(385,87,0,386,20,0,1,1,1590169771,1656010488,'Neurofeedback and Neuromodulation protocols','<p></p>\r\n<p>Neurofeedback is based on the success of operant conditioning, the underlying thesis of which is the Law of Effect, which states, when you reward something, you reinforce that behavior. In the case of neurofedback, the patient is rewarded for making the\r\n    appropriate (programmed) brain wave frequency or connectivity metrics, via either visual or auditory reinforcement.</p>\r\n\r\n<p>Many neurofeedback modalities are preceded by an assessment of the brainwave activity, typically through a Quantitative EEG brainmap; there are schools of neurofeedback that do not do this, including the Othmer method and Valdeen Brown’s Neuroptimal.\r\n    </p>\r\n\r\n<p>There are many different modalities and ways to do neurofeedback. Some are single channel (one active electrode) some are two channels, some are four channels, and some use a 19-channel cap. Since neurofeedback is EEG biofeedback, using the brainwaves\r\n    as the mechanism that is measured is brainwave activity. </p>\r\n<p>Neurofeedback is based on the success of operant conditioning, the underlying thesis of which is the Law of Effect, which states, when you reward something, you reinforce that behavior. In the case of neurofedback, the patient is rewarded for making the\r\n    appropriate (programmed) brain wave frequency or connectivity metrics, via either visual or auditory reinforcement.</p>\r\n\r\n<p>Many neurofeedback modalities are preceded by an assessment of the brainwave activity, typically through a Quantitative EEG brainmap; there are schools of neurofeedback that do not do this, including the Othmer method and Valdeen Brown’s Neuroptimal.\r\n    </p>\r\n\r\n<p>There are many different modalities and ways to do neurofeedback. Some are single channel (one active electrode) some are two channels, some are four channels, and some use a 19-channel cap. Since neurofeedback is EEG biofeedback, using the brainwaves\r\n    as the mechanism that is measured is brainwave activity. </p>\r\n<p>During neurofeedback training, individual EEG electrodes or a full 19-channel cap are placed on the scalp and the EEG activity of the patient is monitored and fed back to them in real time. Based on the feedback and the practitioner’s guidance, changes\r\n    in brainwave patterns occur and are associated with positive changes in physical, emotional, and psychological states of being. </p>\r\n\r\n<p>Often a patient will ask: “how do I make this work?” or “what do I do?” and the answer is they “will” the screen (or tone) to respond positively to them. The answer that I always use is: “get out of your own way and let your brain do its thing, do not\r\n    get too attached to doing better or doing worse, it will continue to ebb and flow.” </p>\r\n\r\n<p>Neurofeedback is based on the principle that the brain responds to ‘information’ on a conscious and nonconscious manner, and typically without any assistance. We have the ability for complex processing. We find most tasks like breathing, eating and digestion\r\n    are ultimately performed without our focused attention.</p>\r\n<p><br></p>\r\n<p><br></p>\r\n<h2><a name=\"_Toc35418104\">LENS and HPN</a></h2>\r\n<p></p>\r\n<div>\r\n    <p>The LENS (<i>Low Energy Neurofeedback System)</i>&nbsp;technology leverages the neuroplasticity, innate within each and every individual, to help alleviate symptoms, optimize functioning, and reclaim lost neurological and physiological potential.\r\n        This unique approach targets the central nervous system and helps to restore functioning that may have been compromised as a result of brain&nbsp;injury including stroke and concussions, trauma, PTSD, surgical procedures, anoxic events, medications,\r\n        birth trauma, environmental influences, etc. These events often leave in their wake&nbsp;anxiety-depression spectrum issues, headaches, migraines, attention deficits, emotional disturbances, explosiveness, behavioral disorders, movement disorders,\r\n        pain, range of motion issues, etc.&nbsp;</p>\r\n    <p>There are four areas that distinguish the LENS from traditional neurofeedback:&nbsp;</p>\r\n    <p>1.&nbsp;<i>Significantly fewer sessions</i>: rather than using operant conditioning to train the brain, the LENS technology utilizes the client’s unique real-time brain wave metrics (also known as EEG) to&nbsp;<i>interrupt the maladaptive mechanisms</i>&nbsp;that\r\n        have been adapted by the CNS in response to head trauma and other events listed above. This produces measurable changes in brainwave activity and subsequent symptom reduction or elimination in significantly fewer sessions, with the number needed\r\n        to improve/restore functioning for the majority of&nbsp;clients&nbsp;falling&nbsp;within the 2-15 session range.</p>\r\n    <p>2.&nbsp;<i>Does not require conscious effort from the client:</i>&nbsp;the LENS has been used successfully with babies (as young as 3 months of age)/toddlers/children, clients on the autism spectrum, those with ADD/ADHD, and even animals (including\r\n        racehorses, giraffes, gorillas&nbsp;and chimpanzees).</p>\r\n</div>\r\n<div>3.&nbsp;<i>Session Duration</i>: a typical LENS session lasts about 6 minutes, and this includes skin prep, sensor placement, running the software, sensor removal and post-session cleanup. For some clients, the&nbsp;actual duration of the LENS itself\r\n    is as little as 1 second. &nbsp;Due to&nbsp;this short session duration, the LENS works well for those who are unable to pay attention to a computer screen for long periods of time, and/or who are not able to understand instructions such as is needed\r\n    with traditional neurofeedback.<br></div>\r\n<div><br></div>\r\n<div>4.&nbsp;<i>Address pain issues</i>: the LENS technology has been applied to other areas of the body (limbs, torso, hands, etc.) to successfully address pain, discomfort, range of motion issues, and more.</div><br>\r\n<p></p>\r\n<h3><a name=\"_Toc35418105\">A LENS Neurofeedback System</a></h3><img src=\"@@PLUGINFILE@@/LENS%20Neurofeedback%20System.png\" alt=\"LENS Neurofeedback System\" width=\"919\" height=\"234\" class=\"img-responsive atto_image_button_left\"><br>\r\n<p></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p></p>\r\n<p><br></p>\r\n\r\n<b>High\r\nPerformance Neurofeedback, </b>aka HPN Ultra Low Power Neurofeedback, was invented by Cory Snook and is thought to be another version of the LENS. HPN&nbsp;is a type of brainwave based&nbsp;<span style=\"font-size: 1rem;\">biofeedback&nbsp;\r\nthat has shown promise of clinical efficacy in addressing the symptoms associated\r\nwith Traumatic Brain Injury (TBI), Post-Concussive Syndrome, Post-Traumatic\r\nStress Disorder (PTSD), Anxiety, Depression,&nbsp; “brain-fog,”&nbsp; and\r\nattention deficit disorders.<br><br></span>\r\n<p>HPN measures and tracks the electrical activity of the brain (brainwaves) and then sends directly back to the brain a very weak, imperceptible signal containing information based on the just preceding brainwave activity.&nbsp; The power in the signal\r\n    is estimated to be about 3 p W (picowatts).&nbsp; Although the power in this signal is amazingly small, the brain appears to be able to adjust its own functioning based on this feedback.\r\n</p>\r\n<h3><a name=\"_Toc3535268\"><br></a></h3>\r\n<h3><a name=\"_Toc35418106\"></a><a name=\"_Toc3535268\">S</a>low Cortical Potential Neurofeedback and Infra Slow Fluctuation&nbsp; Neurofeedback</h3>\r\n\r\n<p></p>\r\n<p><span lang=\"DE\">Slow Cortical Potential Neurofeedback and Infra-Slow\r\nNeurofeedback involve dialing in the right slow cortical potential frequency\r\nfor the client. In a colloquial sense, these neurofeedback modalities are said\r\nto coordinate electrical activity in the brain, controlling activation and\r\ndeactivation of those behavioral networks.