120253),(62,16,'A Review of ADHD Studies','',1,'<p></p><p>Thousands of research\r\narticles on neurotherapy and neurofeedback have been conducted, a very thorough\r\nlist of studies conducted can be found at: <a href=\"https://isnr.org/isnr-comprehensive-bibliography\">https://isnr.org/isnr-comprehensive-bibliography</a></p>\r\n\r\n<h3>ADHD Studies</h3>\r\n\r\n<p>ADHD is one of the most\r\ncommon and most researched disorder: a prevalent, chronic, and impairing\r\ndisorder occurs in 3% to 7% of school-aged populations (Angold et al., 2000;\r\nJensen et al., 1999; Cormier, 2008) and compromises as much as 50% of America’s\r\nchild psychiatry clinic populations (Cantwell, 1996).ADHD is a highly heritable\r\ndisease, with estimated heritability rates of up to 80 % (Faraone et al., 2010).\r\nIt is more common in males (James and Taylor, 1990), with relative rates of up\r\nto 9:1 in clinical samples, and 4:1 in epidemiological studies (APA, 1994),\r\nalthough community-based studies have found ratios as low as 2:1 (Szatmari,\r\n1992; Taylor et al., 1998). </p>\r\n\r\n<h3>ADHD History</h3>\r\n\r\n<p>In 1947, Lehtinen termed what\r\nwe now call ADHD the ‘minimal brain dysfunction’ (MBD) syndrome. In 1957, this\r\nterm was followed by ‘hyperkinetic impulse disorder,’ with symptoms of hyperactivity,\r\nshort attention span, variability, impulsiveness, irritability, explosive anger\r\nfits, and poor school work (Laufer and Denhoff, 1957). In 1962, Clements and Peters (1962) re-introduced the Minimal Brain\r\nDysfunction terminology, including:</p>\r\n\r\n<p></p><ul><li>specific learning deficits</li><li>perceptual motor deficits</li><li>general coordination deficits</li><li>hyperkinesis</li><li>impulsivity</li><li>emotional lability</li><li>short attention span and/or distractibility</li><li>In 1968, the DSM-II (APA, 1968) dubbed the disorder ‘hyperkinetic\r\nreaction of childhood,’ emphasizing inattention, impulsivity and motor\r\nactivity. In 1980, the DSM-III (APA, 1980) renamed it ‘Attention Deficit\r\nDisorder’ (ADD), shifting emphasis from motor activity to attention, with two\r\ntypes: with hyperactivity (ADDh) and without hyperactivity (ADDwo). DSM-III-R (APA, 1987) renamed\r\nit ‘Attention Deficit Hyperactivity Disorder’ (ADHD), and considered\r\nunidimensional in nature, with a single diagnostic checklist. A second\r\ncategory, ‘Undifferentiated Attention Deficit Disorder’ (UADD), featured marked\r\ninattention without specific diagnostic criteria. In the DSM-IV (APA, 1994), the criteria changed again to reflect\r\nthese findings, with 3 main types:<br>&nbsp;• Predominantly Inattentive (AD/HDin)<br>&nbsp;• Predominantly Hyperactive-Impulsive (AD/HDhyp)<br>&nbsp;• Combined Type (AD/HDcom)</li></ul>\r\n\r\n<h3>ADHD Symptoms</h3>\r\n\r\n<p>In adults, the disorder is\r\ntypified by poor concentration, explosive outbursts, impulsivity, restlessness,\r\ncarelessness, ack of attention to detail, poor organizational skills, inability\r\nto focus or concentrate, mood swings, extreme impatience, difficulty keeping\r\nquiet and speaking out of turn, continually losing or misplacing things, as\r\nwell as non-medical drug use, court referrals, incarceration, and personality\r\ndisorders (Hechtman et al., 1984, 1979; Loney et al., 1983; Wender, 1994). </p>\r\n\r\n<p>Symptoms in children and\r\nteens include the following:</p>\r\n\r\n<p><b>Inattentiveness</b></p>\r\n\r\n<p><ul><li>having a short attention span and being easily distracted</li><li>making careless mistakes&nbsp;–&nbsp;for example, in schoolwork</li><li>appearing forgetful or losing things</li><li>being unable to stick to tasks that are tedious or time-consuming</li><li>appearing to be unable to listen to or carry out instructions</li><li>constantly changing activities or task</li><li><!--[endif]-->having difficulty organizing tasks</li></ul><!