[encoded data, 82464 characters]\" alt=\"\"><br></p><h4 style=\"text-align: left;\"><br></h4><h4 style=\"text-align: left;\">qEEG for high amplitude spindling beta (Benzodiazepine use)</h4><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Benzodiazepine%20Map.png\" alt=\"Benzodiazepine Map\" width=\"710\" height=\"919\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem;\"></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><h2 style=\"text-align: left;\"><a name=\"_Toc29328796\">Gamma</a></h2>\r\n\r\n<p style=\"text-align: left;\"><br></p>\r\n\r\n<p style=\"text-align: left;\">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.</p>\r\n\r\n<p style=\"text-align: left;\">Gamma travels in envelopes, which\r\nsurround the oscillation, making it appear with a spindle shape, and it has the\r\nability to arise in any structure of the brain, because interneurons connected\r\nby GABA <sub>A </sub>receptors are ubiquitous throughout the brain (Buzsaki,\r\n2006, p. 75). Of most interest, gamma has been implicated to be the binding\r\nrhythm of consciousness (Buzsaki, 2006, Gold, 1999; Hughes, 2008). It is not\r\ngenerated via a local neurophysiological generator, but is rather an emergent\r\nproperty of networks (Gunkelman, 2015) and is related to subjective awareness (Gunkelman,\r\n2014). &nbsp;Gamma is healthy when it is nested in other\r\nfrequencies, which is a phenomenon known as phase-amplitude cross frequency\r\ncoupling, where the phase of one frequency (e.g., theta) changes the amplitude\r\nof another frequency (e.g., gamma). As the theta goes electro-negative, gamma\r\nis active, but when theta goes positive, gamma attenuates (Gunkelman, 2015).\r\nGamma has also been tied to deep meditative states. Lutz, Greischar, Rawlings,\r\nRichard, and Davidson (2004) found that long-term meditators produce\r\nself-induced high amplitude gamma when meditating.</p><p style=\"text-align: left;\">Gamma-frequency oscillations are\r\ntypically short-lasting, transient events (Buzsaki, 2006, p. 76). One of the\r\nmarkers of pathological gamma is persistence; healthy gamma ought to occur in\r\nbursts or “chirps” (DeRidder, 2014). Low-frequency oscillations (such as those\r\nof delta and theta) have been reported to coordinate long-range communication,\r\nwhile gamma oscillations (40-150) coordinate local communication (Buzsaki &amp;\r\nDraguhn, 2004; von Stein et al., 2000). Local communication is between very\r\nclose neuronal pools. At times brainwaves come into harmony (e.g., 45 Hz gamma\r\nlaid over a background of 9 Hz alpha is a harmonic, since 45 divides into 9),\r\nand other patterns that represent certain states of being and of mind. </p><p style=\"text-align: left;\"><br></p><p></p><p></p>',1),(370,84,368,371,20,0,1,1,1589493136,1594471191,'Developmental EEG','<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Developmental%20EEG.png\" alt=\"Developmental EEG\" width=\"1187\" height=\"1000\" class=\"img-responsive atto_image_button_middle\"><br></p><p><br></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>At 4 weeks, the first brain cells, the neurons,\r\nare establishing at 500,000 per minute. These cells will never turn over,\r\nunlike the skin. Neurons born in fetal life function all the way into old age.\r\nWithin the first 13 weeks of life the reptilian structures of the brain are\r\nfully formed (the brainstem, spinal cord, cerebellum, and pons). The first\r\nstage of wiring is when fundamental networks form via an odyssey of the\r\nneurons, 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><h4><br></h4><h4>Fetal Development</h4><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Fetal%20Development.png\" alt=\"Fetal Development\" width=\"673\" height=\"707\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p></p><p></p><p>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.</p><h4><br></h4><h4>Lissencaphaly, where the brain does not form gyri and sulci, but\r\nis smooth, occurs between 12 – 24 weeks of life.</h4><p><br></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp; &nbsp; &nbsp;&nbsp;</span><span style=\"font-size: 1rem;\">&nbsp;</span></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp; &nbsp;</span><img src=\"@@PLUGINFILE@@/lissencephaly.png\" alt=\"lissencephaly\" width=\"461\" height=\"307\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;&nbsp;</span></p><p></p><p></p><h4 style=\"text-align: center; \"><br></h4><h4 style=\"text-align: center; \"><br></h4><h4 style=\"text-align: left;\">Microcephaly versus a Normal Sized Infant Skull</h4><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/microcephaly.png\" alt=\"microcephaly\" width=\"819\" height=\"472\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p></p><p></p><h3 style=\"text-align: left;\"><a name=\"_Toc29328799\">Premature Babies</a></h3>\r\n\r\n<p style=\"text-align: left;\">&nbsp;</p>\r\n\r\n<p style=\"text-align: left;\">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.</p>\r\n\r\n<p style=\"text-align: left;\">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><p style=\"text-align: center; \"><br></p><p></p><h3 style=\"text-align: left;\"><a name=\"_Toc29328800\">Birth</a></h3>\r\n\r\n<p style=\"text-align: left;\">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.\r\nConsequentially, infants spend a\r\ngreat deal 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><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">The neonatal weeks are crucial for the\r\nneurophysiological effects of nursing on the somato-sensory projection areas of\r\nthe mouth and the relevant associative cortical areas. Chugani et al. (1987)\r\nhave shown in PET recordings that during the first weeks of life there is an\r\nincrease in blood flow in those brain structures (brain stem, cerebellum,\r\nstriatum and the sensory areas of the cortex) that participate in nursing\r\nresponses. At six months, the </span><i style=\"font-size: 1rem;\">theta </i><span style=\"font-size: 1rem;\">rhythm prevailed in&nbsp;</span></p><p style=\"text-align: left;\">both hemispheres, but had a\r\nright hemisphere posterior maximum. Paul et al. (1996) have shown in infants\r\nfrom the age of 2 to 26 weeks that feeding is connected with an amplitude\r\nincrease and a growing degree of synchronization in the EEG, with an exception\r\nof the age of 10 weeks, when no significant EEG changes were recorded. This\r\nnewly acquired neurophysiological organization between subcortical and cortical\r\nstructures can give rise to a synchronized activity in wide brain areas (Scher,\r\n1989). The special 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 style=\"text-align: left;\"><a name=\"_Toc29328801\">Vision</a></h3>\r\n\r\n<p style=\"text-align: left;\">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\r\nlooking at a faded photograph through a tube. This prevents excess stimuli. </p><h3 style=\"text-align: left;\"><a name=\"_Toc29328802\">Breastfeeding</a></h3>\r\n\r\n<p style=\"text-align: left;\">Because the primary\r\nsource of activity of the EEG is in the cortical neural processes, the change\r\nin the EEG pattern in newborn infants during the feeding processes may be\r\nindicative of a shaping of a primitive protomental image, i.e. a sensory memory\r\nformation at the cortical level, that starts after birth and runs in parallel\r\nto the deep automatic brain functions regulating the reflexive and autonomous\r\nneural events of the nursing exchanges. This may be important, since the\r\nparticipation 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 style=\"text-align: left;\">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, illu- minate\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\r\noccur in infant care.</p><h3 style=\"text-align: left;\"><a name=\"_Toc29328803\">Auditory Perception</a></h3>\r\n\r\n<p style=\"text-align: left;\">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 style=\"text-align: left;\">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><h3 style=\"text-align: left;\"><a name=\"_Toc29328804\">Hypnagogic Hypersynchrony</a></h3>\r\n\r\n<p style=\"text-align: left;\">Hypnagogic Hypersynchrony\r\n(HH) is the pattern seen in infants and children during the transition from\r\ndrowsiness to sleep. It consists of high amplitude, paroxysmal, bilateral,\r\nrhythmic bursts of 3 to 5 Hz waves. Unlike, POSTS, which live in the occipital\r\nleads, HH is a diffuse pattern, tending towards anterior dominance. It may\r\nemerge as early as 4 months but is seen in the majority of infants between 6 to\r\n8 months old. HH may be continuous from ages 8 to 12 months but as the child\r\nages a more paroxysmal type of HH is seen. The pattern begins to dissolve by\r\nage 2 years and is usually gone by age 12 years. Since this is only a\r\ntransition pattern, it will disappear once N2 sleep is reached. At three\r\nmonths, the distinctive pattern of hypnagogic hypersynchrony emerges replacing\r\nthe high amplitude 2 to 3 Hz rhythm seen during drowsiness. This high amplitude\r\nbisynchronous rhythmic 3 to 6 Hz activity can be paroxysmal or continuous for\r\nseveral minutes either at the beginning or end of the sleep cycle.</p><p style=\"text-align: left;\"><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">Hypnogogic Hypersynchrony</span></p><img src=\"@@PLUGINFILE@@/Hypnogogic%20hypersynchrony.png\" alt=\"Hypnogogic hypersynchrony\" width=\"603\" height=\"386\" class=\"img-responsive atto_image_button_left\" style=\"text-align: center; \"><p style=\"text-align: center;\"><br></p><p></p>\r\n\r\n<p style=\"text-align: center; \">After 3\r\nmonths of age, all NREM and REM sleep stages show maturation as well as\r\ndevelopment of new patterns. REM now only occupies 25% of the total sleep time.\r\nDuring NREM sleep, patterns reach mature formations. Sleep spindles are fully\r\ndeveloped, synchronous, and symmetrical by 2 years. The amplitude and incidence\r\nof V-waves and K-complexes decrease at 3 to 4 years until the adult waveform is\r\nattained.</p><p style=\"text-align: center;\"><br></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p></p><p style=\"text-align: center; \">&nbsp;</p><p style=\"text-align: center; \"><br></p>\r\n\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc29328805\">Pediatric EEG (Age 1 to Adolescence)</a></h2>\r\n\r\n<p style=\"text-align: left;\">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 style=\"text-align: left;\">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><h3 style=\"text-align: left;\"><a name=\"_Toc29328806\">Language and Auditory\r\nPerception</a></h3>\r\n\r\n<p style=\"text-align: left;\">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 style=\"text-align: left;\"><a name=\"_Toc29328807\"></a><a name=\"_Toc16242767\">Posterior Slow Waves of Youth</a> (PSWY)</h2><p></p><h4 style=\"text-align: center; \"><br></h4><h4 style=\"text-align: center; \">Posterior Slow Waves of Youth in a 2 <sup>1/2</sup> year old\r\nmale</h4><img src=\"@@PLUGINFILE@@/Posterior%20Slow%20Waves%20of%20Youth.png\" alt=\"Posterior Slow Waves of Youth\" width=\"625\" height=\"604\" class=\"img-responsive atto_image_button_left\" style=\"text-align: center; \"><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">Posterior slow waves of youth are physiologically high-voltage theta or delta waves most commonly seen in children aged 8–14 years, but uncommon in children under 2 years. PSWYs &nbsp;occur in 15% of healthy individuals aged 16–20 years but are rare in adults above 21 years of age. These are slow theta and delta waves that are intermixed with alpha waves. They attenuate with eyes opening and they occur as sporadic single waves or as bursts of transient waves interspersed by one or several seconds or regular background activity. PSOY are usually bisynchronous but can have shifting symmetry (Stern 2005).</span></p><p></p><p style=\"text-align: center;\"><br></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p></p><h3 style=\"text-align: left;\"><a name=\"_Toc29328808\">POSTS</a></h3>\r\n\r\n<p style=\"text-align: left;\">Appearing\r\nin children, 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><h4 style=\"text-align: center; \"><br></h4><h4 style=\"text-align: left;\">Positive Occipital Sharp Transients in a child drifting into\r\nNREM2 sleep</h4><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/POSTS.png\" alt=\"Positive Occipital Sharp Transients \" width=\"639\" height=\"513\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: left;\"><a name=\"_Toc29328809\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">OIRDA</a><br></p><p><a name=\"_Toc29328809\"></a></p><p style=\"text-align: left;\"><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 deomnstrated pathological significance. </a></p><h4 style=\"text-align: left;\">OIRDA seen in a 10-year old girl</h4><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/OIRDA.png\" alt=\"OIRDA\" width=\"1007\" height=\"750\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p></p><h2 style=\"text-align: left;\"><a name=\"_Toc29328810\">Adolescence</a></h2>\r\n\r\n<p style=\"text-align: left;\">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 style=\"text-align: left;\">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 hours compared to 8).</p><h2 style=\"text-align: left;\"><a name=\"_Toc29328811\">Adult</a></h2>\r\n\r\n<p style=\"text-align: left;\">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 style=\"text-align: left;\"><a name=\"_Toc29328812\">Senior</a></h2>\r\n\r\n<p style=\"text-align: left;\">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><p></p><p style=\"text-align: left;\">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 style=\"text-align: left;\">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><p style=\"text-align: left;\">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><p style=\"text-align: left;\"><br></p><p></p><p></p>',1),(371,84,370,372,20,0,1,1,1589513452,1614233047,'EEG of Sleep','<p></p><h2><a name=\"_Toc29328813\">EEG of Sleep</a></h2>\r\n\r\n<p>In normal adults, a cycle of sleep\r\nstages repeats throughout the night, about every 90 minutes. This is referred\r\nto as “sleep architecture.”