</span></p>\r\n\r\n<p><span lang=\"DE\">Infra-slow Fluctuation (ISF) electroencephalogram (EEG)\r\nbiofeedback is focused on the lowest energy the brain produces (&lt; 0.1 Hz).\r\nThe intervention is performed with a Direct Current (DC) coupled neurofeedback\r\namplifier. It is distinct from Slow Cortical Potential (SCP) training and\r\nInfra-Low Frequency (ILF) training. It shares a similar optimization process\r\nwith ILF that focuses on emergent state shifts within sessions.</span></p>\r\n\r\n<h4><a name=\"_Toc35418107\"><span lang=\"DE\">What Are Slow Cortical Potentials and what are Infra Slow\r\nOscillations?</span></a><span lang=\"DE\"></span></h4>\r\n\r\n<p><span lang=\"DE\">Slow Cortical Potentials are slow shifts in the EEG that last\r\nfrom 0.3 seconds to several seconds, infra slow oscillations are typically\r\n0.1Hz and lower. These shifts in the EEG reflect the depolarization of large\r\ngroups of pyramidal cells in the cortex. These slow shifts are caused by the\r\nburning of blood glucose, that makes up the hemodynamics of the glial\r\ncells.&nbsp;For two decades researchers have proposed that neurons, glial\r\ncells, and blood may be regarded as compound generators of these infra-slow\r\nbioelectrical phenomena (Hughes, Lőrincz, Parri, &amp; Crunelli, 2011; Zschocke\r\n&amp; Speckmann, 1993). Thalamocortical neurons have been observed to exhibit\r\nrobust infra-slow oscillations (ISOs), in vitro, at approximately 0.005–0.1 Hz\r\n(Lőrincz, Geall, Bao, Crunelli, &amp; Hughes, 2009). After a reappraisal of in\r\nvivo and in vitro evidence, Crunelli and Hughes (2010) have proposed a three\r\ncardinal oscillator model that identifies one cortical and two thalamic sources\r\nof infra-slow frequencies. Astrocytes have recently been identified by Hughes\r\net al. (2011) as a source of ISOs in the 0.003–0.1 frequency range. These researchers\r\nobserved neurons in cat Thalamus succumbing to a cyclic inhibitory influence\r\nthat they proposed was generated in the slow regime by Thalamocortical\r\nastrocytes. These cells create large electro-negative swings when they\r\ndepolarize. Slow Cortical Potentials (SCP) are changes of cortical polarization\r\nlasting several hundred milliseconds to several seconds. SCPs are related to\r\nthe excitability level of underlying cortical regions. Negative SCP shifts\r\nreflect higher cortical excitability while positive shifts reflect reduced\r\nexcitability or even inhibition. Sheets of cortical neurons are depolarized in\r\nthe creation of SCPs. It has been hypothezised that in autism spectrum cases,\r\nthe threshold of depolarization is too high and in ADHD cases, the threshold of\r\ndepolarization is too low. Additionally, in patients with\r\nseizure&nbsp;conditions, large negative potential shifts have been observed\r\nmoments before a seizure. (ADHD children are taught to increase the negativity\r\nof the SCP, while autistic and seizure cases are taught to decrease the\r\nnegativity of the SCP).<br>\r\n<br>\r\n<!--[if !supportLineBreakNewLine]--><br>\r\n<!--[endif]--></span><span lang=\"DE\"></span></p>\r\n\r\n<p><span lang=\"DE\">In Europe Slow Cortical Potential (SCP) neurofeedback is taught\r\nby Ute Strehl , who uses a visual to reflect higher arousal (in\r\nelectro-negative potentials, that is, going up) and lower arousal (in electro-positive\r\npotentials, going down). In clinical thresholding, it is important to verbally\r\nencourage and reward the patient, especially if they are children.&nbsp;SCP\r\ntraining is a “one size fits all protocol” with the majority of the training\r\ndone at the vertex. As first developed, the client attempted to produce\r\ncortical excitation, a negative DC shift, in the case of ADHD; or cortical\r\ninhibition, a positive DC shift, in the case of Epilepsy over the course of\r\nmany short trials (Birbaumer, 1999; Birbaumer et al., 1994, Kotchoubey et al.,2001\r\n). More recently SCP training has evolved to train in both negative and\r\npositive cortical shifts in the same session with proportions of negative and\r\npositive trials dependent on client presentation (Strehl et al., 2006). In\r\nclinical interventions, such as epilepsy or ADHD Ute Strehl always implements\r\nSCP feedback as a technique in the framework of behavior therapy which is being\r\nenumerated by the German statutory health insurance.</span></p>\r\n\r\n<p><span lang=\"DE\">Ute Strehl and colleagues have published extensively in RCT\r\n(randomized controlled trials) studies on their work.They have used a slow-wave\r\nfilter and a 500-millisecond interval moving window. This methodology is\r\navailable using thought technology equipment and screens (</span><span lang=\"DE\"><a href=\"http://www.thoughttechnology.com/\">www.thoughttechnology.com</a></span><span lang=\"DE\">; <a href=\"https://www.neurocaregroup.com/neuroconn-technologie.html\">https://www.neurocaregroup.com/neuroconn-technologie.html</a>;\r\n<a href=\"https://www.mindmedia.com/\">https://www.mindmedia.com/</a>). An\r\nimportant, mandatory feature of SCP feedback is the online artifact control as eye\r\nmovements and huge EMG actitivty may interfere with EEG activity. </span></p>\r\n\r\n<p><span lang=\"DE\">In America, Infra Slow Neurofeedback is being taught by Siegfried\r\nand Sue Othmer. ISF training owes its lineage to the early Beta/SMR training of\r\nSusan Othmer and EEG Spectrum (Kaiser &amp; Othmer, 2000). That intervention\r\nwas done with a single channel of EEG and an intra-hemispheric bipolar montage\r\non the motor strip and temporal lobes. The starting frequency was in the 12–18\r\nHz range depending on the targeted hemisphere. The Othmers and others (Putman,\r\nOthmer, Othmer, &amp; Pollock, 2005; Stokes &amp; Lappin, 2010), modified this\r\ntechnique to include inter-hemispheric placements beginning on the temporal\r\nlobes. Instead of set reward bands, a 3 Hz window was shifted up or down\r\ncontingent upon client response. The intervention produced immediate state\r\nshifts in the client. The trainer targeted state regulation in real time by\r\ndiscovering an optimum frequency through trial and error for each client.\r\nSuccess was defined by the immediate improvement in affect and arousal\r\nregulation in session and ultimately by generalized improvements in behavioral\r\nand&nbsp;state regulation in life. Over time, it became apparent that the vast\r\nmajority of clients were finding an optimum clinical response at lower and\r\nlower frequencies until 2007, when the beginning frequency was established at\r\n0–3 Hz.</span></p>\r\n\r\n<p><span lang=\"DE\">Infra Low neurofeedback is being taught by Mark\r\nSmith.&nbsp;Smith has reported clinical results including increased relaxation,\r\nbetter sleep, profound changes in physiology, and a renewed sense of well-being\r\nin daily life. ISF neurofeedback was put to the test by using Biofeedback\r\nequipment that measured a subject’s physiological response to the training.\r\nWhat was found during that training was blood pressure normalized, heart rate\r\nslowed, hands became warm and dry, breathing became deeper and slower and the\r\nbig muscles in the shoulders (trapezius) relaxed. All direct indications of the\r\nrelaxation response.</span></p><br>\r\n<p></p>\r\n<h3><a name=\"_Toc35418108\"></a><a name=\"_Toc3535269\">Alpha-Theta</a></h3>\r\n\r\n<p>Alpha/theta&nbsp;training,&nbsp;in&nbsp;which&nbsp;the&nbsp;goal&nbsp;is&nbsp;to&nbsp;achieve&nbsp;an&nbsp;altered,&nbsp;hypnogogic&nbsp;state&nbsp;of&nbsp;<span style=\"font-size: 1rem;\">consciousness,&nbsp;useful&nbsp;for&nbsp;therapeutic&nbsp;purposes.