--[if !supportLists]--></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<p><b>Hyperactivity\r\nand&nbsp;impulsiveness</b></p>\r\n\r\n<p><ul><li>being unable to sit still, especially in calm or quiet\r\nsurroundings</li><li>constantly fidgeting</li><li>being unable to concentrate on tasks</li><li>excessive physical movement</li><li>excessive talking</li><li>being unable to wait their turn</li><li>acting without thinking</li><li>interrupting conversations</li><li>little or no sense of danger</li></ul><!--[if !supportLists]--></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<p>&nbsp;</p>\r\n\r\n<h3>Brain Research and ADHD</h3>\r\n\r\n<p>ADHD subjects clearly show a different maturation profile\r\ncomparative to neurotypical populations (Poli et al., 2014). Feinberg, De Bie,\r\nDavis, &amp; Campbell (2011) suggest a decline in EEG power for neurotypicals\r\nis likely a reflective of brain reorganization, which is driven by synaptic pruning,\r\nfurther postulating that slower waves decreased by up to 60% in ages 11 to 17\r\nyears.</p>\r\n\r\n<p>&nbsp;</p>\r\n\r\n<h3>Profiles</h3><h4>Excessive Theta</h4>\r\n\r\n<p>Attention deficit’s relation to EEG has been ever since\r\nthe first description of <b>“fronto-central slow EEG activity at frequencies of\r\n5-6/sec”</b> in <b>“behavioral problem children” </b>in 1938 (Jasper, Solomon,\r\n&amp; Bradley, 1938). Early accounts described <u>defects in moral control</u>,\r\n<u>mischievousness</u> and <u>destructive behavior</u> (Hoffman, 1844; Still,\r\n1902), regarded as resulting from <b>traumatic brain injury </b>(e.g.\r\nGoldstein, 1936; Meyer, 1904), <b>influenza-related encephalitis </b>(e.g.\r\nHohman, 1922; Kennedy, 1924), or <b>various childhood central nervous system\r\n(CNS) infections </b>(e.g. Bender, 1942). </p>\r\n\r\n<p>There are many different ways in which ADHD symptoms\r\nmanifest, as can be seen in EEG. Poil et al. (2014) found that in adults with\r\nADHD there was slowing of alpha frequency along with increased power in alpha-1\r\n(8–10 Hz) when eyes were closed for resting.</p>\r\n\r\n<p>The finding of increased absolute power in the theta EEG\r\nband in ADHD is the most consistently reported finding <i>(Bresnahan, Anderson,\r\n&amp; Barry, 1999; Chabot &amp; Serfontein, 1996; Clarke, Barry, McCarthy,\r\n&amp; Selikowitz, 1998; Clarke, Barry, McCarthy, &amp; Selikowitz, 2001b;\r\nDeFrance, Smith, Schweitzer, Ginsberg, &amp; Sands, 1996; Janzen, Graap,\r\nStephanson, Marshall, &amp; Fitzsimmons, 1995; Lazzaro et al., 1999; Lazzaro et\r\nal., 1998; Mann, Lubar, Zimmerman, Miller, &amp; Muenchen, 1992; Matsuura et\r\nal., 1993).</i> This increase in theta was observed in children and not adults\r\n(<i>Markovska-Simoska &amp; Pop-Jordanova, 2017)</i></p><p><i><img src=\"@@PLUGINFILE@@/Excessive%20theta.png\" alt=\"Excessive Theta\" width=\"571\" height=\"362\" class=\"img-responsive atto_image_button_left\"><br></i></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Excessive%20theta%20vid.mp4\">@@PLUGINFILE@@/Excessive%20theta%20vid.mp4</video>&nbsp;<h3>Slow Alpha Peak</h3>\r\n\r\n<p>There are many different\r\nways in which ADHD symptoms manifest, as can be seen in EEG. Poil et al. (2014)\r\nfound that in adults with ADHD there was slowing of alpha frequency along with\r\nincreased power in alpha-1 (8–10 Hz) when eyes were closed for resting.</p>\r\n\r\n<h3><img src=\"@@PLUGINFILE@@/Slow%20ALpha.png\" alt=\"Slow ALpha\" width=\"696\" height=\"601\" class=\"img-responsive atto_image_button_text-bottom\"><br></h3><p>&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Slow%20ALpha%20Video.mp4\">@@PLUGINFILE@@/Slow%20ALpha%20Video.mp4</video>&nbsp;<br></p><h3>Theta – Beta Ratio</h3>\r\n\r\n<p>Lubar (1991) laid the\r\nfoundation for the concept of the theta/beta power ratio as a measure that\r\ncould discriminate “normal” children from children with ADD, learning disorders\r\nand ADHD (Lubar, 1991). Based on the initial\r\nfindings of increased theta and