</p><h3>Sleep Architecture over the Course of an Evening of Sleep</h3><p></p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Architecture%20of%20Sleep.png\" alt=\"Architecture of Sleep\" width=\"660\" height=\"383\" class=\"img-responsive atto_image_button_left\"><br></p><p></p><p><b>NREM1</b> = Alpha begins to slow\r\nand intermittently drop out of the record and we see a suppression of EEG\r\namplitude, overall. </p>\r\n\r\n<p><b>NREM2</b> = The presence of\r\nVertex Sharp Waves, K-Complexes, and Sleep Spindles</p>\r\n\r\n<p><b>NREM3</b> = The movement towards\r\ncomplete slow waves (Delta and some low frequency theta)</p>\r\n\r\n<p><b>NREM4</b>&nbsp; = Deep dreamless sleep, aka “Slow Wave Sleep\r\n(SWS)</p>\r\n\r\n<p><b>REM</b> = Rapid Eye Movement\r\nSleep</p>\r\n\r\n<p>Some schools of thought now combine\r\nStage 3 and Stage 4 of sleep.</p><p></p><h3><a name=\"_Toc29328814\"><br></a></h3><h3><a name=\"_Toc29328814\">Vertex Sharp Waves</a></h3><img src=\"@@PLUGINFILE@@/V%20Waves.png\" alt=\"V-Waves\" width=\"402\" height=\"683\" class=\"img-responsive atto_image_button_left\">Vertex sharp wave transients, appear in Stage NREM2 sleep. These midline sharp waves run down the vertex and are typically theta in frequency and are of high amplitude. A surround may present at the left and right leads. &nbsp;Vertex sharp waves are usually biphasic. They can occur individually or in runs (repeatedly for a brief time). The morphology of V waves varies in sleeping individuals. In some cases, they are sharply contoured, in other cases they can look like epileptiform discharges.&nbsp;<br><p></p><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></p><h3><a name=\"_Toc29328815\"><br></a></h3><h3><a name=\"_Toc29328815\">Stage NREM 2 Sleep and Sleep Spindles</a></h3><p><a name=\"_Toc29328815\"></a></p><h4><a name=\"_Toc29328815\">Sleep Spindles</a></h4><a name=\"_Toc29328815\"><img src=\"@@PLUGINFILE@@/sleep%20spindles.png\" alt=\"Sleep Spindles\" width=\"492\" height=\"687\" class=\"img-responsive atto_image_button_left\"><br></a><p></p>\r\n\r\n<p>Sleep spindles,\r\nindicate the onset of Stage NREM2 sleep. They serve as a stabilizing mechanism\r\nduring sleep state, which will prevent the individual from awakening. Sleep\r\nspindles are bursts of sinusoidal 12-14 Hz activity, that wax and wane (travel\r\nin an envelope). They are seen over the fronto-central head regions, most often\r\nwith a maximum over the central midline. They last from half a second to two\r\nseconds on average.</p><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></p><h3><a name=\"_Toc29328816\"><br></a></h3><h3><a name=\"_Toc29328816\"><br></a></h3><h3><a name=\"_Toc29328816\">K Complexes</a> </h3><img src=\"@@PLUGINFILE@@/K%20Complex.png\" alt=\"K Complex\" width=\"570\" height=\"683\" class=\"img-responsive atto_image_button_left\"><p>K complexes usually appear\r\nin Stage NREM&nbsp; of 2 sleep, and may also\r\nseen in Stages N3 sleep.. K-complexes consist of a broad vertex sharp waves\r\naccompanied by a run of sleep spindles.</p>\r\n\r\n<p>The slow wave portion of\r\nthe K complex can exceed 1000 milliseconds in duration. The amplitude may\r\nexceed 400 microvolts. K complexes appear spontaneously, or they can be\r\nelicited by an auditory stimulus (the “k” in K-complex stands for “Knock”).&nbsp; Knocking a counter, clapping, or tapping a\r\npencil on a hard surface are good ways to elicit K complexes during EEG\r\nrecordings. K complexes should be of equal voltage over both hemispheres.</p><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></p><p>Stage N3 sleep is\r\ncharacterized by an increase in higher voltage slow waves in the theta and\r\ndelta range. Sleep spindles and K complexes may be present. As Stage N3 sleep\r\nprogresses, the frequencies seen are slower and the number of sleep spindles\r\ndecreases.&nbsp; </p>\r\n\r\n<p>In NREM 4, delta increases, sleep\r\nspindles are no longer present, and the EEG consists of generalized, high\r\nvoltage, irregularly shaped slow waves.&nbsp;\r\nDeeper sleep stages are seldom seen in routine EEG recordings unless the\r\npatient is sleep deprived and the recording period is lengthened.<b></b></p><p></p><h3><a name=\"_Toc29328818\">Rapid Eye Movement (REM) Sleep</a></h3>\r\n\r\n<p>REM sleep begins 60-90 minutes\r\nafter sleep onset. During REM sleep we lose muscle tone, except for eye\r\nmovements. Respiration and heartbeat may become irregular. </p>\r\n\r\n<p>During REM sleep, small muscle\r\nmovements (phasic twitches), are seen in the face and extremities. Saccadic eye\r\nmovements accompany REM sleep, which can be seen under the person\'s closed\r\neyelids. The EEG in REM sleep is of low voltage, with a mixture of rhythms. It\r\nmay look very much the same as the EEG during wakefulness with eyes open,\r\nexcept for the lack of EMG contamination.</p>\r\n\r\n<p>If REM sleep that begins less than\r\none hour after sleep onset, it is called REM onset sleep. This can be an\r\nabnormal finding indicating a sleep disorder called narcolepsy if accompanied\r\nby other symptoms and repeatedly demonstrated.</p><br><h3>The Vigilance Model</h3><p>When you are recording an EEG, its advisable to avoid drowsy data, at all costs. Of course, we first have to know what a drowsy EEG looks like. To understand what data begins to look like as someone falls asleep, it is wise to reference the Vigilance Model.&nbsp;</p><p><br></p><h4>What is Vigilance?</h4><div>The\r\nregulation of vigilance and its flexible adaptation to internal and\r\nenvironmental needs are of fundamental importance for all higher organisms.\r\nVigilance has to be\r\nadapted to the respective environmental situation, ensuring a high vigilance\r\nlevel in situations of danger and a reduced vigilance level during times of\r\nrecreation.</div><div><br></div><h4><span>Vigilance stages</span></h4>\r\n\r\n<div>These states correspond to different levels of alertness at the behavioral\r\nlevel. Several stages can be separated during the transition from tense to\r\nrelaxed wakefulness and further on to drowsiness until sleep onset.</div><p></p><p></p><img src=\"@@PLUGINFILE@@/Vigilance%20Model.png\" alt=\"Vigilance Model\" width=\"673\" height=\"500\" class=\"img-responsive atto_image_button_left\"><br>The VIGALL model of vigilance is meant to be applied to an eyes closed EEG, but it can be even more telling for an eyes open EEG, as you can see when someone descends from the common, eyes closed occipital alpha (A1), to anteriorized alpha (A2) (the first hint that they are getting drowsy and their vigilance is compromised) to a low voltage state (also called desynchronized or alpha drop-out, B1) until you see them descende into NREM2, which corresponds with the C state.&nbsp;<br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>The video just below shows an individual entering stage B1, where we see moments of alpha drop out, where it appears the EEG gets flat.<br>&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/B1.mp4\">@@PLUGINFILE@@/B1.mp4</video>&nbsp;<br>And these are the maps and a spectral plot that correspond with the B2 state, high theta and delta power:<br><img src=\"@@PLUGINFILE@@/Sleep.png\" alt=\"sleep\" width=\"700\" height=\"444\" class=\"img-responsive atto_image_button_left\">&nbsp;<img src=\"@@PLUGINFILE@@/sleep%202.png\" alt=\"sleep 2\" width=\"655\" height=\"560\" class=\"img-responsive atto_image_button_text-bottom\"><br>And the video below is someone actively in stage nREM2 of sleep, noted by the vertex sharp waves and beta spindles.<br><video controls=\"true\"><source src=\"@@PLUGINFILE@@/NREM2.mp4\">@@PLUGINFILE@@/NREM2.mp4</video><br>&nbsp;<br><p></p>',1);
INSERT INTO `mdl_lesson_pages` VALUES (372,84,371,373,20,0,1,1,1589514608,1656008762,'EEG Signatures to Refer Out','<p></p>\r\n<p><a name=\"_Toc29328820\">When you come across an abnormal EEG, one where you see epileptiform discharges, etc., its important you refer your patient to a neurologist.&nbsp;</a></p>\r\n<p><a name=\"_Toc29328820\">However, understanding epileptiform EEG and all the different kinds of seizures is a task on its own.&nbsp;</a></p>\r\n<p><a name=\"_Toc29328820\">Here is a two hour long lecture on the EEG of Seizure and epilepsy, full of videos of what various seizures actually <i>look</i>&nbsp;like, in order to help the budding clinician.&nbsp;</a></p><iframe src=\"https://player.vimeo.com/video/465148872?h=c91f64ca82&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<h2><a name=\"_Toc29328820\">Transient discharges</a> </h2>\r\n\r\n<p>Paroxysmal transients in EEG can indicate: </p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->Epileptogenic activity, indicating a seizure disorder\r\n</p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->Non-convulsive and non-epileptic activity </p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->Cerebral vascular issues, tumors, and lesions</p>\r\n<p></p>\r\n<h2><a name=\"_Toc29328821\">A Transient in the EEG</a></h2><br>\r\n<p></p>\r\n<p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Transient.png\" alt=\"Transient\" width=\"477\" height=\"443\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n<p style=\"text-align: center;\"><br></p>\r\n    <p></p>\r\n    <p style=\"text-align: center; \"><br></p>\r\n    <p style=\"text-align: center; \"><br></p>\r\n    <p style=\"text-align: center; \"><br></p>\r\n    <p></p>\r\n    <h2 style=\"text-align: left;\"><a name=\"_Toc29328822\">Focal Slowing</a> </h2>\r\n\r\n    <p style=\"text-align: left;\">A focal slowing, if seen in the EEG, can indicate trauma, tumor, a lesion, or a healing grey matter injury. If delta is showing it can indicate an injury where the white matter is damaged and myelination is affected, if theta is showing it could indicate\r\n        a grey matter injury (such as we would see in whiplash or a concussive injury). If the focus is at the posterior temporal lobes, good chance it is a cerebral vascular issue.\r\n    </p>\r\n    <h3 style=\"text-align: left;\"><a name=\"_Toc29328823\"></a><a name=\"_Toc3535229\">Cerebro-vascular disorders</a></h3>\r\n\r\n    <p style=\"text-align: left;\">Cerebro-vascular disorders can be indicated by a slowing of alpha at one site. The slow edge of alpha tracks ischemia. An indication of a vascular issue (or impeded flow dynamics) is the presence of headaches or any sort of similar issue.&nbsp; In\r\n        Nuwer et al (1997) there is a finding in cerebrovascular disease that show ischemia-related cerebral impairment to be seen in focal features (perhaps similar to the finding of slowing in the right posterior temporal lobe). </p>\r\n\r\n    <p style=\"text-align: left;\">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). When cerebral\r\n        blood ﬂow (CBF) becomes compromised, changes occur in both the metabolic and electrical activity of cortical neurons, with associated EEG changes.</p>\r\n    <h3 style=\"text-align: left;\"><a name=\"_Toc29328824\">Epileptiform Discharge</a></h3>\r\n\r\n    <p style=\"text-align: left;\">A common feature of the epileptic disorders is a paroxysmal excitatory activity.</p>\r\n\r\n    <p style=\"text-align: left;\">Epileptogenic activity can be seen in the presence of spike waves, sharp waves, and the presence of spike and slow waves. Additionally, fast beta and gamma can indicate a kindling rhythm in the EEG, reflecting an irritable cortex that is pre-disposed\r\n        towards seizure. Very often seizure will manifest in temporal lobes, which are the most vulnerable lobes for this type of pathology.</p>\r\n\r\n    <p style=\"text-align: left;\"><b>Spike:</b> An epileptogenic transient can be seen in a spike (a transient with a duration of less than 70 msec, but more than 20 msec and commonly negative in polarity. Spike morphology has a step incline. </p>\r\n\r\n    <p style=\"text-align: left;\"><b>Sharp Wave</b>: A transient that is 80 – 200msec. Morphology is usually pointed and voltage is usually high.</p>\r\n    <h4 style=\"text-align: left;\">Here is an EEG of an individual going through an absence seizure:<br>&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Seizure%20video.mp4?time=1597384319251\">@@PLUGINFILE@@/Seizure%20video.mp4?time=1597384319251</video>&nbsp;<br></h4>\r\n    <h4 style=\"text-align: center; \">Widespread epileptogenic discharge, affecting the EEG due to shared variance via the ear electrodes</h4>\r\n        <p></p>\r\n        <p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Epileptiform.png\" alt=\"Epileptiform Content\" width=\"531\" height=\"723\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n        <p style=\"text-align: center;\"><br></p>\r\n        <p></p>\r\n        <p style=\"text-align: center;\"><br></p>\r\n        <p></p>\r\n        <p style=\"text-align: center; \"><br></p>\r\n        <p></p>\r\n        <h3 style=\"text-align: left;\"><a name=\"_Toc29328825\">Epileptiform Discharge as seen in classic\r\nSpike and Wave Phenomena</a></h3>\r\n        <p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Epileptiform%202.png\" alt=\"Epileptiform 2\" width=\"500\" height=\"671\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n        <p style=\"text-align: center; \"><br></p>\r\n            <p style=\"text-align: center; \"><br></p>\r\n            <p></p>\r\n            <h3 style=\"text-align: left;\"><a name=\"_Toc29328826\">Phase Reversals</a></h3>\r\n\r\n            <p style=\"text-align: left;\">Phase reversals are a focal finding in the EEG where the waveforms go electro-positive and electro-negative, looking as though they are pointing to each other. This is a marker of a physical abnormality and can point to the seizure focus,\r\n                a lesion, hypoperfusion, localized infarct (a small localized area of dead tissue), or white matter ischemia. This is an “X marks the spot” type of finding. Phase Reversals can be seen using bi-polar montages.