&nbsp;\r\nDuring alpha theta training, the participant is typically reclined or laying\r\nsupine, in a comfortable room in a comfortable position, with their eyes shut,\r\nThey are listening to auditory feedback (one popular set of sounds is the\r\nsounds of ocean waves and the sound of waves upon the shore). The individual in\r\nalpha theta training is trained to increased the amplitude of their theta\r\nfrequencies so that they surpass their alpha frequencies, inducing what is\r\nconsidered a deep state. This increase of theta and decrease of alpha is called\r\na cross-over and is the clinical goal of alpha-theta neurofeedback.</span></p>\r\n\r\n<p>&nbsp;Some clinicians use Alpha-Theta neurofeedback only as polish at the end of many neurofeedback sessions, as the accessing of theta while conscious can create abreactions in individuals who are not ready to access the deeper realms where suppressions\r\n    and repressions reside. On the flip side, this can be a hugely healing protocol for individuals who need to integrate and incorporate the activation behind stress responses. </p>\r\n<h3><a name=\"_Toc35418109\">A diagram showing the concept of an alpha\r\ntheta crossover, the y-axis related to amplitude</a></h3>\r\n<p><a name=\"_Toc35418109\"><img src=\"@@PLUGINFILE@@/Crossover.png\" alt=\"crossover\" width=\"868\" height=\"476\" class=\"img-responsive atto_image_button_left\"><br></a></p><br>\r\n<p></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p></p>\r\n<p>Many of the great minds of our times—artists, musicians, scientists, and geniuses of all sorts—have described arriving at their discoveries and innovations often when in a deep dream-like reverie. The alpha-theta brain wave state that reflects this level\r\n    of trance teeters on the borderline between consciousness and unconsciousness and is the threshold between alpha and theta—a soft, awake brain wave state. This altered state of consciousness has been called different things by different researchers.\r\n    Maury (1848) called it “hypnogogia,” Green, Green, &amp; Walters (1970) called it “the reverie state,” and Budzynski (1977) dubbed it “the twilight state.”</p>\r\n<p>Individuals will often enter this state when daydreaming, resting, meditating, engaging in “mindless” activity (i.e. running, driving long distances), or entering sleep. This state is a calm, relaxed, and unattached presence wherein people report receiving\r\n    imagery, sounds/music, or thoughts of novelty. Einstein reported coming to the notion of this theory of relativity while daydreaming, observing sunbeams and imagining what it would be like to ride on them (Boyd, 1995). Thomas Edison used to intentionally\r\n    induce this state to answer his pressing questions by falling asleep in a chair while holding a ball bearing, with a pie tin placed on the ground underneath his hand. Upon entering light sleep, he would drop the ball bearing onto the pie tin, waking\r\n    him—at which point he would scribble the ideas that arrived in his mind (Robbins, 2000, p. 191). </p>\r\n\r\n<p>In a letter published in 1912, Mozart wrote a colleague about his experience around creativity, music, and this light stage of reverie:</p>\r\n\r\n<p><i>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; When I am . . . completely myself,\r\nentirely alone, and of good cheer—say, traveling in a carriage or walking after\r\na good meal, or during the night when I cannot sleep, it is on such occasions\r\nthat my ideas flow best and most abundantly. Whence and how they come I know\r\nnot, I cannot force them. . . . All this fires my soul, and provided I am not\r\ndisturbed, my subject enlarges itself, becoming methodized and defined, and the\r\nwhole, though it be long, stands almost complete and finished in my mind, so I\r\ncan survey it, like a fine picture or a beautiful statue, at a glance. Nor do I\r\nhear in my imagination the parts successively, but I hear them, as it were, all\r\nat once. What a delight this is, I cannot tell! All this inventing, this\r\nproducing, takes place in a lively dream. (34)</i></p>\r\n\r\n<p>This brain wave state Einstein, Mozart, Edison, and others created their masterpieces in is was likely composed of two frequencies: alpha, which is recorded on an electroencephalogram (EEG) as 9-12 oscillations per second (Hz), and theta, 5-8 oscillations\r\n    per second (Hz).&nbsp; Alpha theta is used for many clientele populations, including &nbsp;peak performance neurofeedback training. This training is a means of inducing in the performer heightened amplitudes and presence of alpha and theta brain wave\r\n    states, theorized to bring about “flow” states, or experiences of “being in the zone.” The goal of this type of neurotherapy is to increase the ratio of theta to alpha, encouraging a crossover, whereby the amplitude of theta brainwaves supersedes\r\n    the amplitude of alpha being produced. In personal neurofeedback practice as clinician, I often incorporate alpha-theta training into neurotherapy sessions once an individual has worked through their major psychological or emotional problems via psychotherapy\r\n    or other forms of neurofeedback, demonstrating self-regulation. Otherwise there is risk in accessing the unconscious memories residing in theta state and bringing them into conscious awareness while the individual is psychologically unprepared. Alpha-theta\r\n    training is like a polish, used once a subject displays evidenced psychological readiness to fine-tune their higher-level functioning skills.</p>\r\n\r\n<p>In Egner and Gruzelier’s 2003 study on the enhancement of musicianship in music conservatoires with the aid of neurofeedback, it was discovered that individuals training alpha-theta brainwave states had a positive trend in three criteria of instrumental\r\n    competence (notably, “perceived instrumental competence, especially rhythmic accuracy”), musicality (notably “stylistic accuracy, interpretive imagination, and expressive range”), and communication (notably “emotional commitment and conviction, ability\r\n    to cope with the stress of the situation and with deportment”), whereas the study’s control group (without any neurofeedback) evidenced no improvements (p. 3). In the conservatoires’ real-life quantification, the neurofeedback recipients also saw\r\n    an average a jump of two class grades. </p>\r\n\r\n<p>Another study testing novice singers’ singing abilities as a result of alpha-theta training found similar results in performance communication (specifically “scales of commitment, confidence, enjoyment, attention holding, and deportment”) as well as in\r\n    the technical areas of “breathing, diction, and pitch.” Lastly, the individuals subject to alpha-theta neurofeedback experienced “increased expressiveness, confidence, and stage presence,” all of which positively corresponded with their respective\r\n    alpha-theta learning indices (Leach et al., 2008). While these studies are exciting and noteworthy, they are the first of few and there remains to be a lack of science linking alpha-theta brainwave states and musical abilities.