decreased beta, in 1991, Lubar suggested the\r\nTheta/Beta power ratio (TBR) as a measure for discriminating “normal” children\r\nfrom children with ADD, learning disorders, and ADHD (Lubar, 1991). </p>\r\n\r\n<p>Excess theta and elevated\r\nTBR have been found favorable predictors for treatment outcome to stimulant\r\nmedication (Arns, Gunkelman, Breteler, &amp; Spronk, 2008; Clarke, Barry,\r\nMcCarthy, Selikowitz, &amp; Croft, 2002; Suffin &amp; Emory, 1995) and neurofeedback\r\n(Arns et al., 2012; Monastra, Monastra, &amp; George, 2002), thereby\r\ndemonstrating the prognostic value of this measure (assuming a slow alpha peak\r\nfrequency is ruled out (Arns et al., 2008; Lansbergen, Arns, van Dongen, Boomsma,\r\nSpronk, &amp; Buitelaar, 2011). Based on studies, the excess theta and TBR is\r\nfound in a substantial subgroup of patients with ADHD (25%-40%) and has been\r\ndemonstrated to be of prognostic value in predicting treatment outcome to\r\nstimulant medication and neurofeedback.</p><img src=\"@@PLUGINFILE@@/theta%20beta%20atio.jpg\" alt=\"Theta Beta Ratio\" width=\"500\" height=\"592\" class=\"img-responsive atto_image_button_left\"><h3>Other Profile Types</h3>While these profiles are some of the most widely researched and written about, there are a few others that occur in clinic that the well-versed clinician should know about. They are:<br>* Mu Rhythm<br>* Frontal Beta Spindles<br>*Excessive Delta<br>* Complex Types (composed of one or more of the subtypes)<br>* Paroxysms&nbsp;<br>*Epileptiform Content (An ADHD Impostor)&nbsp;<br><p></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',4,1654222234),(63,16,'A Review of Epilepsy Research','',1,'<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/gUzTE_sG2eQ\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe><p>Seizures and epileptogenic content is the wheelhouse of neurology, however EEG is the main modality used to study and understand seizure and, because of this, it is an important education for neurotherapists.&nbsp;</p>\r\n<p>\r\n    </p><div>A seizure is a <u>transient</u> symptom and or sign that is produced by abnormal, paroxysmal, and disorderly neuronal discharges in the brain.&nbsp;<span style=\"font-size: 1rem;\">Paroxysmal&nbsp;attacks\r\nor&nbsp;paroxysms&nbsp;(from\r\nGreek παροξυσμός)\r\nare a sudden recurrence or intensification of symptoms, such as a spasm or\r\nseizure. These short, frequent symptoms can be observed in various clinical\r\nconditions.&nbsp;</span><span style=\"font-size: 1rem;\">A seizure is an “ictal” event.\r\nInter-ictal is what occurs between seizures. Post-ictal is the time just after\r\nthe seizure.</span></div>\r\n    <div><span style=\"font-size: 1rem;\"><br></span></div>\r\n    <div><span style=\"font-size: 1rem;\"><div>Epilepsy is a chronic disorder of the\r\nbrain characterized by recurrent (two or more) seizures unprovoked by any\r\nimmediate identified cause and is sometimes called a seizure disorder.&nbsp;<span style=\"font-size: 1rem;\">Often the cause of epilepsy is idiopathic\r\n– unknown and not associated with neurological abnormalities.</span></div>\r\n    <div><span style=\"font-size: 1rem;\"><br></span></div>\r\n    <div><span style=\"font-size: 1rem;\">There are many kinds of seizures, here is a list of all the types:</span></div><div><span style=\"font-size: 1rem;\"><div><ul><li><span style=\"font-size: 1rem;\">Status Epilepticus</span></li><li>Psychogenic Seizures</li><li>Unclassified Epileptic Seizures</li><li>Generalized Seizures (convulsive\r\nor non-convulsive)</li><li>Absence\r\nSeizures (typical or atypical)</li><li>Myoclonic\r\nSeizures</li><li>Clonic\r\nSeizures</li><li>Tonic\r\nSeizure</li><li>Tonic-clonic\r\nseizures</li><li>Atonic\r\nSeizures</li><li>Partial&nbsp;</li><li>Simple\r\nPartial Seizures</li><li>Complex\r\nPartial Seizures</li><li>Partial\r\nSeizures evolving to secondarily generalized