</p>\r\n            <h3></h3>\r\n            <h2 style=\"text-align: left;\"><a name=\"_Toc29328827\">Multi-focal spikes in the EEG</a></h2>\r\n            <p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/multi%20focal%20spike.png\" alt=\"Mulit focal spike\" width=\"672\" height=\"1097\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n            <p style=\"text-align: center;\"><br></p>\r\n            <p></p>\r\n            <h3 style=\"text-align: left;\">Phase Reversals</h3>\r\n            <p style=\"text-align: center;\"><br></p>\r\n            <h2 style=\"text-align: center;\"><br></h2>\r\n            <p></p>\r\n            <p style=\"text-align: center;\"><a name=\"_Toc29328827\" style=\"background-color: rgb(255, 255, 255); color: rgb(82, 96, 105); font-size: 1rem;\">&nbsp;<img src=\"@@PLUGINFILE@@/Phase%20Reversals.png\" alt=\"Phase Reversals\" width=\"772\" height=\"1104\" style=\"text-align: center;\" class=\"atto_image_button_middle\"></a></p>\r\n            <a name=\"_Toc29328827\">\r\n                <p style=\"text-align: center;\"><br></p>\r\n                </a>\r\n                <p style=\"text-align: center; \"><br></p>\r\n                <p style=\"text-align: left;\"><a name=\"_Toc29328829\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Encephalopathy</a><br></p>\r\n\r\n                <p style=\"text-align: left;\">Encephalopathy (low voltage slow)—you must also find the etiology, see if it is metabolic, toxic, traumatic, anoxic, electrolytic—no medication will work as long a there is insufficient support for brain function. You will treat this by\r\n                    identifying and rectifying the root of the problem.\r\n                </p>\r\n\r\n                <h3 style=\"text-align: left;\">Low Voltage Slow Profile</h3>\r\n                <p style=\"text-align: center; \"><img src=\"data:image/png;base64,[encoded data, 285864 characters]\" alt=\"\"><br></p>\r\n                <p style=\"text-align: center;\"><br></p>\r\n                <p></p>',1),(373,84,372,374,20,0,1,1,1589515757,1656009101,'EEG Profiles and Clinical Presentations of Pathology','<p></p>\r\n<h5>Jay Gunkelman has done a service to the field in his explanation of the 11 phenotypes in EEG.&nbsp;</h5>\r\n<p>Here is a short video of Jay explaining the Phenotype model:&nbsp;</p>\r\n<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/429426691?h=875f70a63c&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 - PHENOTYPES\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script>\r\n<p>And here is a long video (2 hours) of Jay discussing phenotypes:</p>\r\n<div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/589486357?h=cb70efe2cb&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=\"Phenotypes Tools for Advanced Neurotherapy\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script>\r\n<p><br></p>\r\n<p></p>\r\n<h3>Electroencephalography (EEG)/Quantitative EEG Phenotypes</h3>\r\n<p><br></p>\r\n<table border=\"0\" cellspacing=\"0\" cellpadding=\"7\" width=\"100%\">\r\n    <tbody>\r\n        <tr>\r\n            <td valign=\"top\"><b>Candidate Phenotype</b></td>\r\n            <td valign=\"top\"><b>EEG Findings</b></td>\r\n            <td valign=\"top\"><b>Associated Neurofeedback Approach<br><br></b></td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Low-voltage fast</td>\r\n            <td valign=\"top\">Low-voltage EEG overall</td>\r\n            <td valign=\"top\">Reward alpha activity posteriorly<br><br></td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Epileptiform</td>\r\n            <td valign=\"top\">Transient spike/wave, sharp waves, paroxysmal EEG</td>\r\n            <td valign=\"top\">Inhibit low and high frequencies; sensorimotor rhythm training; also consider slow cortical potential control<br><br></td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Diffuse slow activity (with or without lower alpha)</td>\r\n            <td valign=\"top\">Increased delta and theta (1-7 Hz) with or without slower posterior alpha</td>\r\n            <td valign=\"top\">Inhibit midline fronto-central activity slower than 10 Hz, add reward for anterior beta for increased stimulating effect</td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Focal abnormalities (not epileptiform)</td>\r\n            <td valign=\"top\">Focal slow activity or focal lack of activity</td>\r\n            <td valign=\"top\">Inhibit slower activity and reward higher frequencies (consider medical referral)<br><br></td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Mixed fast and slow</td>\r\n            <td valign=\"top\">Increased slower activity, lack of organized alpha, increased beta</td>\r\n            <td valign=\"top\">Inhibit slow frequencies, reward alpha and SMR, inhibit faster beta<br><br></td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Frontal lobe hypoperfusion disturbances</td>\r\n            <td valign=\"top\">Frontally dominant excess theta or alpha frequency activity</td>\r\n            <td valign=\"top\">Inhibit midline fronto-central activity below 10Hz, reward anterior beta for increased effect</td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Frontal asymmetries</td>\r\n            <td valign=\"top\">Frontal asymmetry primarily measured at F3, F4<br><br></td>\r\n            <td valign=\"top\">Adjust frontal symmetry with alpha, theta, and beta</td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Excess temporal lobe alpha</td>\r\n            <td valign=\"top\">Increased alpha activity generated in temporal lobe</td>\r\n            <td valign=\"top\">Inhibit alpha over affected temporal region(s),and inhibit frontal slow activity<br><br></td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Faster alpha variants, not low voltage</td>\r\n            <td valign=\"top\">Alpha peak frequency greater than 12 Hz over posterior and parietal cortex<br><br></td>\r\n            <td valign=\"top\">Reward 8-10 Hz alpha at Pz, shift alpha frequency slower with alpha/theta protocol</td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Spindling excessive beta</td>\r\n            <td valign=\"top\">Rhythmic beta with a spindle morphology, often with an anterior prominence<br><br></td>\r\n            <td valign=\"top\">Inhibit beta’s spindle frequencies, wide band inhibit; alpha-theta training may help</td>\r\n        </tr>\r\n        <tr>\r\n            <td valign=\"top\">Persistent eyes-open alpha</td>\r\n            <td valign=\"top\">Alpha doesn’t attenuate by at least 50% with eyes open; it is generally slower alpha</td>\r\n            <td valign=\"top\">Reward beta frequencies, inhibit alpha; reward higher frequency alpha</td>\r\n        </tr>\r\n    </tbody>\r\n</table><br>\r\n<p></p>\r\n<p>His research on Phenotypes can be seen in the article in the Articles section of this chapter.</p>\r\n<p>Johnstone, Gunkelman, and Lunt (2005), Clinical database development: Characterization of EEG phenotypes. Clinical EEG and Neuroscience, 2, 99-107, and is used with the permission of Clinical EEG and Neuroscience.</p>\r\n<h2><a name=\"_Toc29328831\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Low\r\nVoltage Fast EEG</a><br></h2>\r\n\r\n<p>The low voltage fast EEG phenotype is driven by over arousal. This profile shows a genetic alteration of gene number 4, the gene that controls GABA A receptors, and if you make more receptors than you can saturate, you are over aroused. This is a prominent\r\n    variant of people who have alcoholism. Behaviorally, this would show as someone who is over aroused, perhaps nervous, anxious, or tense. This is someone who will not do well in a highly stressful work environment. But, overall, this it is a normal\r\n    variant that is present in about 10% of the population. Typically, their alpha is fast and desynchronized.</p>\r\n\r\nThe low voltage fast EEG phenotype is driven by over arousal. This profile shows a genetic alteration of gene number 4, the gene that controls GABA A receptors, and if you make more receptors than you can saturate, you are over aroused. This is a prominent\r\nvariant of people who have alcoholism. Behaviorally, this would show as someone who is over aroused, perhaps nervous, anxious, or tense. This is someone who will not do well in a highly stressful work environment. But, overall, this it is a normal&nbsp;variant\r\nthat is present in about 10% of the population. Typically, their alpha is fast and desynchronized.\r\n<br>\r\n<p></p>\r\n<p></p>\r\n<h4>Low Voltage Fast EEG</h4>\r\n<p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Low%20VOltage%20Fast.png\" alt=\"Low Voltage Fast\" width=\"723\" height=\"942\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n<p style=\"text-align: center;\"><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; text-align: left;\"><br></span></p>\r\n<h4 style=\"text-align: left;\">Low Voltage Individual Hertz Bins</h4>\r\n<p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/Low%20Voltage%20Individual%20Hz%20Bins.png\" alt=\"individual hz bins low voltage\" width=\"717\" height=\"462\" style=\"text-align: center;\" class=\"img-responsive atto_image_button_middle\"></p>\r\n<p style=\"text-align: center;\"><br></p>\r\n    <p></p>\r\n    <h2 style=\"text-align: left;\"><a name=\"_Toc29328832\">Trauma</a></h2>\r\n\r\n    <p style=\"text-align: left;\">According to Porges: there is no way to understand trauma without understanding the biology of trauma: first hyperarousal, crying then screaming, the best clinical term that describes the state of the infant at the level of abuse is panic. In panic\r\n        there is a dysregulation of the body—the sense of self collapses or explodes in a reenactment of the abandonment.</p>\r\n\r\n    <p style=\"text-align: left;\">Sympathetic excitation is now in the body, as well as in the organs, but its being shut down by a parasympathetic inhibition that tries to regulate this via disassociation—this is considered a moment of psychic death. Dissociation by means of parasympathetic\r\n        inhibition is the role of the unmyelinated subdiaphrammatic vagus nerve, which is reptilian in its evolutionary origin. It is this dissociative mechanism that creates the feigning of death.</p>\r\n    <p style=\"text-align: left;\">Dissociation is a right brain survival defense against overwhelming, unbearable, painful emotional experiences. This can manifest, symptomatically, in a number of ways. Dissociation can arrive in the presence of mu rhythm (covered earlier in this\r\n        chapter), dissociation can occur in the presence of Temporal lobe Alpha. </p>\r\n\r\n    <h2 style=\"text-align: left;\"><a name=\"_Hlk530979595\"></a><a name=\"_Toc29328833\">Temporal Lobe Alpha</a></h2>\r\n\r\n    <p style=\"text-align: left;\">With eyes open, in Temporal Lobe alpha, 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. This appearance suggests an affective perceptual problem, a prosodic\r\n        comprehension difficulty, and even a deficit in spatial reasoning. “Excess Temporal Lobe Alpha” (TLA) classification is used when evidence exists that the temporal lobe generates abnormal amounts of alpha. TLA suggests frontal lobe disengagement\r\n        which results in temporal lobe idling. This excessive gating is often seen in individuals dealing with trauma or anxiety.</p>\r\n    <h2 style=\"text-align: left;\"><a name=\"_Toc29328834\">PTSD</a></h2>\r\n\r\n    <p style=\"text-align: left;\">Sometimes an individual dealing with post-traumatic stress disorder will create alpha blocking or a rise in the amplitude of beta with eyes closed. For most individuals, when we close our eyes we are able to relax. The brain signals to the body that\r\n        we are safe and able to rest or fall asleep. The parasympathetic nervous system kicks in, assuring the body (and the brain) that it is safe to rest, digest and recuperate from the activities of the day. </p>\r\n\r\n    <p style=\"text-align: left;\">In the case of PTSD, the opposite happens. When the eyes are closed again, vigilance appears (which can be seen in the rise of amplitude in beta brainwaves). &nbsp;Beta and high beta are the frequencies in which we process cognitive data. These are\r\n        the brainwaves in which we think. Typically, the waveforms of alpha and ultimately theta and delta rise when we close our eyes. Additionally, we may see a drop in delta and theta when eyes are closed, signifying a further inability to relax.</p>\r\n    <p style=\"text-align: left;\">What can be expected from an EEG response such as this is difficulty falling asleep and staying asleep, nightmares&nbsp; (due to an overly active brain at rest), and the results from poor or compromised sleep (fatigue, grumpiness, feelings of heaviness,\r\n        poor attention, inability to stay on task, difficulty sequencing thoughts, et cetera.).</p>\r\n\r\n        <h3 style=\"text-align: left;\"><a name=\"_Toc29328835\">OCD and Mood Disorders</a></h3>\r\n\r\n        <p style=\"text-align: left;\">Very often obsessive compulsive disorder will live at the anterior cingulate cortex and will have the presence of alpha and other frequencies. This appears as a malfunction in a network node in the error detection and processing network. Usually\r\n            if you are getting a lot of error codes (“that’s wrong,” “did you forget to lock the door,” “your hands are not yet clean,” etc.) this maker could signify an obsessive compulsive or oppositional defiant marker. </p>\r\n\r\n        <p style=\"text-align: left;\">The anterior midline holds a model of what is going on in the world at the subgenual anterior Cingulate location. When that spot is not working properly, you end up having error codes. In addition, Mood Disorders are often seen stemming from a\r\n            dysregulation in this area and can manifest as depression, amotivational, and angry behaviors.</p>\r\n        <h2 style=\"text-align: left;\"><a name=\"_Toc29328836\">Reactive Attachment Disorder and Trauma</a></h2>\r\n\r\n        <p style=\"text-align: left;\">There are different attachment styles: (1) secure attachment, (2) insecure attachment with anxious/avoidant and anxious/resistant subtypes, and (3) disorganized attachment (Ainsworth, Blehar, Waters &amp; Wall, 1978; Bowlby, 1988; Main &amp; Solomon,\r\n            1986).&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; The child needn’t be abused to be in trouble, he merely needs to experience himself as abandoned by his mother. Reactive Attachment Disorder describes the effects of pathogenic care on\r\n            the child’s ability to bond appropriately. These children are either hypervigilant, aggressive, and averse to comfort, or in fewer cases, inhibited, ambivalently needy, and withdrawn. They are suspicious of caretakers, a suspiciousness that,\r\n            sadly, they come by honestly. They are prone to dissociative states and in the fugue of mother loss, they do not readily perceive their primary caretaker (Fisher, 2014, p. 4).</p>\r\n\r\n        <p style=\"text-align: left;\">Often the mother of a baby may be physically present but emotionally absent.