<i></i></p>\r\n\r\n<p><b>&nbsp;\r\n\r\n</b></p>\r\n<h3><b><a name=\"_Toc35418110\"></a><a name=\"_Toc3535270\">Amplitude</a> Training</b></h3>\r\n<p></p>\r\n<p>Amplitude training was the first neurofeedback “protocol” to be developed, and is uptraining or downtraining the size (or amplitude) of an EEG frequency or range of frequencies. Peak to peak (P – P) and root mean squared (RMS) are measures of a frequency’s\r\n    amplitude from peak to valley. Single channel EEG feedback is usually simple amplitude training, where the individual is suppressing or enhancing frequency bands of delta, theta, alpha, beta, or hight beta. The Neurofield amplitude training is currently\r\n    the only modality that allows for the uptraining of gamma frequencies. In the use of single channel training, a clinician can use ear electrodes as references, or they can use bi-polar training, where one area of the head is trained relative to another\r\n    area of the head. Amplitude training can also be undertaken using a full 19-channel EEG cap. </p>\r\n<h3><a name=\"_Toc35418111\"></a><a name=\"_Toc3535271\">Single Channel  v 19-channel</a></h3>\r\n\r\n<p>At one time in the history of the field, there was a debate as to whether single channel was better than full 19-channel, and vice versa. The difference is the difference in training one to four channel locations, as opposed to training with 19 active\r\n    electrodes. One is not better than the other, and the question to ask is: is it preferable to train the entire brain (based on the client’s presentation and EEG brainmap) or is it preferable to train single channels? There are many single channel\r\n    amplifiers&nbsp; on the market.&nbsp; </p>\r\n<h3><a name=\"_Toc35418112\"></a><a name=\"_Toc3535272\">Z-score Neurofeedback</a></h3>\r\n<p><a name=\"_Toc3535272\"></a></p>\r\n<p><a name=\"_Toc3535272\">Z-score neurofeedeback is used to\r\ntrain the individual towards the “Z of zero.” This means that the individual’s\r\nEEG is bring driven towards the normal range. Z-score neurofeedback can be used\r\nfor measures of coherence, phase, and power differentials in the brain.&nbsp; Providers that offer Z-score training\r\nsoftwares are Brainmaster, Neurofield, and Neuroguide.</a></p>\r\n<p style=\"display: inline !important;\"><a name=\"_Toc3535272\">Live Z-scores can be used either for live assessment or for feedback training, depending on how the system is configured and used. When used for assessment, live Z-scores can be viewed during&nbsp;data&nbsp;acquisition,&nbsp;and&nbsp;can&nbsp;also&nbsp;be&nbsp;recorded&nbsp;and&nbsp;reviewed.\r\nZ-score neurofeedback relies upon a database of neurotypical EEGs as a basis of\r\nrelatively. &nbsp;The z-scores are integrated into the feedback design and they\r\nare used to control displays, sounds, and other information for the purpose of\r\nopreant conditioning and other learning paradigms.<br></a></p>\r\n<p><a name=\"_Toc3535272\"></a></p>\r\n<p><a name=\"_Toc3535272\">In Neuroguide, for instance, the\r\nlive z-scores are monitored using a dynamic JTFA mode (joint time frequency\r\nanalysis), as opposed to a fast fourier transform (FFT), which is more commonly\r\nused for QEEG results (an average of data over time). A Joint time frequency\r\nanalysis allows for instant z-score feedback, providing real-time information\r\nabout the state of the brain. </a></p>\r\n<a name=\"_Toc3535272\">\r\n\r\n    <p>The&nbsp;rapid&nbsp;analysis&nbsp;and&nbsp;feedback&nbsp;of&nbsp;Z-scores is essential for timely feedback. Z-score training can be&nbsp;accomplished&nbsp;with&nbsp;2&nbsp;or&nbsp;4&nbsp;channels&nbsp;of&nbsp;EEG, or with 19 channels. However, the\r\n        live feedback is not the same as those observed using the postprocessed QEEG results.</p>\r\n</a>\r\n<p style=\"display: inline !important;\"><a name=\"_Toc3535272\">When inspecting individual live Z-scores in Neuroguide,&nbsp;it&nbsp;is&nbsp;observed&nbsp;that&nbsp;their&nbsp;&nbsp; &nbsp;typical&nbsp;values&nbsp;are&nbsp;not&nbsp;the&nbsp;same&nbsp;as&nbsp;those&nbsp;observed&nbsp;when&nbsp;using&nbsp;postprocessed&nbsp;QEEG&nbsp;results. This&nbsp;is&nbsp;not&nbsp;a&nbsp;problem&nbsp;or&nbsp;defect&nbsp;in&nbsp;the&nbsp;system,&nbsp;it&nbsp;is&nbsp;a&nbsp;natural&nbsp;consequence&nbsp;of&nbsp;watching&nbsp;a&nbsp;live&nbsp;</a>statistic,&nbsp;versus&nbsp;a&nbsp;static&nbsp;statistic.&nbsp;Live&nbsp;zscores&nbsp;can&nbsp;be&nbsp;used&nbsp;to&nbsp;train&nbsp;a&nbsp;combination&nbsp;of&nbsp;variables&nbsp;including&nbsp;absolute&nbsp;and&nbsp;relative&nbsp;power,&nbsp;power&nbsp;ratios,&nbsp;coherence,&nbsp;phase,&nbsp;and&nbsp;asymmetry.&nbsp;&nbsp;When&nbsp;used&nbsp;in&nbsp;this&nbsp;manner,&nbsp;the\r\n    EEG&nbsp;Biofeedback&nbsp;Training&nbsp;Using&nbsp;Live&nbsp;Z­Scores&nbsp;and&nbsp;a&nbsp;Normative&nbsp;Database system is no longer targeting just a single variable or attribute. Rather, the possibility arises of training the brain in a complex\r\n    multi-dimensional manner, s that it learns a comprehensive brain state.&nbsp;</p>\r\n<p style=\"display: inline !important;\">WIth Z-score training, we can also choose to uptrain or downtrain any components we like, including&nbsp;combinations&nbsp;of&nbsp;components,&nbsp;or&nbsp;relationships&nbsp;between&nbsp;components.&nbsp; So&nbsp;we&nbsp;can&nbsp;train&nbsp;to&nbsp;a&nbsp;Z&nbsp;score&nbsp;of&nbsp;­2&nbsp;or&nbsp;­3,&nbsp;or&nbsp;+2&nbsp;or&nbsp;+3&nbsp;or&nbsp;even&nbsp;+6&nbsp;if&nbsp;we&nbsp;choose.&nbsp;\r\n</p>\r\n<p style=\"display: inline !important;\">Real time Z-score neurofeedback uses instantaneous measures of the EEG data compared to a Gaussian&nbsp;distribution&nbsp;to&nbsp;averaged&nbsp;“instantaneous”&nbsp;time&nbsp;domain&nbsp;spectral&nbsp;measures&nbsp;from&nbsp;groups&nbsp;of&nbsp;normal&nbsp;subjects&nbsp;and&nbsp;then&nbsp;cross­&nbsp;validates&nbsp;the&nbsp;means&nbsp;and&nbsp;standard&nbsp;deviations&nbsp;for&nbsp;each&nbsp;subject&nbsp;for&nbsp;each&nbsp;instant&nbsp;of&nbsp;time.\r\n    <br></p>\r\n<h3><a name=\"_Toc35418113\"></a><a name=\"_Toc3535273\">Wide Band Inhibit (aka “squash”)&nbsp;</a>&amp; Neuroptimal</h3>\r\n<p>Little is known about the mechanism of action in Valdeen Brown’s Neuroptimal. This program is a simple set up, where the active electrodes are placed at C3 and C4 and the references are place on the upper ear cartilage and the ground electrode is placed\r\n    on the ear lobe. The activity of the EEG is measured and displayed (using&nbsp; feedback visual called a “mind mirror”) . The slowest activity measured is 0.1Hz and the fastest is 64 HZ. The frequencies are squashed, overall, and this is thought of\r\n    as a squash protocol to many in the field. As stated on the Neuroptimal website: “The differences in electrical signal are measured in terms of Duration, Intensity, Frequency and Shift and is unique to Neuroptimal. This information is offered back\r\n    to the brain in real time via auditory and visual interruptions of the media.” The Neuroptimal approach involves training both sides of the brain at the same time, over the motor strip, using multiple frequencies and reinforcement tones. There are\r\n    three basic stages of training, and the system alters training frequencies at each stage. The neuroptimal system is dedicated to reducing abnormal variability in the EEG to enhance system integration and functioning.</p>\r\n\r\n<p>The system is described on the website as “a unique and highly expanded Neurofeedback process that is more sophisticated than the antiquated linear approaches that only include the 2-D model of frequency and amplitude as initially founded in the field\r\n    of [NF. As a result, Neuroptimal is able to recognize the incredible natural potential of the brain and give information (or communication) that mirrors what the CNS just did. This information takes the form of mathematical interruptions in the auditory\r\n    and visual fields that offers the individual a “mirror” into their own electrical activity. Thereby reminding the individual to move away from discomfort.” </p>\r\n\r\n<p>The Neuroptimal system is marketed to non-clinical users, noting that brain maps and other means of clinical assessment are not necessary, since the device has not been termed a medical device by the FDA, but instead as a personal wellness device. They\r\n    are explicit that the system does not diagnose, treat, mitigate, prevent, or cure any disease, disorder, or abnormal physical state.