seizures</li></ul></div>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<div><br></div><h3>Research on Epilepsy</h3></span></div>\r\n    </span>\r\n    </div>\r\n<p></p>\r\n<p>Sterman &amp; Egner (2006) published a comprehensive review of earlier key studies regarding this disorder. The first single-case study was reported in 1972 (Sterman &amp; Friar, 1972). Sterman observed that, on average, 80% of patients who entrained sensory motor rhythm (12 - 15Hz) amplitudes displayed significant clinical improvements (Kaplan, 1975; Seifert &amp; Lubar, 1975; Sterman, MacDonald, &amp; Stone, 1974). These results were achieved in a difficult subgroup of epilepsy patients who had been unresponsive to pharmacological treatment. In addition, a number of investigations employing ABA crossover designs emphasized the causal and frequency-specific nature of SMR training by documenting symptom reversal when reversing\r\n    training contingencies (Lubar &amp; Bahler, 1976; Lubar et al., 1981; Sterman &amp; MacDonald, 1978).<br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',3,1654222307),(64,16,'A Review of Substance Abuse Research','',1,'<p></p><div>Addiction\r\nresearch has largely targeted regions of the ventral striatum (the nucleus\r\naccumbens core and shell), as well as the dopamine-releasing neurons of the\r\nventral mesencephalon. The ventral mesencephalon (i.e.\r\nmidbrain) densely innervate the nucleus accumbens.&nbsp;<span style=\"font-size: 1rem;\">Activation\r\nof the dopaminergic innervation of the nucleus accumbens (termed the mesolimbic\r\ndopamine system) is the neuronal substrate for the rewarding or reinforcing\r\nproperties of drugs of abuse (Roberts et al. 1980; Di Chiara and Imperato\r\n1988; Wise 1989, 1996; Kuhar et\r\nal. 1991; Koob\r\n1992; Fibiger et al. 1992; Dworkin and Smith 1993; Schulteis\r\nand Koob\r\n1996; White 1996).</span></div><img src=\"@@PLUGINFILE@@/Nucleus%20Accumbens.png\" alt=\"Nucleus Accumbens\" width=\"400\" height=\"293\" class=\"img-responsive atto_image_button_left\"><br><p></p><p>In short, t<span style=\"font-size: 1rem;\">he\r\nrelease of dopamine from the mesolimbic pathway into the nucleus accumbens\r\nregulates&nbsp;</span><span style=\"background-color: rgb(255, 255, 255); font-size: 1rem;\">incentive salience</span><span style=\"font-size: 1rem;\">&nbsp;(e.g.\r\nmotivation and desire for&nbsp;</span><span style=\"background-color: rgb(255, 255, 255); font-size: 1rem;\">rewarding stimuli</span><span style=\"font-size: 1rem;\">)\r\nand facilitates&nbsp;</span><span style=\"background-color: rgb(255, 255, 255); font-size: 1rem;\">reinforcement</span><span style=\"font-size: 1rem;\">&nbsp;and\r\nreward-related motor function learning.&nbsp;</span>The\r\ndysregulation of the mesolimbic pathway and its output neurons in the nucleus\r\naccumbens plays a significant role in the development and maintenance of\r\nan&nbsp;addiction.</p><h3><br></h3><h3><br></h3><h3><br></h3><h3>Crack / Cocaine</h3><p></p><div>Alper, et al., (1990) determined: “The\r\nmajor QEEG finding was increased absolute and relative alpha power” in crack\r\ncocaine users.&nbsp;<span style=\"font-size: 1rem;\">Prichep,\r\net al (2002) discovered in 57 male users, two\r\nmajor subtypes:</span></div>\r\n\r\n<div>◦1)\r\nan alpha cluster characterized by significant deficits of low frequency\r\nactivity (&lt;8Hz), significant excess of alpha activity (8-12Hz) and\r\nrelatively more normal levels of beta activity; and </div>\r\n\r\n<div>◦2)\r\na beta cluster characterized by deficits of delta, normal amounts of theta and\r\nanterior excess of alpha and beta activity. (Prichep et al., 2002).&nbsp;</div><br><p></p><h3>Stimulants</h3><p></p><div>Stimulants increase the activity in the Reticular Activating System, with the Raphe\r\nnucleus releasing norepinephrine,\r\ndecreasing the polarization in the reticular nucleus of the thalamus, and thus increasing the “clocking” or peak frequency\r\nof the rhythmic alpha activity and increasing faster activity.