&nbsp; Even though mother may change diapers, feed her baby, and pick baby up from the crib, she may have difficulty interacting with the baby—that is, mirroring facial\r\n            expressions, mimicking baby’s coos, etc. The depressed mother who cannot, from her own deadened state, enliven her baby. </p>\r\n        <p style=\"text-align: left;\">This could result in a dissociative EEG presentation, such as <b><u>mu rhythm</u></b>. Attachment research has shown that babies depend on face--, eye-to-eye, voice-to-voice emotional reciprocity (Bowlby, 1988; Ainsworth et al., 1978; Main &amp;\r\n            Solomon, 1986; Tronick, 2007). Alexithymia means inability to describe or articulate feelings, and for some it means trouble recognizing that they even have feelings. (107), this type of symptomology would be present in a child who was not\r\n            mirrored.</p>\r\n\r\n        <p style=\"text-align: left;\">Sebern Fisher has seen excess slow wave (as low as 2 Hz) in the temporal lobes of people with developmental trauma. High amplitude, of 50 microvolts, is also seen. This can indicate dissociative processes. If there is excess slow wave—particularly\r\n            delta to slow theta—at a particular site, it is not communicating adequately with the outside world; it is mainly talking to itself.</p>\r\n        <h3 style=\"text-align: left;\">Dementias</h3>\r\n        <p></p>\r\n        <p style=\"text-align: left;\">Parahippocampal slowing and slow alpha will indicate an Alzheimer’s type dementia. If there is a frontal slowing of alpha fronto-temporally, with a steady pace of alpha parietally and occipitally, that indicates vascular dementia, working away\r\n            at the frontal lobes memory content. If there is a generalized slow EEG, there are tropic changes, which can indicate Korsakov’s syndrome (which we see in severe alcoholics). Thalamo-cortical dysrhythmias and subcortical abnormal activity\r\n            indicate Parkinson’s disease (which is seen in the substantia nigra) and Lewy body disease is seen in cortical and subcortical abnormalities. However, Parkinson’s dementia can have a Lewy body mix in it. The anterior temporal pole and insulae\r\n            deteriorate disproportionately in Lewy Body dementia, which can lead to hallucinations, loss of sense of smell (which is the mesial temporal surface, the uncus, degrading). Lewy body is difficult because the individual will drift in and out\r\n            from hallucinatory states to normal states, making the hallucinations seem all that more real. This is the same disorder that Robin Williams had when he died. </p>\r\n        <h3 style=\"text-align: center; \"><br></h3>\r\n        <h3 style=\"text-align: left;\">Diffuse Slowing in the Raw EEG in Lewy Body Dementia</h3>\r\n        <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/diffuse%20slowing.png\" alt=\"diffuse slowing\" width=\"655\" height=\"976\" style=\"text-align: left;\" class=\"img-responsive atto_image_button_middle\"></p>\r\n        <h3 style=\"text-align: center; \"><br></h3>\r\n            <h3 style=\"text-align: left;\">Diffuse Slowing as seen in WinEEG Spectral Analysis</h3>\r\n            <p style=\"text-align: center; \">&nbsp; &nbsp;&nbsp;<img src=\"@@PLUGINFILE@@/Diffuse%20Slowing.png\" alt=\"Diffuse Slowing\" width=\"930\" height=\"494\" style=\"text-align: center;\" class=\"img-responsive atto_image_button_middle\">&nbsp;</p>\r\n            <p style=\"text-align: center; \"><br></p>\r\n                <h3 style=\"text-align: center; \">Diffuse Slow Sources at the Anterior Cingulate Cortex and the right insula in a Lewy Body Dementia Case</h3>\r\n                <p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/ACC%20and%20Insula.png\" alt=\"ACC and insula\" width=\"858\" height=\"548\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p>\r\n                <p style=\"text-align: center;\"><br></p>\r\n                    <p></p>\r\n                    <p style=\"text-align: center; \"><br></p>\r\n                    <p></p>\r\n                    <p></p>',1),(374,84,373,375,20,0,1,1,1589517025,1594474898,'Physiological Pathologies','<p></p><h3><a name=\"_Toc29328838\">Head Injury and Concussion</a></h3>\r\n\r\n<p><a name=\"_Hlk3298282\">Often in a concussion, the </a><span lang=\"EN-CA\">initial impact\r\nwill lead the brain to release the excitatory neurotransmitter glutamate at the\r\nareas of damage, which causes a rapid depolarization of the local neurons.\r\nAfter this, the axonal sodium/potassium pump goes into overdrive to rebalance\r\nion/voltage imbalance, more ATP (energy) is required,</span> there is a <span lang=\"EN-CA\">jump in glucose metabolism, and </span>e<span lang=\"EN-CA\">xtracellular\r\nswelling starts, reducing blood flow. Then the increase in metabolism with\r\nreduced blood flow causes an energy crisis in the cell. Cell is unable to carry\r\nout regular activity due to lack of energy and</span><span lang=\"EN-CA\"> </span>o<span lang=\"EN-CA\">ften entire cell groups will go dormant to preserve themselves. This\r\ncauses a low voltage EEG. However, for the record, a low voltage EEG is also a\r\nnormal phenotype (Johnstone et al, 2005). </span></p>\r\n\r\nIt is very likely that, after a career of having\r\nhard knocks to the skull, that clients’ brains will form scar tissue at the\r\nsites of the accident (after initially experiencing a state of inflammation).\r\nIf the inflammation is not able to properly heal the brain—which is its’\r\nfunction—then the brain will ultimately learn to handle the inflammation by\r\naltering cellular structures to form tougher tissues, which would\r\nconsequentially prevent blood perfusion at the&nbsp;<span style=\"font-size: 1rem;\">sites of the\r\ninjury and prevent the slower brainwaves of delta and theta from being read\r\nfrom the surface.</span><p>&nbsp;</p>\r\n\r\n<h3><a name=\"_Toc29328839\"></a><a name=\"_Toc3535239\">TBI, Stroke and Concussion</a></h3>\r\n\r\n<p><a name=\"_Hlk3544972\">When brain\r\ntrauma occurs, the brain sends slow, healing brainwaves to the areas receiving\r\ndamage. Typically, a recent wound (whether open or closed) will result in an\r\nabundance of delta and theta brain waves—indicating damage to the white matter\r\nof the brain. Birnbaumer&nbsp;(2007)&nbsp;has&nbsp;suggested&nbsp;that&nbsp;if&nbsp;the&nbsp;neuronal&nbsp;assemblies&nbsp;adjacent&nbsp;to&nbsp;the&nbsp;injury,&nbsp;</a><span style=\"font-size: 1rem;\">rather&nbsp;than&nbsp;the&nbsp;homologue&nbsp;in&nbsp;the&nbsp;contra­lateral&nbsp;hemisphere,&nbsp;assume&nbsp;the&nbsp;function&nbsp;of&nbsp;</span><span style=\"font-size: 1rem;\">damaged&nbsp;neurons&nbsp;more&nbsp;recovery&nbsp;is&nbsp;possible.</span><a name=\"_Hlk3544950\" style=\"color: rgb(82, 96, 105); font-size: 1rem; background-color: rgb(255, 255, 255);\"> Other signs and symptoms of frontal lobe injury are\r\ndifficulty with flexibility, problem solving, attention span and memory\r\n(Thompson &amp; Thompson, 2015, p. 39).</a></p><p><a name=\"_Hlk3544950\" style=\"color: rgb(82, 96, 105); font-size: 1rem; background-color: rgb(255, 255, 255);\"><br></a></p><h2><a name=\"_Toc29328840\">Anxiety via Low Theta-Beta Ratio</a></h2>\r\n\r\n<p>A high theta over beta ratio at Cz\r\nhas been confirmed by the Food and drug administration as an indicator of ADHD.\r\nThe theta/ beta ratio is best known as a predictor of Attention Deficit\r\ndisorders. Typically, when one has too much theta and not enough beta, their\r\nabilities to focus and concentrate are compromised. In the case of a low\r\ntheta/beta ratio, the amount of theta is too low and the amount of beta is too\r\nhigh, suggesting one who veers to the other end of the attention spectrum. This\r\ncould manifest in many ways, including someone who is rigid or fixed in\r\nthought, someone who pays meticulous attention to detail, sometimes to a fault.\r\n</p>\r\n\r\nThere is the possibility\r\nthat the “small stuff” is a source of stress, where details can become\r\noverwhelming and the component parts of a task, job, or endeavor are\r\nscrutinized and&nbsp;<span style=\"font-size: 1rem;\">overthought to a detrimental\r\ndegree.&nbsp; There could be signs or symptoms\r\nof obsession, rumination, and the desire to take care of things oneself,\r\ninstead of having others handle tasks, under the belief that “my way is the\r\nbest way” or “only I know how to do it right.” In its best light, this low\r\nratio may indicate a high level of proficiency and efficiency; someone who\r\nproduces meticulous, detail oriented, high quality work. The question then is:\r\nis this effort pleasurable?</span><p>&nbsp;</p>\r\n\r\n<h2><a name=\"_Toc29328841\">ADD/ADHD via High Theta-Beta Ratio</a></h2>\r\n\r\n<p>The theta/beta ratio is a predictor of attention deficit\r\ndisorder according to the FDA and American Academy of Pediatrics.&nbsp; However, 30% of ADHD kids show excessive\r\nalpha frontally.</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->T/B ratio is driven largely by slow alpha</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->The theta beta ratio changes over time</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Monastra/Lubar (1999) shows accuracy of 95% of\r\nusing the T/B/ ratio for the diagnosis of attention spectrum disorders</p><p>\r\n\r\n</p><p>20% of\r\nADD/ADHD cases is the variation of&nbsp;\r\nfrontal beta spindles. This profile manifests is an inability to\r\nregulate attention, its not a deficit of attention. Easily kindled or excitable\r\ncortex will show in beta spindle. </p><p></p>\r\n\r\n<p></p><h2><a name=\"_Toc29328842\"><br></a></h2><h2><a name=\"_Toc29328842\">ADD/ADHD\r\nSpindling Beta Variant in Raw EEG</a></h2><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Spindling%20Variant.png\" alt=\"Spindling Variant\" width=\"650\" height=\"466\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><h3 style=\"text-align: left;\">ADHD/ADD Spindling Beta Variant in qEEG</h3><p style=\"text-align: center; \"><a name=\"_Toc29328843\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; text-align: left; background-color: rgb(255, 255, 255);\"><br></a></p><p style=\"text-align: center; \"><a name=\"_Toc29328843\">&nbsp;&nbsp;<img src=\"@@PLUGINFILE@@/ADD%20QEEG.png\" alt=\"ADD/ADHD QEEG\" width=\"709\" height=\"918\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></a></p><p style=\"text-align: center; \"><br></p><p></p><h2 style=\"text-align: left;\"><a name=\"_Toc29328844\">Spectrum Based Disorders</a></h2>\r\n\r\n<p style=\"text-align: left;\">The rate of brain growth is\r\nabnormal in autistic children. Researchers speculate in autism that too few connection\r\nare created between the frontal cortex and other regions of the brain (Seung, 2009).\r\nAlong with the phase dynamics of the\r\nbrain, aberrant brain connectivity, especially as it pertains to long-distance\r\nunderconnectivity, has been recognized as a candidate pathophysiology of autism\r\nspectrum disorders.&nbsp; The current\r\nmeta-analysis of diffusion tensor imaging studies in subjects with autism\r\nspectrum disorders emphasizes important roles of connections in the superior\r\nand inferior longitudinal fasciculi, inferior fronto-occipital fasiculus,\r\nuncinate fasciculus, and the anterior portion of the corpus callosum that\r\nextends into the frontal lobes in the pathophysiology of autism spectrum\r\ndisorders (Bashat et al, 2010; Joe et al., 2010).&nbsp; </p><h4 style=\"text-align: left;\"><br></h4><h4 style=\"text-align: left;\">Abnormal Phase Dynamics as seen\r\nin Spectrum-Based Disorders</h4><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Autism.png\" alt=\"Autism\" width=\"530\" height=\"540\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p></p><p></p>',1),(375,84,374,0,20,0,1,1,1589517109,0,'References','<p><p>Ainsworth, M.D. S., Blehar, M. C., Waters, E. &amp; Wall, S.\r\n(1978).<i> Patterns of attachment: A\r\npsychological study of the strange situation</i>. Hillside, NJ: Erlbaum.</p>\r\n\r\n<p>Barrett, M.D. (1985). <i>Children’s\r\nsingle-word speech</i>. Chichester, England: Wiley.</p>\r\n\r\n<p>Bland BH, Oddie SD (2001). Theta band oscillation and\r\nsynchrony in the hippocampal formation and associated structures: The case for\r\nits role in sensorimotor integration. <i>Behav Brain Res </i><b>127</b>:119–36.</p>\r\n\r\n<p>Bloom, L. (1973). <i>One\r\nword at a time: The use of single word utterances before syntax</i>. The Hague:\r\nMorton.</p>\r\n\r\n<p>Bowlby, J. (1988). <i>A\r\nsecure base.</i> New York, NY: Basic Books.</p>\r\n\r\n<p>Chugani HT (1998). A critical period of brain development:\r\nStudies of cerebral glucose utilization with PET. <i>Prev Med </i><b>27</b>:184–8.</p>\r\n\r\n<p>Chugani HT, Phelps ME, Mazziotta JC (1987). Positron\r\nemission tomography study of human brain functional development. <i>Ann Neurol </i><b>22</b>:487–97.</p>\r\n\r\n<p>Cortina, M. and Marrone, M. (eds) (2003) Attachment Theory\r\nand the Psychoanalytic Process, London: Whurr Publishers.</p>\r\n\r\n<p>de Boysson-Bardies,\r\nB., Sagart, L., &amp; Durand, C. (1984). Discernible differences in the\r\nbabbling of infants according to target language. <i>Journal of Child Language, 11</i>. 1-15.</p>\r\n\r\n<p>Damasio AR (1996). <i>Descartes’ error. Emotion, reason,\r\nand the human brain</i>. London: Papermac.</p>\r\n\r\n<p>Damasio AR (2000). <i>The feeling of what happens. Body,\r\nemotion and the making of consciousness</i>. London: Vintage.</p>\r\n\r\n<p>Fonagy, P. (1999) “Psychoanalysis and attachment theory”, in\r\nJ. Cassidy and P. Shaver (eds), Handbook of Attachment. Theory, Research and\r\nClinical Applications, New York and London: Guilford Press.</p>\r\n\r\n<p>Freud S (1923). <i>The ego and the id. </i>SE <b>19</b>, p.\r\n3–66.</p>\r\n\r\n<p>Futagi Y, Ishihara T, Tsuda K, Suzuki Y, Goto M (1998).\r\nTheta rhythms associated with sucking, crying, gazing, and handling in infants.\r\n<i>Electroencephalogr Clin Neurophysiol </i><b>106</b>:392–9. Ginzburg A (2004).</p>\r\n\r\n<p>Green, K.P. &amp; Kuhl, P.K. (1989). The role of visual\r\ninformation in the processing of place and manner features in speech\r\nperception. <i>Perception and psychophysics,\r\n45</i>. 34-42.</p>\r\n\r\n<p>Greenfield, P., &amp; Smith, J. (1976). <i>The structure of communication in early language</i>. New York:\r\nAcademic Press.