</p>\r\n<h2><a name=\"_Toc35418114\">Mind Mirror Neurofeedback, Displaying the\r\nAmplitude on the Y-axis and the frequencies on the X-axis</a></h2><img src=\"@@PLUGINFILE@@/Mind%20Mirror.jpg\" alt=\"Mind Mirror\" width=\"865\" height=\"503\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><a name=\"_Toc35418115\"></a><a name=\"_Toc3535274\">Multi-Variate Training</a></h3>\r\n\r\n<p>Four channel multi-variate training is a type of neurofeedback that Rob Coben invented, which measures and trains coherence between four electrodes. The protocol works when inputs from sensors are transformed into multivariate coherence values across\r\n    all possible combinations of the four locations or sensors. This information makes up the reward band. Additionally, there are three user-defined inhibit hands that encourage a decrease in EEG frequencies, as a form of amplitude training.&nbsp; </p>\r\n\r\nThe multivariate nature of how coherence is calculated comes close to the brain’s noise, itself, and Coben theorizes this makes it easier for the client to train, as opposed to the typical coherence model, where cross correlations between pairs of electrodes\r\nis used (bivariate coherence). The compromise to using pairwise coherence measures include inter-electrode&nbsp;\r\n<p>distance, volume conduction of the brain, and the inability to capture three-dimensional brain activity (Nnez, 1994; Nunes and Srivinasan, 2006).</p>\r\n\r\n<p>This method has been demonstrated on the EEGer Training system (developed by Ed Hamlin). Coben and Myers (2010) have shown that four channel multi-variate training has had greater efficacy than single or dual channel coherence training; they believe that\r\n    one advantage to four-channel multi variate training is the number of electrodes used, as well as the statistical sophistication of what is actually fed back to the client.\r\n</p>\r\n\r\n<p>Coben intends to continue to refine his model of four channel multi-variate coherence training, foreshadowing future enhancements involving functional connectivity. </p>\r\n<p><br></p>\r\n<h3><a name=\"_Toc35418116\"></a><a name=\"_Toc3535277\">HEG</a></h3>\r\n\r\n<p>Hemoencephalography (HEG) is a method of measuring brain function by measuring the brain blood flow. <a href=\"http://www.biocompresearch.org\">Hershel Toomim</a> first coined the term hemoencephalography in 1997. Toomim discovered that the manipulation\r\n    of brain blood flow is voluntary and can be trained using neurofeedback techniques. With the sensor giving feedback of increased blood flow, we can voluntarily increase brain blood flow at the location of the sensor. HEG trains the subject to increase\r\n    blood ﬂow to a targeted area of the brain. Neurofeedback, as we have known it so far, measures the electrical activity of the brain, EEG, as a feedback signal to be controlled by the patient. Here EEG is substituted with blood oxygenation for the\r\n    same purpose.</p>\r\n\r\nThere are two kinds of HEG, pIR and nIR (near infrared), the former is up training temperature and the latter is uptraining oxygen via interaction with an infrared light. Near-infrared HEG (nirHEG): uses a spectrophotometer to measure the oxygenated blood\r\nflow inside&nbsp;<span style=\"font-size: 1rem;\">the skull.\r\nThe bone is translucent and lets light in. The Instrument measures the amount\r\nof blood that\'s carrying oxygen. This is similar to the\r\n\"pulse-oximeter\" that is used as a finger clip in the hospital, and\r\nthat shines a red light through your skin to measure the blood oxygen level.&nbsp;</span><br>\r\n<p>\r\n    The advantage to using the nirHEG is that the elastic band on the head is easily moved to any location on the scalp to train the corresponding area of the brain. HEG is used on the frontal lobes and other areas where skin is showing. it will not work\r\n    when placed on the hair, however. U<span style=\"font-size: 1rem;\">nlike traditional neurofeedback, HEG is not affected by eye blinks\r\nor facial movement which cause distortion when using EEG.</span></p>\r\n<p><span style=\"font-size: 1rem;\">Neurofeedback using this new technique provides\r\na means to exercise selected brain areas. Exercise increases blood ﬂ ow to the\r\nchosen brain module.&nbsp; Capillaries and\r\ndendrites grow with brain exercise (Kaiser 1997, Thompson et al. 1998, Joyce\r\nand Seiver 1997, Rossiter 1996, 1996, Kaiser 1997). An audible tone was devised\r\nthat increased in pitch to signify increased blood oxygenation. To increase\r\noxygenation one would merely attend to the highest note in each trill and will\r\nthe next higher note to sound. Application of the headband and monitoring\r\npatient progress is simple. The treatment process is divided into ten-minute\r\nsegments. Usually three to four such segments constitute a treatment session.<br>\r\n<u>Why\r\nis brain blood flow important?</u><br>\r\nActive areas of the brain are marked by high oxygen density and higher than\r\nnormal temperature. The blood carries the fuel for the brain: oxygen and\r\nglucose. When an area of the brain is more active, it has increased blood\r\nsupply. The brain dilates the capillaries of the area in use to bring more\r\nblood supply. With continued use, more capillaries and more synaptic&nbsp;<span style=\"font-size: 1rem;\">connections\r\nbetween neurons are built in that area. When we increase blood flow, that area\r\nof the brain is able to do it\'s job better and more efficiently.</span>\r\n\r\n    </span>\r\n</p>\r\n<p>Sequential processing, including using language and executing tasks in proper order, takes place in the frontal lobes. Increased blood supply helps the brain accomplish these tasks. </p>\r\n\r\n<p>The frontal cortex is in charge of inhibiting impulses, when appropriate. If the frontal cortex is not functioning well, a person will show a lot of impulsive behaviors. Also involved in this inhibition is control of migraines. <a href=\"http://www.stopmymigraine.com\">Jeffrey\r\nCarmen</a> has shown that when the frontal cortex has increased blood supply, migraine headaches are well controlled. The frontal lobes are important in the function of working memory. Working memory is important for reading comprehension and carrying\r\n    out tasks.</p>\r\n<p></p>\r\n<h3><a name=\"_Toc35418117\">Single Photon Emission Computerized\r\nTomography (SPECT Scan) demonstrating blood flow pre-and post-treatment</a></h3><img src=\"@@PLUGINFILE@@/HEG%20Image.png\" alt=\"HEG Before and After Image\" width=\"679\" height=\"364\" class=\"img-responsive atto_image_button_left\"><br>\r\n<p></p><br>\r\n<p></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><a name=\"_Toc35418118\"></a><a name=\"_Toc3535278\">Othmer Method</a></h3>\r\n\r\n<p>The Othmer method (can be found at eeginfo.com) is recommended for intractable brain based disorders of childhood, such as seizures, conduct disorder, bipolar disorder, spectrum based disorders, pervasive developmental delays, cerebral palsy, birth trauma,\r\n    and acquired birth injuries.&nbsp; Their device is an amplifier, and they rely exclusively on bipolar montages. </p>\r\n\r\n<p>Building primarily on the work of Sterman, they developed a basic and reliable approach to neurofeedback that does not utilize brain mapping. Much of their early techniques involve balancing left and right hemispheres with respect to levels of arousal\r\n    (1999).