<br></div><br><p></p><p><img src=\"@@PLUGINFILE@@/Reticular%20Activating%20System.png\" alt=\"Reticular Activating System\" width=\"600\" height=\"341\" class=\"atto_image_button_middle\"></p><div>Both&nbsp;Dextrostat and Adderal&nbsp;are similar in\r\neffect, with&nbsp;<u>decreased slower activity </u>and <u>increased beta </u>from 12-26 Hz. There is a paradoxical\r\nincrease in alpha noted in the QEEG (Itil et al., 1980). </div>\r\n\r\n<div><br></div><div>Methylphenidate:&nbsp;Ritalin&nbsp;produces\r\na <u>decrease in delta and theta</u>,\r\nwith a more pronounced <u>posterior\r\nalpha increase and an increase in low beta</u>, with effects delayed up to 6 hours,\r\ncompared to the rapid effects of the amphetamines.</div><h3>Methamphetamines</h3><p></p><div>Methamphetamine dependent volunteers with 4 days of abstinence had\r\nincreased EEG power in the delta and theta bands.&nbsp;&nbsp;<span style=\"font-size: 1rem;\">Within the methamphetamine dependent group, a majority of the conventional EEGs were\r\nabnormal (64%), compared to 18% in the non-methamphetamine using group (Newton\r\net al., 2003).&nbsp;</span><span style=\"font-size: 1rem;\">Methamphetamine exposure is associated with long-lasting reductions in\r\nmarkers for dopaminergic neurons.</span></div><div><span style=\"font-size: 1rem;\"><br></span></div><h3></h3><h3>Alcohol</h3><div><span style=\"font-size: 1rem;\"><div>Acute\r\nalcohol increases dopamine release across the striatum primarily due to\r\nincreased firing of midbrain dopaminergic neurons.</div>\r\n\r\n<div>With alcoholism, tolerance\r\ndevelops, and more alcohol is consumed.&nbsp;<span style=\"font-size: 1rem;\">Concomitantly,\r\nadaptations in glutamatergic, GABAergic, and dopamine transmission occur and\r\ngreater or continued amounts of alcohol can result in allostatic changes to\r\npreserve normal brain function. This allostasis is characterized by aberrant\r\nglutamate, GABA, and opioid signaling, as\r\nwell as, a dysfunction in nigrostriatal\r\nand mesolimbic dopamine transmission.</span></div><img src=\"@@PLUGINFILE@@/Ventral%20Striatum.png\" alt=\"Ventral Striatum\" width=\"500\" height=\"423\" class=\"img-responsive atto_image_button_middle\"><p></p><ul><li>Alcohol consumption is the third\r\nlargest risk factor for poor health (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4106030/\">WHO, 2011</a>)</li><li>One profile\r\nthat has a predisposition to alcohol: Low voltage</li><li>Low Voltage\r\nEEG can be due to excessive GABAA receptor sites</li></ul></span></div><p><img src=\"@@PLUGINFILE@@/Low%20Voltage%20EEG.png\" alt=\"Low Voltage EEG\" width=\"605\" height=\"537\" class=\"img-responsive atto_image_button_left\"><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><h3>Cannabis / Hashish / THC&nbsp;</h3><p></p><div><span style=\"font-size: 1rem;\">Marijuana and its sister drugs will:</span><br><ul><li>Increase\r\nfrontal alpha amplitude, </li><li>increased\r\nfrontal coherence across the hemispheres</li><li>Increased\r\nphase synchrony (hypo phase lag).&nbsp; These findings are reported in chronic\r\nexposures.</li><li>Effects on dampening reaction times\r\nin evoked potentials have been noted as well</li></ul></div>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\nRegular\r\nuse of cannabis over many years lowers levels of dopamine, a key chemical in\r\nthe brain’s reward center. <br>The dopamine system is central to learning and motivation. We conclude that\r\nlong-term cannabis use in people is linked to blunting of the dopamine\r\nsystem.<br><p></p><p><img src=\"@@PLUGINFILE@@/Dopamine.png\" alt=\"Dopamine\" width=\"400\" height=\"366\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>',1,0,NULL,5,'a:3:{s:12:\"printheading\";s:1:\"1\";s:10:\"printintro\";s:1:\"0\";s:17:\"printlastmodified\";s:1:\"1\";}',3,1654213930),