</p>\r\n\r\n<p>Hagmann, P., CAmmoun, L., Gigandet, X., Meuli, R., Honey,\r\nC.J., Wedeen, V.J., Sporns, O. (2008) Mapping the structural core of the human\r\ncerebral cortex. PLoS Biol. 6, e159. </p>\r\n\r\n<p>He, B.J. et al (2008) Electrophysiological correlates of the\r\nbrains intensive large-scale functional architecture. Proc. Nat’l Acad. Sci.\r\nUSA, 105, 16039 – 16044.</p>\r\n\r\n<p>Kandel, E. (2012). Biology and the future of psychoanalysis:\r\nA new intellectual framework for psychiatry revisited. <i>Psychoanalytic\r\nReview, 99</i>(4),\r\n607-644.</p>\r\n\r\n<p>Kouvelas, E.D. (2012). Unconscious and plasticity: Bridges\r\nbetween psychoanalysis and neuroscience. <i>International\r\nForum of Psychoanalysis</i>, 21. 214-217.</p>\r\n\r\n<p>Lehtonen J (2006) In search of early mental organization of\r\nthe infant. Contributions from the neurophysiology of nursing. In: Mancia M,\r\neditor. <i>Psychoanalysis and neuroscience</i>, p. 419– 31. Milan: Springer.\r\n392 p.</p>\r\n\r\n<p>Lewin B (1946). Sleep, the mouth, and the dream screen. <i>Psychoanal\r\nQ </i><b>15</b>:419–34.</p>\r\n\r\n<p>Lewin B (1955). Dream psychology and the analytic situation.\r\n<i>Psychoanal Q </i><b>24</b>:169–99.</p>\r\n\r\n<p>Main, M., &amp; Solomon, J. B. (1986). <i>Discovery of an insecure-disorganized/disoriented attachment pattern. </i>Westport,\r\nCT: Ablex.</p>\r\n\r\n<p>Mandler, J. (1992) “‘How to build a baby’: II. Conceptual\r\nprimitives”, Psychological Review, 99(4), 587– 604.</p>\r\n\r\n<p>McEwen BS, Sapolsky RM: Stress and cognitive\r\nfunction. Curr Opin Neurobiol 1995; 5:205–216  </p>\r\n\r\n<p>McGurk, H. &amp; MacDonald, J. (1976). <i>Hearing lips and seeing voices</i>. Nature (London), 264, 746-748.</p>\r\n\r\n<p>Mehler J, Bertoncini J, Barriére M, Jassik-Gerschenfeld D\r\n(1978). Infant recognition of mother’s voice. <i>Perception </i><b>7</b>:491–7.</p>\r\n\r\n<p>Sapolsky RM: Why stress is bad for your\r\nbrain. Science 1996; 273:749–750</p>\r\n\r\n<p>Scher MS (1989). Pediatric electroencephalography and\r\nevoked potentials. In: Swaiman KF, editor. <i>Pediatric neurology: Principles\r\nand practice</i>, vol. I, p. 67–103. St Louis, MO: Mosby.</p>\r\n\r\n<p>Schore, A.\r\nN. (1994). <i>Affect regulations and the\r\norigin of the self. The neurobiology of emotional development. </i>New Jersey:\r\nL. Erlbaum &amp; Associates.</p>\r\n\r\n<p>Schore, A. (2014). Book Review: The Emotional Life of Your\r\nBrain, by Richard J. Davidson and Sharon Begley. <i>Psychoanalytic Psychology, 32(</i>3). 539-547.</p>\r\n\r\n<p>Shalev, I., Moffitt, T. E., Sugden, K., Williams, B., Houts,\r\nR.M., Danese, A. et al. (2013) Exposure to violence during childhood is\r\nassociated with telomere erosion from 5 ro 10 years of age: A longitudinal\r\nstudy. <i>Molecular Psychiatry, 18</i>(5).\r\n576-581.</p>\r\n\r\n<p>Spitz RA: Hospitalism: an inquiry into the\r\ngenesis of psychiatric conditions in early childhood. Psychoanal Study Child\r\n1945; 1:53–74</p>\r\n\r\n<p>Tronic, E. Z. (2007). <i>The\r\nneurobehavioral and social-emotional development of infants and children. </i>New\r\nYork: Norton.</p>\r\n\r\n<p>Vaslamatzis, G. (2010). Framework for a new psychoanalytic\r\napproach between psychoanalysis and neurosciences: Is the combined\r\nneuropsychoanalytic approach the missing link? In M. Issidorides-Radovich and\r\nG. Vaslamatzis (Ed.), Dialogue of psychoanalysis and neurobiology:\r\nTheoretical and therapeutic aspects (pp. 169?78). Athens:\r\nBETA Medical Publishers.</p>\r\n\r\n<p>Winson J (2002). The meaning of dreams. <i>Sci Am </i>(Special\r\nissue 12):54–61.</p>\r\n\r\n<p>Yamaguchi Y, Aota Y, Sato N, Wagatsuma H, Wu Z (2004).\r\nSynchronization of neural oscillations as possible mechanism underlying\r\nepisodic memory: A study of <i>θ</i>-rhythm in the hippocampus. <i>J Integr\r\nNeurosci </i><b>3</b>:143–57.</p><br></p>',1),(376,85,0,377,20,0,1,1,1589824234,1596164485,'Definitions','<p></p><p><b>Absolute\r\nPower: </b>The total voltage, or energy, that the brain is emitting, measured\r\nin disparate frequencies and typically portrayed after processed via a\r\n“normative database.”</p>\r\n\r\n<p><b>Amplitude:\r\n</b>The\r\nheight of the brainwave, measured in microvolts squared.<b> </b></p>\r\n\r\n<p><b>Asymmetry:</b> is the absence of, or a violation of,\r\nsymmetry or the lack of balance.</p>\r\n\r\n<p><b>Coherence:\r\n</b><a name=\"_Hlk484153241\">The stability of phase relationship between any two areas of the\r\nbrain. Two areas are said to be coherent if they have constant respective\r\nrelative phase. Coherence in excess is hypercoherence; coherence in deficiency\r\nis hypocoherence. </a></p>\r\n\r\n<p><b>Common mode rejection:</b>&nbsp; The input amplifier is\r\nmore sensitive in relation to the signal components that are different at the\r\nelectrodes than to those components that are of equal amplitude and polarity.\r\nIt indicates the ability of the amplifier to accurately cancel voltages that\r\nare common to both inputs.</p>\r\n\r\n<p><b>Complex\r\nAdaptive System</b></p>\r\n\r\n<p>The statistical properties of the brain’s dynamics reflect the\r\nstatistics of the environment , this is because our brain is a complex adaptive\r\nsystem (CAS) which arises when two conditions are fulfilled: 1) structure has\r\nsmall world topology and 2) the presence of noise (variability)—the brain is a\r\ncomplex adaptive system. </p>\r\n\r\n<p><b>Fast Fourier transforms</b>: The fast Fourier transform is a\r\nmathematical method for transforming a function of time into a function of\r\nfrequency. Sometimes it is described as transforming from the time domain to\r\nthe frequency domain. It is very useful for analysis of time-dependent phenomena. FFT’s are of great importance to digital signal processing\r\nin EEG applications.</p>\r\n\r\n<p><b>Frequency</b>: How many\r\nwaves are made per second interval, represented in hertz (Hz), or cycles per\r\nsecond.</p>\r\n\r\n<p><b>Phase:</b> Any one\r\npoint or portion in a recurring series of changes, as in the changes of motion\r\nof one of the particles constituting a wave or vibration.</p>\r\n\r\n<p><b>Relative\r\nPower:</b> A measure of clients’ EEGs, viewed in relation to their absolute\r\npower profile, used to determine what may be deviant, in relative terms. </p>\r\n\r\n<p><b>Symmetry:</b> Generally conveys two primary meanings. The first\r\nis an imprecise<b> </b>sense of harmonious or aesthetically-pleasing\r\nproportionality and balance; such that it reflects beauty or perfection. The\r\nsecond meaning is a precise and well-defined concept of balance or\r\n\"patterned self-similarity\" that can be demonstrated or proved\r\naccording to the rules of a formal system: by geometry, through physics or\r\notherwise.</p><br><h4></h4><br><p></p>',1),(377,85,376,378,20,0,1,1,1589826516,1595620606,'Montages','<p></p><p><a name=\"_Hlk530944452\">Here is a video on Morphology and Montages. If you want to skip straight to montages, go to minute 24.</a></p><p><a name=\"_Hlk530944452\"><a href=\"https://www.youtube.com/watch?v=dpY2F_2nrAo&amp;t=1580s\">Morphology and Montages Video</a><br></a></p><p><a name=\"_Hlk530944452\">An EEG montage is the placement of\r\nelectrodes. All EEG signals are measured by subtracting the signal measured at\r\n2 sites: the active electrode and the reference electrode.&nbsp; This is called\r\ncommon mode rejection.&nbsp; The reason for this is that we need to subtract\r\nout all the environmental electrical noise (which is much larger than the\r\nbrainwave signal) in order to see the brain\'s activity.&nbsp; Any scalp\r\nelectrode site measurement must be referenced to some other measured\r\nsite.&nbsp; In the past, the most common site for reference was linked ears.&nbsp;</a> But you can use the nose, or any other scalp location or, as explained\r\nabove, any average of multiple sites.&nbsp; So, there are many montages\r\navailable and they all have strengths and weaknesses.&nbsp; There is no best\r\nmontage for all purposes.</p><h3><a name=\"_Toc29929020\">Referential\r\nMontages</a></h3>\r\n\r\n<p>Many will refer to the “active”\r\nelectrode and the “reference“&nbsp; electrode.\r\nCommonly used “referential montages” include the ear references (linked ear,\r\nipsilateral or contralateral ear), the Cz location or a “vertex”\r\nreference.&nbsp; Local function in the EEG\r\ndoes not shown well with linked ears (that is, if you had a focal slowing,\r\nLinked Ears would not be a good montage to view it). Linked ears montages show\r\nglobal firings well.</p>\r\n\r\n<p>The linked ear montage can spread\r\ntemporal lobe activity into reference electrodes. The activity seen at T5 and\r\nT6 are most likely to be seen in the electrodes on the ears but activity at T3\r\nand T4 may influence the ear electrodes, as well as F7 and F8 in rarer cases.</p><h2><a name=\"_Toc29929021\">Linked Ears Montage</a></h2><p></p><p style=\"text-align: center;\"><a name=\"_Toc29929021\" style=\"background-color: rgb(255, 255, 255); color: rgb(82, 96, 105); font-size: 1rem;\">&nbsp;&nbsp;</a></p><a name=\"_Toc29929021\"></a><p style=\"text-align: center;\"><a name=\"_Toc29929021\"></a><a name=\"_Toc29929021\" style=\"background-color: rgb(255, 255, 255); color: rgb(82, 96, 105); font-size: 1rem;\">&nbsp; &nbsp; &nbsp;<img src=\"@@PLUGINFILE@@/LE%20Montage.png\" alt=\"Linked Ears\" width=\"519\" height=\"512\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></a></p><p style=\"text-align: center;\"><br></p><p></p><br><p></p><p></p><h2><a name=\"_Toc29929022\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Cz Reference Montage</a><br></h2><p style=\"text-align: center; \"><a name=\"_Toc29929022\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\"><img src=\"@@PLUGINFILE@@/Cz%20Montage.png\" alt=\"Cz Montage\" width=\"800\" height=\"522\" class=\"atto_image_button_middle\"><br></a></p><br><p></p><p><br></p><p><a name=\"_Toc29929023\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Sequential\r\nMontages</a><br></p>\r\n\r\n<p>Sequential\r\nreferences (commonly termed “bipolar”) are those that we see in the transverse\r\nbi-polar and longitudinal transverse bi-polar montage. Sequential montages\r\n(such as transverse or longitudinal transverse, are often used in neurology\r\npractices to determine the location of any focal findings in the EEG. This is\r\nseen with “phase reversals’ in the EEG, where two electrodes seem to “point” to\r\none another (i.e. one line moves eletro-negative and the one next to it moves\r\nelectro-positive.&nbsp; This is a marker of a\r\nphysical abnormality and can point to the seizure focus, a lesion,\r\nhypoperfusion, localized infarct (a small localized area of dead tissue), or\r\nwhite matter ischemia. This is an “X marks the spot” type of finding. You can\r\ndetermine the site of the finding based upon the <u>shared electrode between\r\nthe two pairs</u>. Phase reversals are relevant in slow frequencies (typically\r\n8Hz and under).</p><h3><a name=\"_Toc29929024\">Phase Reversals located at T5 in a\r\ndouble banana montage</a></h3><p><a name=\"_Toc29929024\"><img src=\"@@PLUGINFILE@@/Phase%20Reversals.png\" alt=\"Phase Reversals\" width=\"600\" height=\"1036\" class=\"img-responsive atto_image_button_left\"></a></p><p><a name=\"_Toc29929024\">Phase reversals are a\r\nmarker of a physical abnormality and can point to the seizure focus, a lesion,\r\nhypoperfusion, localized infarct (a small localized area of dead tissue) or\r\nwhite matter ischemia. This is an “X marks the spot” type of finding. When\r\nthere is a lack of blood flow and oxygen to the area, there is often a\r\nconsequential slowing of alpha at the area. As the area degrades, sometimes the\r\nalpha slows considerably below the band. But this depends on how severe the damage\r\nis (Classen and Foreman, 2012). </a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p><a name=\"_Toc29929024\"><br></a></p><p></p><h3><a name=\"_Toc29929025\"><br></a></h3><h3><a name=\"_Toc29929025\"><br></a></h3><h3><a name=\"_Toc29929025\"><br></a></h3><h3><a name=\"_Toc29929025\"><br></a></h3><h3><a name=\"_Toc29929025\">Video of localization of ischemia via\r\nidentifying phase reversals in a bipolar montage</a></h3>\r\n\r\n<p><a href=\"@@PLUGINFILE@@/Ischemias.mp4\">Ischemias.mp4</a><br></p><p><br></p><p><br></p><p><br></p><p></p><p></p><h2><a name=\"_Toc29929026\">Transverse Bi-Polar Montage</a></h2><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/transverse%20bi-polar%20montage.png\" alt=\"Transverse bi-polar montage\" width=\"600\" height=\"551\" class=\"atto_image_button_middle\" style=\"font-size: 1rem;\"></p><p></p><p><br></p><p><br></p><p><a name=\"_Toc29929027\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Longitudinal Bi-Polar Montage (aka “double banana montage”)</a><br></p><br><p></p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Double%20Banana%20Montage.png\" alt=\"Double Banana\" width=\"683\" height=\"610\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p></p><h3><a name=\"_Toc29929028\">Double Banana Montage</a></h3><br><p></p><p></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Double%20Banana%20Montage%20%281%29.png\" alt=\"Double Banana Montage\" width=\"548\" height=\"383\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: center;\"><br></p><p></p><p></p><h2><a name=\"_Toc29929029\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Average Montages</a><br></h2>\r\n\r\n<p>An average reference that is often\r\nused in EEG is based on Laplacian mathematics; it is variously called the\r\nLaplacian reference, Hjorth reference, and local average. Other computerized\r\nreferences (meaning no individual reference electrode is required) include the\r\ncommon average or global average and the weighted average reference (Scherg, et\r\nal., 2002). A Laplacian montage is useful for understanding what is happening\r\non a focal level (i.e. Laplacian montages are good at seeing focal findings).\r\nAn average reference is a good way to understand what is happening without\r\nreferencing the ear electrodes, which are often contaminated with real (EEG) or\r\nfake (artifactual) findings.