</p>\r\n\r\n<p>The Othmers now largely proffer &nbsp;a new paradigm called Infra-low Frequency Training that involves training sub-delta frequencies that are actually slow shifts in dc brain potentials. This method involves training in frequency ranges of .0003 Hz or\r\n    lower. Despite considerable controversy over whether present day amplifiers are actually capable of accurately providing data on such low frequencies, the Othmers claim that they have modified their amplifiers to achieve this feat. These slow frequencies\r\n    are thought to be base frequencies of the EEG, also considered frequencies of hemodynamics—or the burning of blood glucose. A large number of clinicians have adopted this approach. It has gained recognition among clinicians for being very effective,\r\n    especially in developmentally challenged children. Mark Smith has adopted a more conservative approach with this paradigm by building on more accepted frequency ranges of .001-.003 Hz or higher that can be easily measured with modern amplifiers. </p>\r\n<p></p>\r\n<h2><a name=\"_Toc35418119\">How does It Work?</a></h2>\r\n\r\n<p>Slow cortical potentials are slow event-related direct-current shifts of the electroencephalogram. Slow cortical potential shifts in the electrical negative direction reflect the depolarization of large cortical cell assemblies, reducing their excitation\r\n    threshold. They change periodically from being electrically positive to electrically negative. They are described as a phasic tuning mechanism related to activities in the brain stem reticular process, the thalamus and the basal ganglia. These dc\r\n    shifts are reflected in the superficial cortical layers and represent synaptic activities in the apical dendrites in those layers. Negative shifts represent increased probability of firing while positive shifts represent decreased probability or inhibition.\r\n    Negative shifts are described as related to the utilization of resources for attention, memory, and other related cognitive mechanisms.</p>\r\n<h3><a name=\"_Toc35418120\"></a><a name=\"_Toc3535279\">At Home Trainers</a></h3>\r\n\r\n<p>There are at home trainers on the market currently, some offered through New Mind Academy (Richard Soutar’s work), others offered through a program called Myndlift, which uses a muse device to train the pre-frontal cortex of the brain. Through this program,\r\n    people are directed through at home use with the assistance of a local clinician. </p>\r\n\r\n<h3><a name=\"_Toc35418121\">LORETA (Low Resolution Electromagnetic Tomographical\r\nAnalysis)</a></h3>\r\n<iframe src=\"https://player.vimeo.com/video/443110917?h=bbd6d9f3ed&amp;color=13979b&amp;title=0&amp;portrait=0\" width=\"640\" height=\"360\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n\r\nWhen recording an EEG, 50% of the data arriving at the site of the electrode is from neurons directly underneath it, and 95% of the data comes from within 6 centimeters distance (that’s a circle with a diameter of 2 <sup>1/3</sup> inches—big) (Nunez,\r\n1982; 1995, Cooper et al., 1965). This is one of the reasons that EEG is limited in terms of what it can determine spatially (i.e. where something lives in the brain). LORETA neurofeedback training is Z-score training that uses three dimensional source\r\nlocalization so that the location within the interior of the brain can be&nbsp;&nbsp;<span style=\"font-size: 1rem;\">pinpointed with accuracies of 1cm. LORETA\r\nneurofeedback is thought to target subcortical structures that are showing\r\ndeviance in the amount of frequency generated.</span>\r\n<p></p>\r\n<p></p>\r\n<h3><br>LORETA Z-score </h3>\r\n\r\n<p>LORETA Z-Score neurofeedback is thought to regulate the deep structures of the brain and improve connectivity between the brain networks through targeting the central voxel within certain regions of the brain. In each session, a cap with 19 sensors is\r\n    applied to your head. During training, your brainwaves learn to become balanced and normalized as they are rewarded.</p>\r\n\r\n<p>The goal of LORETA is to reinforce stability of information processing in dysregulated networks and connections based on the client’s symptoms. It targets the specific areas of the brain and connections between nodes that are linked to the symptoms. In\r\n    doing so it specifically targets deep brain structures that are out of balance. Similar to traditional Neurofeedback (single channel Neurofeedback) training it provides operant conditioning (rewards) based on your brainwaves compared to the brainwaves\r\n    of a healthy population.</p>\r\n\r\n<p>It is possible to train coherence, phase, and power from 88 Brodmann areas in LORETA Z-score neurofeedback. </p>\r\n<p>There are a few ways to choose what regions of the brain to train using LORETA Z-score Neurofeedback. One means is using a symptom checklist, which is created from the patient’s EEG. Another method is using Neurodesigner.</p>\r\n<h2><a name=\"_Toc35418122\">Image from NeuroGuide Z-Score LORETA\r\nNeurofeedback</a></h2><img src=\"@@PLUGINFILE@@/LORETA%20in%20Neuroguide.png\" alt=\"LORETA in Neuroguide\" width=\"762\" height=\"1640\" class=\"img-responsive atto_image_button_text-bottom\"><br><br><br>\r\n<p></p>\r\n<p></p>\r\n<h2><a name=\"_Toc35418123\"></a><a name=\"_Toc3535280\">Neuromodulation protocols</a></h2>\r\n\r\n<p>Neuromodulation is also known as neurostimulation is different than neurofeedback, but fits under the umbrella of neurotherapy. Neurofield’s neurotherapy system is known for the blending of neurostimulation into neurofeedback training. Neuromodulation,\r\n    at the clinical level, is comprised of transcranial alternating current stimulation (tACS), transcranial direct current stimulation (tDCS), transcranial random noise stimulation (tRNS), transcranial pink noise stimulation (tANS) and pulsed electro-magnetic\r\n    field stimulation (PEMF).</p>\r\n<h3><a name=\"_Toc35418124\">Three Stimulation Modalities used in Neuromodulation</a></h3>\r\n<p><a name=\"_Toc35418124\"><img src=\"@@PLUGINFILE@@/Three%20Stimulation%20Modalities.png\" alt=\"Three Stimulation Modalities\" width=\"904\" height=\"912\" class=\"img-responsive atto_image_button_left\"><br></a></p>\r\n<p></p><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><a name=\"_Toc35418125\">Transcranial Alternating Current Stimulation (tACS)</a></h3>\r\n\r\n<p>tACS is a form of electrical stimulation that uses two electrodes (a positive electrode called an anode and a negative electrode, the cathode) to pass current back and forth through either the brain or the body. It is called alternating current because\r\n    the side which is giving and receiving electrons (anode and cathode) continuously switches. Any frequency, or blend of frequencies, can be given with these devices. So, if a patient is in need of more delta, the clinician can stimulate them in the\r\n    delta frequencies. This technology is engineered, developed, and sold through Neurofield, Inc, (founded by Nicholas Dogris and Brad Wiitala). Clinicians use stimulation devices to help their patients heal, recover, and change the behavior of the brain\r\n    and their bodies. As opposed to neurofeedback, neurostimulation shows the brain how to behave and the brain, like a copy cat, mimics the stimulation frequency. </p>\r\n<h3>The NeuroField System</h3>\r\n<p><img src=\"@@PLUGINFILE@@/Neurofield%20System.jpg\" alt=\"Neurofield System\" width=\"700\" height=\"426\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n\r\nIn transcranial alternating current stimulation, one applies current and encourages neural synchronization. As electrons pass through the brain (from anode to cathode) the populations of neurons they go through become more likely to fire. This increased\r\nlikelihood of firing is generalized to the entire area where current is applied. This can cause neurons which were formerly out of phase with each other to align. This happens not just during treatment, but is hypothesized to cause lasting changes to\r\nthe brain. This is called Spike Timing Dependent Plasticity.<br>\r\n<h2><a name=\"_Toc35418126\"><br></a></h2>\r\n<h2><a name=\"_Toc35418126\"><br></a></h2>\r\n<h2><a name=\"_Toc35418126\"><br></a></h2>\r\n<h2><a name=\"_Toc35418126\"><br></a></h2>\r\n<h2><a name=\"_Toc35418126\"><br></a></h2>\r\n<h2><a name=\"_Toc35418126\">The Mechanism of Transcranial Alternating\r\nCurrent Stimulation</a></h2><img src=\"@@PLUGINFILE@@/tACS.png\" alt=\"tACS\" width=\"777\" height=\"415\" class=\"img-responsive atto_image_button_left\"><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\r\n<h3><a name=\"_Toc35418127\">Transcranial Direct Current Stimulation (tDCS)</a></h3>\r\n\r\n<p>tDCS is transcranial direct current stimulation. It is a form of electrical stimulation that is used to treat many conditions and pathologies, both in the brain and in the body. The technology uses a positive and a negative electrode (called the anode\r\n    and the cathode, respectively). Direct current passes a one-way current through the brain or the body. In the brain, a surge in calcium ions and in sodium ions creates a condition of neuroplasticity, which makes the brain more susceptible to neurofeedback\r\n    and pEMF conditioning. tDCS &nbsp;It increases the potential of the brain to change, learn and grow.</p>\r\n\r\ntDCS 1) increases blood flow at the targeted areas and, thus, leads to vaso-profusion (which helps to heal wounds on the brain and the body and also encourages angiogenesis and neurogenesis), 2) causes large scale network organization, 3) stimulates/excites\r\nthe positive electrode site (anode) which increases glutamate and decreases GABA, and inhibits the negative&nbsp;electrode site (cathode) creating more GABA at the site of stimulation, and causes calcium and sodium surges in the glial cells, which leads\r\nto flexibility in polarity shifting. TDCS does not force the brain to fire. Some of the symptoms and pathologies addressed by tDCS include migraines, age-related cognitive decline, and other disorders where the tissues of the brain agree damaged or compromised\r\n(such as cerebro-vascular issues, stroke, and some epileptogenic profiles). tDCS protocols cause the underlying blood vessels to dilate, which allows oxygenation of the affected areas.&nbsp;A recent meta-analysis showed no serios adverse effets on over\r\n1,000 people across 33,200 sessions (Bikson et al., 2016).<br>\r\n<h3><a name=\"_Toc35418128\">The application of transcranial direct\r\ncurrent</a></h3><img src=\"@@PLUGINFILE@@/tDCS.png\" alt=\"tDCS\" width=\"700\" height=\"674\" class=\"img-responsive atto_image_button_text-bottom\"><br><br><br>\r\n<h3><a name=\"_Toc35418129\">Transcranial Random Noise Stimulation</a></h3>\r\n\r\n<p>tRNS is a form of electrical stimulation that is used to pass noise (like the white noise of a television screen) through the brain and/or the body. One way to consider tRNS is as a “Wall of noise”. tRNS is different from tDCS because instead of giving\r\n    steady current from anode to cathode, it is giving current at randomized frequencies and milliamperes between the two sites. This means that the region of the brain between the electrodes are stimulated, increasing neuroplasticity and reducing stuck\r\n    patterns.&nbsp; This is one modality used to unlearn problematic fixed patterns. tRNS has also shown benefit for learning in people with developmental abnormalities. When tRNS stimulation is given during math lessons, it helps more than sham stimulation\r\n    or behavioral therapy.&nbsp;&nbsp; Issues of hyper or hypo coherence and hyper or hypo phase lag are addressed by white noise, in addition, white noise is often used at the first layer of multi-layer protocols. </p>\r\n<h3><a name=\"_Toc35418130\">Different Forms of White Noise Stimulation</a></h3>\r\n<p><a name=\"_Toc35418130\"><img src=\"@@PLUGINFILE@@/Whit%20Noise%20Stim.png\" alt=\"White Noise Stim\" width=\"956\" height=\"346\" class=\"img-responsive atto_image_button_left\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"></a></p>\r\n<h3><a name=\"_Toc35418131\">Pink Noise Stimulation</a></h3>\r\n\r\n<p>Pink Noise is filtered white noise. This form of stimulation affects the restng membrane potneitl and has the same types of de-coupling properties as white noise. It also creates increased blood perfusion. Pink noise appears to have an effect on microstates,\r\n    which are associated with the “on-off” switching of a neuon. In using pink noise, you can saturate a neuron with a failtered set of frequencies, that influence the switching of the neurons, effectively changing the ways that they fire. tRNS is one\r\n    modality that can be used to address stuck patterns, such as thalamo-cortical dysrhythmias (which are found in many hearing disorders, form of mood and affect regulation disorders, some attention deficit disorders, and some movement disorders). Thalamo-cortical\r\n    dysrhythmias are disorders where there is a persistent gamma waveform attached to&nbsp; a slower carrier wave (typically 8hz or less). Pink noise is typically one step in a multi-step protocol.\r\n</p>\r\n<h3><a name=\"_Toc35418132\">The bell curve of pink noise</a></h3>\r\n<p><a name=\"_Toc35418132\"><img src=\"@@PLUGINFILE@@/Pink%20Noise.png\" alt=\"pink noise in NF\" width=\"686\" height=\"426\" class=\"img-responsive atto_image_button_left\"><br></a></p><br>\r\n<p></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"></a></p>\r\n<h3><a name=\"_Toc35418133\"></a><a name=\"_Toc3535282\">pEMF (Pulsed Electro-Magnetic Frequency)</a></h3>\r\n<p></p>\r\n<p><a name=\"_Toc35418130\"></a></p>\r\n<p><a name=\"_Toc35418130\">Pulsed Electromagnetic Field (pEMF)\r\nstimulation is imperceptible, yet the effects are real. pEMF creates an\r\nelectromagnetic field, which allows cells and tissues in its wake to oscillate\r\nat the same frequency. The frequency and duration of the pEMF are important\r\ncomponents of the effectiveness of the treatment. This modality is gentle\r\ncompared to other stimulation technologies. You can\'t feel it because an\r\nelectromagnetic field is generated through a wire coil that flows through the\r\nair and passes through your body effortlessly. One of the happy benefits of\r\npEMF is the increase in blood flow at the site of the stimulation, which can\r\nincrease angiogenesis by way of allowing more oxygen rich blood to make its way\r\nto the site. &nbsp;At low intensity pEMF is safe and has numerous clinical\r\nbenefits, including affecting the resting membrane potential (without the\r\nforced depolarization of the membrane), inflammation reduction, nerve healing,\r\nthe healing of bones, the remediation of depression and other affective\r\ndisorders, and postoperative pain. </a></p>\r\n<p><a name=\"_Toc35418130\">Due to the low-level voltage output of pEMF, it is safe for\r\ninfants, the elderly, and animals. </a></p>\r\n<h4><a name=\"_Toc35418130\">pEMF devices are known for the\r\nability to help reduce pain</a></h4><a name=\"_Toc35418130\"><img src=\"@@PLUGINFILE@@/pEMF%20for%20Pain.png\" alt=\"pEMF for Pain\" width=\"976\" height=\"618\" class=\"img-responsive atto_image_button_left\"><br></a>\r\n<p></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"><br></a></p>\r\n<p><a name=\"_Toc35418130\"></a></p>\r\n<h3><a name=\"_Toc35418134\"></a><a name=\"_Toc3535283\">CES</a></h3>\r\n\r\n<p><b>Cranial</b>&nbsp;electrotherapy&nbsp;<b>stimulation</b>&nbsp;(CES) is a form of neurostimulation that delivers a small, pulsed, alternating current via electrodes on the head. Recently, a systematic review (2018) found insufficient evidence that CES\r\n    has clinically impactful effects on&nbsp;<a href=\"https://en.wikipedia.org/wiki/Fibromyalgia\" title=\"Fibromyalgia\">fibromyalgia</a>, headache, neuromusculoskeletal pain, degenerative joint pain, depression, or insomnia and there is low-strength evidence\r\n    suggesting modest benefit in patients with anxiety and depression (Shekelle et al, 2018)</p>Dave Siever\'s company, Mind Alive creates cranial electric stimulators, that use photic stimulation, as well as ear clips that deliver small stimulation through\r\nthe ear lobes.