</p><h3><a name=\"_Toc29929030\">An EEG with an Ear Reference contaminated\r\nby a heartbeat (which is thus seen in every channel)</a></h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp; &nbsp;</span></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Contaminated%20Ear%20Reference.png\" alt=\"Contaminated Ear Reference\" width=\"775\" height=\"541\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p></p><p style=\"text-align: left;\">The Laplacian technique (aka\r\n“local average” or “Hjorth” montage) is quite good at showing localized\r\nfindings. The Laplacian montages are good at eliminating cardioballistic\r\nartifacts (as seen in the previous image). However, Laplacian montages are\r\nthought to have an “unforgiving” nature of display, due to minor distortions at\r\nthe edge electrodes, commonly a small percentage error (not a real problem for\r\nclinical utility). </p>\r\n\r\n<p style=\"text-align: left;\">The Laplacian montage is not good\r\nat displaying global or regional EEG findings, due to false localization to the\r\nperimeter or edge of the finding (Scherg et al., 2002). </p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">An “average” montage uses\r\nthe average of all electrodes as the reference. This technique is not good for\r\ndisplaying generalized changes, especially generalized paroxysmal activity. However,&nbsp;</span></p><a name=\"_Toc29929024\"><p style=\"text-align: left;\">this “weighted average” reference is very popular when using dense arrays in topographic mapping</p></a><p></p><span style=\"font-size: 1rem;\"><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">No montage is the “right one” or\r\nthe “best” montage, they each have their own strengths and weaknesses. It is\r\nimportant to switch references from a linked ears (or other referential\r\nmontage) to an average or a Laplacian or Hjorth, to understand the differences\r\nbetween montages. One example where linked ears may be deceiving is when strong\r\ntemporal alpha contaminates the ear lobe. In this case, the ear references will\r\ncreate the appearance that alpha is global, when it is in fact located in the\r\ntemporal and picked up (and thus transmitted) by the reference electrode\r\nsite—the ear. Thus, the ear references when contaminated create “false alpha.”</span></p></span><p></p><p></p><h2 style=\"text-align: left;\"><a name=\"_Toc29929031\">Switching from Linked Ears to an Average\r\nReference to identify focal findings</a></h2><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;&nbsp;</span><img src=\"@@PLUGINFILE@@/Switching%20from%20Linked%20Ears.png\" alt=\"Switching\" width=\"1000\" height=\"563\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p></p><h2 style=\"text-align: left;\"><a name=\"_Toc29929032\">Appearance of Diffuse Alpha in Lined Ears\r\nReference, due to a contaminated reference electrode, properly localized to T3\r\nwhen montage is shifted</a> </h2><p style=\"text-align: left;\"><a name=\"_Toc29929032\"></a><a href=\"@@PLUGINFILE@@/Shared%20%20Variance.mp4\">Shared  Variance.mp4</a><br></p>\r\n\r\n<p style=\"text-align: left;\">&nbsp;In the above video, you will see that every channel looks similar in phase and waveform. I confirm this by examining small portions of the record, seeing that there is shared variance (meaning that the ear electrode is picking up a real brainwave and casting it across all the channels, as the reference. When switching the montage to a Laplacian montage, we are able to confirm that the alpha signal is coming from one of the temporal leads (affected the ear in a linked ears reference). This kind of EEG must be read from an average montage for accuracy.</p>\r\n\r\n<p style=\"text-align: left;\">The failure to shift montages\r\ncreates problematic coherences, which are impossible for the human brain to\r\ncreate. When we failed to shift montages, in cases of shared variance, we will\r\noften end up with global hypercoherence, which is artifactual and should never\r\nbe considered real. </p><h3 style=\"text-align: left;\"><a name=\"_Toc29929033\">QEEG Map with False Hypercoherence, due\r\nto contaminated reference</a></h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Contaminated%20Reference.png\" alt=\"Contaminated Reference\" width=\"717\" height=\"953\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: center;\"><br></p><p style=\"text-align: center;\"><br></p><p></p><p style=\"text-align: left;\">Using a variety of\r\nmontages is a part of the minimum guidelines for EEG and a commonly adopted\r\nguideline developed by the American Society of Electroneurodiagnostic\r\nTechnologists (ASET). This practice of switching perspectives avoids the reader\r\nbeing fooled by a false localization when a reference is contaminated with\r\nvoltages as described above. The proper selection of montages will allow the\r\nreader to get a good view of the EEG phenomenon and its distribution across the\r\ncortex. Understanding of the topographic distribution of brain function is\r\nrequired to understand what the neuropsychological impacts of the EEG changes\r\nmight be. If you switch to global and you see that it is very different, you\r\nmust determine which EEG is accurate and which is not.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; </p>\r\n\r\n<p style=\"text-align: left;\">The montage is like a perspective,\r\nit is used to present information from a particular point of view. Each montage\r\nhas strengths as well as weaknesses, including the problem of failed neutrality\r\nof the reference. A single ear reference will avoid any problem associated with\r\nthe other ear’s contamination though it does not cancel the EKG as well as the\r\nlinked ear reference, as well as creating an apparent asymmetry due to the\r\nsystematically different inter-electrode distances between the two hemispheres.\r\nThe Cz reference will give good resolution for the temporal areas but not the\r\ncentral area. The Cz montage is also a poor choice where there is drowsiness,\r\nwith the associated vertex sharp waves and spindles which are seen maximally\r\nalong the midline anteriorly and at the vertex which will contaminate the\r\nvertex electrode.</p><h3 style=\"text-align: left;\"><a name=\"_Toc3535249\">Power displays</a></h3><p><a name=\"_Toc29929034\"></a></p>\r\n\r\n<p style=\"text-align: left;\">There are a number of ways power is\r\nseen in EEGs. Different power metrics are: 1) raw power measured in amplitude\r\n(microvolts squared) or magnitude (microvolts); 2) absolute power (seen in\r\nnorm-referenced quantitative EEGs); and 3) relative power (seen in\r\nnorm-referenced EEGs).&nbsp; Furthermore,\r\npower can be displayed in spectrometers, head maps, and other ways. </p><h3 style=\"text-align: left;\">Depiction of Power Display in IsyncBrain</h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;&nbsp;</span><img src=\"@@PLUGINFILE@@/isync%20map.png\" alt=\"isync map\" width=\"703\" height=\"681\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: left;\"><br></p><p></p><h3 style=\"text-align: left;\">Absolute Power</h3>\r\n\r\n<p style=\"text-align: left;\">Absolute Power is power\r\nmeasured in discreet Hertz bins, by amplitude or magnitude. This can be\r\ndisplayed in a norm-referenced fashion or in raw individual hertz bins. </p><h3 style=\"text-align: left;\">Absolute Power Displayed in Raw EEG (not norm-referenced)</h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Raw%20Data%20in%20Neuroguide.png\" alt=\"Raw Data in Neuroguide\" width=\"717\" height=\"874\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p></p><h3 style=\"text-align: left;\">Absolute Power Displayed in Z-Score EEG\r\n(norm-referenced)</h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;&nbsp;</span><img src=\"@@PLUGINFILE@@/Absolute%20Power.png\" alt=\"Absolute Power\" width=\"716\" height=\"825\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p></p><h2 style=\"text-align: left;\"><a name=\"_Toc29929035\"></a><a name=\"_Toc3535250\"></a><a name=\"_Toc525053815\">Relative\r\nPower</a></h2>\r\n\r\n<p style=\"text-align: left;\">The\r\ndifferences in absolute and relative power are differences between the\r\ntotal voltage, or energy, that the brain is emitting, measured in disparate\r\nfrequencies and typically portrayed after processed via a “normative database”\r\n(absolute power) and the measure of clients’ EEGs, viewed in relation to their\r\nabsolute power profile, used to determine what may be deviant, in relative\r\nterms (relative power).&nbsp; Relative maps\r\nare subject-specific, in the sense that we are witnessing the deviances (and\r\nexcesses) in and of the client, taking into account the particulars of the\r\nsubject’s overall amplitudes.</p>\r\n\r\n<p style=\"text-align: left;\">Relative power is especially telling when a\r\nclient is low amplitude overall, or high amplitude overall. In the next\r\nfigures, we see an individual who has a high amplitude EEGs—meaning that the\r\noverall voltage that their brain emits is larger than their same aged peers, in\r\nevery bandwidth. In this case, we can see in what frequency band they spend the\r\nmost time.</p><p style=\"text-align: left;\">Because the absolute power row is high voltage\r\n(2+ Z-scores above the norm in every frequency bin) we have to use the relative\r\npower rows to determine where this person has the most energy allocated. In the\r\nimage we can see that the client spends the most time (relatively) in the alpha\r\nband and the least amount of time in the delta range.</p><h3 style=\"text-align: left;\">High Amplitude Absolute Power EEG</h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/map.png\" alt=\"Map of High Amplitude Absolute Power\" width=\"560\" height=\"721\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: left;\"><br></p><p></p><p style=\"text-align: left;\">In the next figure, we see an EEG that is low\r\nvoltage, overall. We can see that the client is 1-2+ standard deviations low in\r\nevery bandwidth. When looking at relative power, we learn that the balance of\r\nhis EEG is quite good—he is spending similar amounts of time in all five\r\nbandwidths measured. </p><h3 style=\"text-align: left;\">Low Voltage EEG</h3><p><br></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Low%20Voltage%20EEG.png\" alt=\"Low Voltage EEG\" width=\"560\" height=\"739\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p></p><p></p>',1),(378,85,377,379,20,0,1,1,1589827506,1594477598,'Transforms','<p></p><h3><a name=\"_Toc29929037\"></a><a name=\"_Toc3535252\">JTFA (Joint Time Frequency Analysis)</a></h3>\r\n\r\n<p>Joint-Time Frequency-Analysis\r\n(JTFA)is used for real-time EEG biofeedback and is used to compute statistical\r\nZ scores in real-time. JTFA relies on complex demodulation, which is an\r\nanalytic technique that multiples a time series by a sine wave and a cosine\r\nwave and then applies a low pass filter (Granger et al, 1964; Otnes and\r\nEnochson, 1977). JTFA computes instantaneous power, instantaneous phase\r\ndifferences, and instantanous coherences. Unlike the Fourier transform, &nbsp;which depends on windowing and integration\r\nover an interval of time, JTFA complex demodulation computes and creates an\r\ninstantaneous Z score within subject variance of instantaneous electrical\r\nactivity as well as the between subject variance for subjects of a given age.\r\nThe summation of instantaneous Z scores is Gaussian distributed and has high\r\ncrossvalidation (Thatcher et al, 1987; 2007), however, the individual time\r\npoint by time point Z score is always smaller than the summation due to within\r\nsubject variance.</p><p>INSERT\r\nVIDEO OF JTFA POWRE ANALYSIS</p><p></p><h3><a name=\"_Toc29929038\"></a><a name=\"_Toc3535253\">FFT (Fast Fourier Transform)</a></h3>\r\n\r\n<p>Jean Baptiste Fourier demonstrated\r\nthat any repetitive signal, over the course of time, could be broken down into\r\na series of sine waves by boiling it down into its component parts, in integral\r\nnumbers. His Fast Fourier Transform is a mathematical calculation that\r\ntransforms time-related EEG into a frequency domain. So, in Fast Fourier\r\ndecomposition, the raw EEG is broken down into disparate frequencies, divided\r\ninto bandwidths: delta (0.5 – 4HZ), theta (4 – 8Hz), alpha (8-12 Hz), Beta 1\r\n(12-15Hz), Beta 2 (15 – 19Hz), Beta 3 (19-25 Hz) and High Beta (25 – 30Hz), as\r\nwell as individual hertz bins. Many normative databases also break down gamma\r\ninto individual Hz bins, thought not all give normative data for gamma\r\nfrequencies.</p>\r\n\r\n<p>Essentially, the Fast Fourier\r\nTransform takes a signal and breaks it down into sine waves of different amplitudes\r\nand frequencies. Fourier’s theorem states that any waveform within a time\r\ndomain can be represented by the <b><u>weighted sum of sines and cosines</u></b>.\r\n</p><p></p><p>In the below image, we are first\r\nseeing two sine waves, where one is three times as fast as the other.&nbsp; When you add them, you can see you get a\r\ndifferent signal. This is the sum of the two frequencies. A Fast Fourier\r\ntransform will allow us to see them as separate frequencies.</p><h3>The summation of two signals</h3><p></p><br><p></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Summation%20of%20Two%20Signals.png\" alt=\"Summation of Two Signals\" width=\"561\" height=\"450\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p>In Fisch, it is written: “The FFT\r\nfunction is based on the fact that any signal can be described as a combination\r\nof sine and cosine waves of various places, frequencies and amplitudes (Fisch,\r\n1999, p. 125).&nbsp; Although the etiology of\r\nEEG does not neatly compartmentalize into individual frequency bins, FFT is one\r\nway to better understand the role of various frequencies. When using a\r\ndecomposition method, such as FFT, you lose the morphology of the raw EEG,\r\nwhich is essential for understanding the fundamentals of the person’s data.</p><p>If we were to take a signal\r\ngenerator and create a perfect 10 Hz wave, but receive electrical contamination\r\nat 60Hz, we would see a sharp peak at 10Hz and at 60Hz in a spectrogram. In the\r\nbelow picture, 10HZ is represented by the blur arrow and 60Hz is represented by\r\nthe red arrow.</p><h3>How a perfect 10Hz (blue) and perfect 60Hz (red) signal would\r\nlook in a spectrogram with Amplitude on the Y-axis and frequency on the X-axis</h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Noise%20and%20Sine%20Wave.png\" alt=\"Noise and Sine Wave\" width=\"600\" height=\"321\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p></p><p style=\"text-align: left;\">One way to tell real EEG from\r\nartifact generated by electricity, is the spectrogram will show an abnormal\r\npeak, signifying one frequency. Subharmonics of electricity in the United\r\nStates and western nations are at 16Hz and at 28Hz. The peak seen at 16Hz in\r\nthe following image is the result of a saltbridge that occurred at the ground\r\nelectrode, contaminating every other electrode, as a consequence. A real human\r\nEEG signal will have “kurtosis,” which means “curved” or “arching” in Greek and\r\nis a measure of tailedness within the probability distribution of EEG\r\nfrequency. We expect to see kurtosis in all dominant frequencies of the EEG.<span lang=\"EN\"></span></p><h2 style=\"text-align: left;\">Spectrogram showing diffuse electrical contamination at 16Hz</h2><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Spectrogram.png\" alt=\"Spectrogram\" width=\"603\" height=\"548\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span></p><p></p><p style=\"text-align: center; \"><br></p><p></p><h3 style=\"text-align: left;\">A peak showing sides, or kurtosis in real human EEG, indicating\r\nthat this client not only produces 10Hz, but the also produce the frequencies\r\nsurrounding 10Hz, as one would in a normal distribution</h3><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/alpha%20peak.png\" alt=\"alpha peak\" width=\"604\" height=\"553\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p></p><h3 style=\"text-align: center; \">The mathematical equation for frequency decomposition and\r\nthe summation of frequencies </h3><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/FFT.png\" alt=\"FFT\" width=\"1209\" height=\"682\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p><p></p><p></p><p style=\"text-align: center;\">The&nbsp;mathematical&nbsp;details&nbsp;of&nbsp;complex&nbsp;demodulation&nbsp;used&nbsp;to&nbsp;compute&nbsp;the&nbsp;instantaneous&nbsp;Z&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">scores&nbsp;as&nbsp;contained&nbsp;in&nbsp;the&nbsp;Applied&nbsp;Neuroscience,&nbsp;Inc.&nbsp;“dll”&nbsp;are&nbsp;published&nbsp;in&nbsp;Otnes&nbsp;and&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">Enochson,&nbsp;(1977);Granger&nbsp;and&nbsp;Hatanaka,&nbsp;(1964);&nbsp;Bloomfield,&nbsp;2000;&nbsp;Thatcher&nbsp;et&nbsp;al,&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">(2007).&nbsp;Complex&nbsp;demodulation&nbsp;is&nbsp;a&nbsp;time&nbsp;domain&nbsp;digital&nbsp;method&nbsp;of&nbsp;spectral&nbsp;analysis&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">whereas&nbsp;the&nbsp;fast&nbsp;Fourier&nbsp;transform&nbsp;(FFT)&nbsp;is&nbsp;a&nbsp;frequency&nbsp;domain&nbsp;method.&nbsp;&nbsp;These&nbsp;two&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">methods&nbsp;are&nbsp;related&nbsp;by&nbsp;the&nbsp;fact&nbsp;they&nbsp;both&nbsp;involve&nbsp;sines&nbsp;and&nbsp;cosines&nbsp;and&nbsp;both&nbsp;operate&nbsp;in&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">the&nbsp;complex&nbsp;domain&nbsp;and&nbsp;in&nbsp;this&nbsp;way&nbsp;represent&nbsp;the&nbsp;same&nbsp;mathematical&nbsp;descriptions&nbsp;of&nbsp;the&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">power&nbsp;spectrum.&nbsp;&nbsp;The&nbsp;advantage&nbsp;of&nbsp;complex&nbsp;demodulation&nbsp;is&nbsp;that&nbsp;it&nbsp;is&nbsp;a&nbsp;time&nbsp;domain&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">method&nbsp;and&nbsp;less&nbsp;sensitive&nbsp;to&nbsp;artifact&nbsp;and&nbsp;it&nbsp;does&nbsp;not&nbsp;require&nbsp;windowing&nbsp;nor&nbsp;even&nbsp;integers&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">of&nbsp;the&nbsp;power&nbsp;of&nbsp;2&nbsp;as&nbsp;does&nbsp;the&nbsp;FFT.&nbsp;&nbsp;&nbsp;The&nbsp;FFT&nbsp;integrates&nbsp;power&nbsp;in&nbsp;a&nbsp;frequency&nbsp;band&nbsp;over&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">the&nbsp;entire&nbsp;epoch&nbsp;length&nbsp;and&nbsp;requires&nbsp;windowing&nbsp;functions&nbsp;which&nbsp;can&nbsp;dramatically&nbsp;affect&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">the&nbsp;power&nbsp;values&nbsp;whereas,&nbsp;as&nbsp;mentioned&nbsp;previously,&nbsp;complex&nbsp;demodulation&nbsp;does&nbsp;not\r\nrequire&nbsp;windowing&nbsp;(Otnes&nbsp;and&nbsp;Enochson,&nbsp;1972).&nbsp;&nbsp;&nbsp;Complex&nbsp;demodulation&nbsp;was&nbsp;computed&nbsp;</p>\r\n\r\n<p style=\"text-align: center;\">for&nbsp;the&nbsp;linked&nbsp;ears&nbsp;and&nbsp;eyes&nbsp;open&nbsp;and&nbsp;eyes&nbsp;closed&nbsp;conditions&nbsp;for&nbsp;all&nbsp;625&nbsp;subjects&nbsp;in&nbsp;the normative database.</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/JTFA%20Imaging.png\" alt=\"JTFA feedback for Z-scores\" width=\"586\" height=\"592\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: center;\"><br></p><p></p>',1),(379,85,378,380,20,0,1,1,1589827589,1656010000,'Windowing, Voltage, Symmetry and Synchrony','<p></p><h3></h3><h4>Windowing</h4><p><span style=\"font-size: 1rem;\">You will have to match the ends up when you cut the EEG and\r\nmake epochs. If you splice ends together and there’s discontinuity you get\r\nGibb’s artifact or “leakage.” A square wave (a square wave is all of the\r\nfrequencies combined)</span><br></p>\r\n\r\n<p>Windowing- gently turns on the epoch at the beginning and\r\nturns it off at the end, this is called smearing—this is preferential to Gibb’s\r\nartifact.</p>\r\n\r\n<p>An ideal window starts at 0 . The Hamming Window does not\r\nstart at 0—it does not get down to the 0 point. Bartlett (triangular window)\r\nhas a narrow peak at the top. There are various ways of fixing the\r\nEEG—(Bartlett, Hamming, Hanning, Blackman)—the QEEG is a extension of the\r\nanalysis of the EEG.</p><p><br></p><div><div><p></p><h4>Voltage vs. Amplitude</h4>Voltage and amplitude are terms that are closely linked but are not synonymous.&nbsp;<p></p><p>The voltage of an EEG waveform is measured in microvolts. The voltage can vary depending on the recording technique. The voltage seen on the EEG recording is the difference in electrical potential between the 2 inputs. It may appear higher or lower depending on the type of montage used to record it. Remember, the montage selection, bipolar or referential, will alter the display or deflection due to cancellation or summation of the EEG signal.&nbsp;<b>This makes it difficult to know the true or absolute voltage of a waveform</b>.&nbsp;</p><p><img src=\"@@PLUGINFILE@@/bipolar%20montages.png\" alt=\"Bipolar Montages\" width=\"600\" height=\"310\" class=\"img-responsive atto_image_button_left\"><br></p><p>Bipolar&nbsp;<a title=\"Montages\" href=\"https://schoolofneurotherapy.com/classroom/mod/lesson/view.php?id=183\">montages</a>&nbsp;with closely spaced electrode derivations produce lower voltage than widely spaced referential electrode derivations.&nbsp;</p><p>The amplitude of the EEG waveform is dependent on the sensitivity setting of the EEG instrument, and the voltage of the EEG signal being recorded. The amplitude which is the peak to-peak measurement (millimeters) is multiplied by the sensitivity, in microvolts per millimeter to calculate the voltage of the EEG wave or in some digital instruments the sensitivity may be \"full scale\" such as 50uV or 100 uV, in other words, the maximum voltage that can be displayed full scale. A waveform with a peak-to-peak measurement of 9 millimeters recorded at a sensitivity of 10 microvolts per millimeter would have a voltage of 90 microvolts or a peak to peak amplitude measurement of 13 millimeters recorded at a sensitivity of 10 microvolts per millimeter has a voltage of 130 microvolts.&nbsp;</p><p><br></p><h4>Symmetry vs. Asymmetry</h4><p>Symmetry is used to describe EEG amplitude and frequency in homologous, or similar, regions&nbsp;of the head. In general, normal EEG activity that occurs over both hemispheres in expected to be&nbsp;symmetric. It may be difficult to assess the symmetry of a sinusoidal pattern because of&nbsp;amplitude changes that are characteristic of the pattern. The range of amplitude changes,&nbsp;however, should be similar.</p><p><b>Symmetric - EEG waveforms that are equal in frequency and voltage&nbsp;in homologous (corresponding) regions of the head.&nbsp;</b></p><p><b>Asymmetric - EEG waveforms that are NOT equal in frequency and voltage&nbsp;in homologous (corresponding) regions of the head.&nbsp;</b><br></p><p>Asymmetry describes EEG activity that is different (present/absent or increased/decreased) in one hemisphere when compared to the same region of the opposite hemisphere. Asymmetry can be caused by damage to an area of the brain or even by skull defects, which are changes in the skull bone caused by injuries or medical procedures. An increase in the amplitude is seen over the skull defect. A minimal degree of asymmetry is acceptable in normal EEG recordings. Alpha rhythm, for example, is usually of higher amplitude over the right hemisphere.&nbsp;<br></p><p>In right-handed individuals, alpha should be found to be somewhat higher in amplitude in the right hemisphere.&nbsp; However, when alpha frequency is found to be slower by 1 Hz or more in one hemisphere, this should be considered as potentially indicative of a focal abnormality (Markand, 1990) warranting a neurological consult, and should particularly be considered abnormal if it is greater than 1.5 Hz (Duffy, et al., 1989).&nbsp; Likewise, an amplitude difference in alpha between the two sides of more than 50% is considered significant (Hughes, 1994), and because in right handed individuals, alpha rhythm is usually of higher amplitude on the right side, a decrease of even 35% on the right may be significant (Duffy et al., 1989).&nbsp; Focal lesions may cause alpha to be disorganized ipsilaterally, to be of lower or higher amplitude, and may cause alpha to fail partially or totally to block following eye opening on the affected side.&nbsp; But, “in the absence of other findings, one should use caution in interpreting isolated&nbsp;<i>amplitude</i>&nbsp;asymmetry of the alpha rhythm, because amplitude asymmetries of the order as high as 2:3 are not uncommon in normal subjects” (Markand, 1990, p. 181, emphasis added).&nbsp; &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;<br></p><p><b>Both muscle contamination and poor electrode application can lead to asymmetry.</b></p><p><img src=\"@@PLUGINFILE@@/symmetry%20vs.%20asymmetry.jpg\" alt=\"Symmetry vs. Asymmetry\" width=\"720\" height=\"540\" class=\"img-responsive atto_image_button_left\"><br></p><h4>Synchrony</h4><p>Synchrony describes waveforms that occur simultaneously. Patterns that occur at the same time in both hemispheres may be called bilaterally synchronous. Eye blinks seen on an EEG are an example of activity that is bilaterally synchronous. Asynchronous - waveforms with timing that is not the same. The eye blinks in the above image are synchronous.</p></div></div><br><p></p>',1),(380,85,379,390,20,0,1,1,1589827947,1597384516,'Connectivity','<p></p><p>THREE KINDS OF CONNECTIVITY</p>\r\n\r\n<p><!--[if !supportLists]-->1)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Structural – anatomical connectivity DTI/DSI</p>\r\n\r\n<p><!--[if !supportLists]-->2)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Functional Connectivity</p>\r\n\r\n<p><!--[if !supportLists]-->3)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Effective connectivity</p><p>&nbsp;</p><p><i>Human intelligence is directly correlated to brain\r\ncomplexity as measured by the EEG (Anokhin et al, 1999; Giannitrapani, 1985;\r\nThatcher et al, 1983; 2005)</i></p><p><i><br></i></p><p></p>\r\n\r\n<h2><a name=\"_Toc29929042\"></a><a name=\"_Toc3535256\">Coherence</a></h2>\r\n\r\n<p>&nbsp;</p>\r\n\r\n<p>Coherence is generally thought of as connectivity.&nbsp;<span style=\"font-size: 1rem;\">There is a two compartmental level model of\r\ncoherence. Coherence is cortical-cortico connectivity.</span><span style=\"font-size: 1rem;\">When cortical-cortico connections are cut, this\r\ndoes not affect coherence! Coherence is Cortical-thalamo-cortical.</span></p>\r\n\r\n<p><a name=\"_Hlk488301210\"></a><a name=\"_Hlk523304243\"></a><a name=\"_Hlk491673952\">The measure of coherence is the measure of\r\nthe stability of the phase relationship between different sites in the brain.\r\nThat is to say, we are measuring connectivity from the perspective of\r\nflexibility.&nbsp; </a>Hypercoherence\r\nshows a lack of flexibility in the connection relationships; firings are locked\r\ninto the same rhythm. Imagine\r\nsoldiers goose-stepping or a crowd clapping in unison. Hypercoherence is\r\nproblematic in the sense that it can create “tunnel vision” or the inability to\r\nswitch tasks readily. On the other hand, it may lead to a sort of frenetic\r\ndistractibility, where nothing gains the complete attention and the individual\r\nalways feels “scattered,” “distracted,” and busied.</p>\r\n\r\n<p>Coherence is stability of the phase relationship in the\r\nbrain. Hypocoherence is a lack of stability, in terms of the brain waves never\r\nremaining consistent in their relative relationship to other areas of the\r\nbrain. Hypercoherence is an “over-connectivity,” or the stability of the phase\r\nrelationship between the areas of the brain are in a locked pattern.</p>\r\n\r\n<p>For example, hypocoherence, as we see in the delta range and\r\nat the sites of C4 and P4 (the axis of the sensory part of the sensory motor\r\nstrip and the superior parietal lobe), is a deviance in phase relationship in\r\nthe sense that the affected site is not cooperating or coming into any reliable\r\nrelationship with any of the surrounding areas.&nbsp;\r\nIn these maps, C4 (correlating with Brodmann areas 3, 4, 5, and 7) and\r\nP4 (correlating with Bas 5 and 7) area those areas committed to visuospatial\r\nfunctions motor imagery and processing, memory (working memory and visuospatial\r\nmemory), language processing (attention to sentence comprehension and\r\nphonological relations) and even the processing of emotion ( 5 and 7), as well\r\nas motor movements, the control of motor tasks, kinesthetic perception of limb\r\nmovement, contralateral lower limb movement, and the localization of pain,\r\ntemperature, vibration, and touch (Bas 3 and 4).</p>\r\n\r\n<p><a name=\"_Hlk523384356\">Hypercoherence is an\r\n“over-connectivity,” or the stability of the phase relationship between the\r\nareas of the brain are in a locked pattern. In this case, there is a\r\npreponderance of alpha activity with the eyes closed (partially due to\r\nmedication), and in this state we also see the 9-12 Hz bandwidth come into a\r\n“locking” of sorts. </a>Alpha synchrony (or hypercoherence) is often seen in\r\nmeditators, and it shows (often) a certain presence about the individual.\r\nFeeling alert and “here and now.” This is, for the time being, not the primary\r\nconcern, especially since the client reported becoming drowsy with the eyes\r\nclosed state.</p><h3><a name=\"_Toc29929044\">Asymmetry</a></h3>\r\n\r\n<p><a name=\"_Hlk523168956\">Asymmetry is a reflection of a power\r\ndifferential in the brain, that is to say, the lines coming from the back of\r\nthe head in the above picture represent an excess of energy that lives\r\noccipitally. As the excessive power in the occiput diminishes, so will the\r\nreflections of asymmetry in amplitude.</a></p>\r\n\r\n<p>&nbsp;</p>\r\n\r\n<h2><a name=\"_Toc29929045\">Phase</a> </h2>\r\n\r\n<p>The phase measures have also been normed. It is clear that\r\nphase is an important measure in understanding propagation of neuronal\r\nactivity. Progressive phase delays are measurable as a volley travels from a\r\nsource to a destination. In addition, 180 degree differences in phase denote\r\npolarity inversion and suggest the location of underlying generators. Using\r\npolarity inversion to model the source of brain macropotentials is useful in\r\nlocalizing activity and is commonly used in electroencephalography (Niedermeyer\r\nand Lopes da Silva, 1999). However, the meaning and utility of measures of\r\n“average phase” over time is not as clear.</p><p>Click <a href=\"https://vimeo.com/443082983\">\"here\"</a> to watch a video on phase shift and phase lock.&nbsp;</p><h3><a name=\"_Toc29929046\">Phase Shift, Phase Lock, and Phase Reset</a></h3>\r\n\r\n<p>For 200 – 1,0000 msec clusters of neurons assemble into phase\r\nsynchrony (aka “phase lock”); conversely, for 200-1,000 msec clusters of\r\nneurons disassemble into loss of phase synchrony (aka “phase shift”).&nbsp; The dominant acting force for these\r\nsynchronizatons and desycnhronizations&nbsp;\r\nis that of stochastic resonance (“stochasm” is latin for “purposeful\r\nrandomness”).</p>\r\n\r\n<p>Phase reset is made of phase shift and phase lock, which is the\r\nsynchronization and desynchronization of neurons. Phase shift is like a “shout\r\nout,” where neurons are recruited to synchronize with the action potential\r\nactivity at the time.</p>\r\n\r\n<p>&nbsp;Thatcher et al. (2008)\r\nidentified that longer phase shift dynamic is related to superior I.Q., with an\r\noptimized balance between phase shift and phase lock being ideal. &nbsp;Phase shift duration is related to the average\r\nlocal inhibitory post synaptic potential duration on cell bodies and the phase\r\nlock duration is positively related to the average excitatory post synaptic\r\npotential summation on the dendrites of cortical pyramidal cells.</p>\r\n\r\n<p>When <u>phase shift duration is too short</u> then there are fewer\r\nneural resources available to be phase locked into a stable dynamic. <u>Longer\r\nphase shift</u> duration increases the probability of identifying larger\r\nnumbers of neurons capable of being phase locked (this is why there is a direct\r\nrelationship between shift duration and I.Q.). However, when <u>phase shift\r\nduration is too long</u> then there is increased noise and reduced number of\r\nneurons available for phase locking. When <u>phase lock duration is too long</u>\r\nthen there is less flexibility and there are reduced resources available to be\r\nallocated by the phase shift mechanism.&nbsp;However, <u>too short of phase\r\nlocking</u> will result in less information processing and less efficiency of\r\nthe allocated resources with premature release of the resources by a subsequent\r\nphase shift. &nbsp;In short, an optimal\r\nbalance between phase shift duration and phase lock duration is related to\r\nhigher levels of intelligence because of an optimal balance results in maximum\r\nspeed and efficiency of information processing.<b>&nbsp;</b></p>\r\n\r\n<p>The dynamic balance between synchronization and desynchronization\r\nis essential for normal brain function and abnormal balance is often associated\r\nwith pathological conditions such as epilepsy (Lopes da Silva and Pihn, 1995;\r\nLeVan Quyen et al, 2001b; Chevez et al, 2003; Netoff and Schiff, 2002),\r\nschizophrenia (Lee et al., 2002) and dementia (Stam et al., 2002a; 2002b).</p>\r\n\r\n<p>Phase dynamics are represented in Bob Thatcher’s qEEG analysis as\r\nthe metric of “Phase Lag.” Phase lag can be normal (no lines presented), hyper\r\nphase lag (red lines) or hypo phase lag (blue lines). Hyper phase lag indicates\r\n<i>too much phase lag</i> and not enough phase synchrony (i.e. not enough phase\r\nlock). This can result in increased neuronal noise and a reduced amount of\r\nneurons available for phase locking.</p><h3><a name=\"_Toc29929047\">Hyper Phase Lag in Theta in a 60-year-old\r\nman complaining of memory difficulties</a></h3><p style=\"text-align: center; \"><a name=\"_Toc29929047\"><img src=\"@@PLUGINFILE@@/Hyper%20Phase%20Lag.png\" alt=\"Hyper Phase Lag\" width=\"626\" height=\"454\" class=\"img-responsive atto_image_button_middle\"><br></a></p><p><a name=\"_Toc29929047\"><br></a></p><p><a name=\"_Toc29929047\"><br></a></p><p><br></p><p><a name=\"_Toc29929047\"></a></p><p><a name=\"_Toc29929047\">Hypo phase lag indicates not enough phase lag (and too long phase\r\nlock) indicating that neuronal assemblies are coming into synchrony too\r\nfrequently and for longer duration than is ideal. The individual in the\r\nfollowing image report difficulty keeping attention on any given task.</a></p><p></p><h2><a name=\"_Toc29929048\">Hypo Phase Lag in all Frequencies in a\r\n12-year-old girl who has poor organization skills, focus and concentration</a></h2><br><p></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Hypo%20Phase%20Lag.png\" alt=\"Hypo Phase Lag\" width=\"528\" height=\"384\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem;\"></p><p></p><p></p>',1),(381,85,390,0,3,0,1,1,1589828279,0,'Page 1','Asymmetry is:',1),(382,86,0,383,20,0,1,1,1589902547,1596129166,'Introduction','<p></p><p></p><p>The definition of quantitative EEG is very broad and encompasses all quantified EEG in term of phase, coherence, power and/or other brain-computer interfaces. However, for the sake of simplicity, we will refer to the quantitative EEG as a test comparing the electroencephalography of the individual (EEG) to a normative database, which is a database of “normal” people within the clients age range who are physiologically and psychologically healthy. The individual is assessed from the perspective of how many standard deviations from the norm their EEG data occurs within.&nbsp; This creates what we know as a “brain map.” Maps are taken using standard deviations from the norm by way of or power output (measured in microvolts squared or pure microvolts).&nbsp;&nbsp;&nbsp;&nbsp;</p><p>When recording, traditionally in the field of neurotherapy, the international 10-20 system for electrode placement is used (a 19-channel cap) and electrode impedance of less than five kilo ohms is used. Activity at the functional regions of the brain, including Brodmann areas, can be incorporated into the findings with the use of Low Resolution Brain Electromagnetic Tomography (LORETA) software.</p><h3>Low Resolution Tomographical Analysis Image</h3><p><img src=\"@@PLUGINFILE@@/LORETA%20Imagery.png\" alt=\"LORETA Imagery\" width=\"928\" height=\"653\" class=\"img-responsive atto_image_button_left\"><br></p><p>Typically, an EEG is recorded in two conditions: eyes open and eyes closed. A clinician can use as many or as few databases as they wish, each database has its own high points and short comings. &nbsp;Depending on the database, data can be understood from a variety of different montages. Some of the more well-known databases include: Neuroguide, HBI, BrainDx, iSyncBrain, and more.&nbsp;<i></i></p><p>The images created by quantitative EEGs will show an overall view of the client’s brain waves (EEG) relative to a normative database of other people their own age. Colors are often used to indicate how many standard deviations they are from the normal population. Also (often) shown are connectivity issues in coherence (the stability of the phase relationship between different sites in the brain) and phase lag (a measure of how waveforms come into and out of synchronization).</p><p>Quantitative databases usually give an overall view of the individual’s data from a Fast Fourier Transform (FFT) perspective. &nbsp;Absolute Power is the total voltage, or energy, that the brain is emitting, measured in microvolts squared in disparate frequencies. Relative Power<b>&nbsp;</b>is<b>&nbsp;</b>a measure of clients’ EEGs, viewed in relation to their absolute power profile, used to determine what may be deviant, in relative terms. Magnitude is measured in pure microvolts.</p><p>A measure of clients’ EEGs, viewed in relation to their absolute power profile, is used to determine what may be deviant, in relative terms.&nbsp;&nbsp;<span style=\"font-size: 1rem;\">When reading a Z-score map, 1.64 standard deviations is considered the threshold of clinical significance.</span></p><h3><span>Interpreting the Data</span></h3><p>The summary pages of many QEEG reports give an overall view of the goings on from a neurophysiological perspective. Each column contains the activity for one bandwidth (delta, theta and so on). Each row contains a separate metric. The colors indicate how many standard deviations, or Z-scores, the client is from the normal population. The thickness of the lines also depicts deviance in Z-score measures. Absolute Power is the total voltage, or energy, that the brain is emitting, measured in disparate frequencies and typically portrayed after processed via a “normative database.” Relative Power<b>&nbsp;</b>is<b>&nbsp;</b>a measure of clients’ EEGs, viewed in relation to their absolute power profile, used to determine what may be deviant, in relative terms.&nbsp;</p><p>Coherence is<b>&nbsp;</b>the stability of phase 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. Phase is any one point or portion in a recurring series of changes, as in the changes of motion of one of the particles constituting a wave or vibration; the metrics of phase are very similar to coherence and will be discussed further in the document. In the articles folder, you will find an entire report from the Neuroguide Quantitative Database, as well as an entire report from the iSyncBrain Database.</p><p><a name=\"_Toc35418096\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">A summary Page from a Quantitative Database (NeuroGuide)</a><br></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Summary%20Map.png\" alt=\"Summary Map\" width=\"716\" height=\"955\" style=\"font-size: 1rem;\"></p><p></p><p></p><h2><a name=\"_Toc35418097\">A summary page from a Quantitative Database (SKIL)</a></h2><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/SKIL%20Summary%20Map.png\" alt=\"SKIL Summary Map\" width=\"729\" height=\"453\" style=\"font-size: 1rem;\"></p><p></p><h2><a name=\"_Toc35418098\">A Summary Page of Individual Hz bins in SKIL</a></h2><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Individual%20Hz%20Bins.png\" alt=\"SKIL Individual Hz Bins\" width=\"638\" height=\"332\" style=\"font-size: 1rem;\"></p><p></p><p style=\"text-align: center;\"><br></p><p></p>',1),(383,86,382,384,20,0,1,1,1590093627,1656010293,'How to get a valid qEEG Brain Map','<p></p>\r\n<h2><span style=\"color: rgb(82, 96, 105); font-size: 1rem; font-family: &quot;Open Sans&quot;, sans-serif;\">When gathering data, the clinician\r\nmust begin with visual analysis of the data and proceed to edit the EEG\r\ninformation, removing all artifacts and, if they are persistent or\r\nunremovable,&nbsp; denoting how they will\r\naffect the qEEG, so as to not misinterpret the artifactual findings as real.</span><br></h2>\r\n\r\n<h2><a name=\"_Toc35418100\">Impedance</a></h2>\r\n\r\n<p>Typically, when gathering QEEG data, the clinician starts by ensuring the electrodes have a low impedance. They might use a checktrode impedance meter or another built-in impedance checking system. </p>\r\n<p>Here is short video on checking impedance with Neurofield software:&nbsp;&nbsp;&nbsp;<video controls=\"true\"><source src=\"https://www.youtube.com/watch?v=OPof2CEqYq8\">https://www.youtube.com/watch?v=OPof2CEqYq8</video>&nbsp;</p>\r\n<h2><a name=\"_Toc35418101\"></a><a name=\"_Toc3535259\">QEEG databases</a> </h2>\r\n\r\n<p>Many quantitative EEG Databases use Z-scores to measure how deviant the individual is from the normal population, in terms of amplitude/magnitude (often referred to as “power”), coherence, phase measures, and symmetry. </p>\r\n<p>Here is a short video of Bob Thatcher describing the creation of Z-Scores:</p>\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><script src=\"https://player.vimeo.com/api/player.js\"></script>\r\n<p><b><u>Z scores</u></b></p>\r\n\r\n<p>Z = subject value – mean value of the same/ SD of the sample</p>\r\n\r\n<p>Z= probability that the subject value lies within the normal range. 1.96 Z scores is 2 SDs.</p>\r\n<h3>Image of a bell curve denoting Z-scores&nbsp;</h3>\r\n<p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Z-score%20chart.jpg\" alt=\"z scores\" width=\"546\" height=\"368\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n<p></p>',1),(384,86,383,0,20,0,1,1,1590093665,1596769314,'LORETA','<p></p><h2><a name=\"_Toc35418102\">LORETA</a></h2><p>&nbsp;</p><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><h3>&nbsp;Here are two videos showing a few ways LORETA is used in EEG Analysis&nbsp;</h3><h2>&nbsp;</h2><h2><video controls=\"true\"><source src=\"@@PLUGINFILE@@/Loreta%20video%202.mp4\">@@PLUGINFILE@@/Loreta%20video%202.mp4</video>Here is a video of LORETA as used in EEGLab in MatLab by Arnaud DeLorme</h2><h2>&nbsp;<a href=\"https://www.youtube.com/watch?v=amttvN_Sb6A\">LORETA in EEGLab</a>&nbsp;<br><a name=\"_Toc35418103\"></a></h2><p><h2>Here is a video of LORETA and ICA as used in WinEEG by Juri Kropotov</h2></p><p><a href=\"https://www.youtube.com/watch?v=CrrA771v-WY\">Juri Kropotov and LORETA in WinEEG</a><br></p><p><h2>Here is a video of LORETA as used in Neuroguide by Bob Thatcher</h2><p><a href=\"https://www.youtube.com/watch?v=VzQoLg-FKBQ\">Bob Thatcher on LORETA in Neuroguide</a><br></p></p><p></p>',1),