&nbsp;<br><img src=\"@@PLUGINFILE@@/Mind%20Alive%20hardware.jpg\" alt=\"Mind Alive Hardware\" width=\"713\" height=\"246\" class=\"img-responsive atto_image_button_left\"><br>\r\n<p></p>\r\n<p></p>',1),(386,87,385,0,20,0,1,1,1590169822,0,'References','<p><p>Adnan, Tatheer &amp; Mourdoukoutas, Antonios &amp; Kronberg,\r\nGreg &amp; Truong, Dennis &amp; Boggio, Paulo &amp; Brunoni, Andre &amp;\r\nCharvet, Leigh &amp; Fregni, Felipe &amp; Fritsch, Brita &amp; Gillick, Bernadette\r\n&amp; Hamilton, Roy &amp; Hampstead, Benjamin &amp; Jankord, Ryan &amp; Kirton,\r\nAdam &amp; Woods, Adam. (2016). Safety of Transcranial Direct Current\r\nStimulation: Evidence Based Update 2016. Brain Stimulation. 9.\r\n10.1016/j.brs.2016.06.004.</p>\r\n\r\n<p>Coben, R., and Myers, T. E.\r\n(2010). The relative efficacy of connectivity guided and symptom based EEG\r\nbiofeedback for autistic disorders.&nbsp;<i>Appl. Psychophysiol. Biofeedback</i>&nbsp;35,\r\n13–23. doi: 10.1007/s10484-009-9102-5 </p>\r\n\r\n<p>Nunez, P. (1994).&nbsp;<i>Neocortical\r\nDynamics and Human EEG Rhythms.</i>&nbsp;New York, NY: Oxford University Press.</p><p>\r\nNunez, P., and Srivinasan, R. (2006).&nbsp;<i>Electrical\r\nFields of the Brain: The Neurophysics of EEG.</i>&nbsp;New York, NY: Oxford\r\nUniversity Press, doi: 10.1093/acprof:oso/9780195050387.001.0001</p>\r\n\r\n<p>Shekelle PG, Cook IA,\r\nMiake-Lye IM, Booth MS, Beroes JM, Mak S (2018). \"Benefits and Harms of\r\nCranial Electrical Stimulation for Chronic Painful Conditions, Depression,\r\nAnxiety, and Insomnia: A Systematic Review\".&nbsp;<i>Ann Intern Med</i>.&nbsp;<b>168</b>&nbsp;(6):\r\n414–421.&nbsp;<a href=\"https://en.wikipedia.org/wiki/Digital_object_identifier\" title=\"Digital object identifier\">doi</a>:<a href=\"https://doi.org/10.7326%2FM17-1970\">10.7326/M17-1970</a>.&nbsp;<a href=\"https://en.wikipedia.org/wiki/PubMed_Identifier\" title=\"PubMed Identifier\">PMID</a>&nbsp;<a href=\"https://pubmed.ncbi.nlm.nih.gov/29435567\">29435567</a>.</p><br></p>',1),(387,88,0,0,20,0,1,1,1590172019,1592716148,'Ethical and Professional Conduct','<p></p><p>&nbsp;</p><h2><a name=\"_Toc31009226\">Preamble</a></h2><p>This module covers all ethical and professional considerations for neurotherapy clinicians and technicians. The practice of neurotherapy is both an art and a science. It will vary in terms of approach, modality, method of delivery, and services provided. This chapter covers a code of ethics that neurotherapist need adhere to. When working with patients, may situations can arise; if a situation is not covered in this chapter on ethics, it does NOT mean that ethics do not apply. While the specific wording behind these standards is important, it is the spirit and intent of these standards which must be applied to situations. Violation of these standards by any QEEG-D or neurotherapist ought to be brought to the Attention of the QEEG-D Certification Board, at: iqeegcb@gmail.com and/or 561-247-1347.</p><p>Neurotherapy members are encouraged to apply for membership to either the AAPB (Association of Applied Psychophysiology and Biofeedback) or ISNR (international Society for Neurofeedback and Regulation) for belonging to a larger board and for inclusion in a group of colleagues and professionals engaging in the same business. The professional standards adhered to by the professional organizations of neurofeedback professionals all maintain the highest ethics, values of competence, promotion of intellectual freedom, respect, integrity, honesty, fairness, and trustworthiness.</p><p>Because the trade organizations supporting and advocating for neurofeedback professionals are committed to the protection of human rights, they strive to maintain respect amongst other professional communities, fostered by professionalism, integrity and dignity.&nbsp; Clinicians must hold themselves accountable for their clients welfare as it pertains to the their neurotherapy regimens, and they mist limit their services only to those areas in which they have expertise and are competent.</p><p>&nbsp;</p><p>&nbsp;</p><h1><a name=\"_Toc31009227\">RESPONSIBILITY TO PATIENT WELFARE</a></h1><p>The goal of the neurotherapist is to advance the patient’s well being and maintain their best interests at all times.</p><h3><a name=\"_Toc31009228\">Non Discrimination</a></h3><p>Neurotherapists will not discriminate or deny services to anyone based upon religion, gender identity,&nbsp; sexual orientation, ethic or national origin, race, socioeconomic status, or disability. Within reason, neurotherapists make accommodations to treat all individuals within their scope of practice. If a neurotherapist believes someone is outside of their scope of practice (e.g. an infant), they will do their best to find a suitable referral for those seeking help.</p><p>&nbsp;</p><h3><a name=\"_Toc31009229\">Dual Relationships</a></h3><p>A dual relationship is one that occurs outside of the neurotherapy clinic as a separate and distinct relationship during or after the termination of the neurotherapeutic relationship. Neurotherapists avoid dual relationships with patients that are able to impair professional judgment, as they are aware of their influential position in the patient-therapist dynamic. Not all dual relationships are unethical and some dual relationships cannot be avoided.</p><p><a name=\"_Toc31009230\">Unethical dual relationships</a>&nbsp;are those wherein a therapist borrows money from a patient, hires a patient, engages in business ventures with a patent, or enters a close personal relationship with a patient (this applies to patient’s spouses, partners and family members, as well). Sexual contact, intimacy or intercourse with a patient during the therapeutic relationship or two years following the relationship is unethical and strictly prohibited. If a neurotherapist engages in intimacy with a former patient or their spouse or partner, or immediate family member, within two years of the termination of the patient-therapist relationship, the neurotherapist risks the revocation of their quantitative EEG diplomacy and/or their board certification in neurotherapy. This type of conduct is considered harmful and potentially exploitative to the patient.&nbsp;</p><h4><b>Treatment disruption, abandonment or termination&nbsp;</b></h4><p>It is a neurotherapists professional and clinical responsibility to maintain practices and procedures that assure undisrupted care. This may include providing contact information in case an emergency situation arises while the therapist is away. It is important that a neurotherapist uses clinical judgment when terminating a relationship, as termination must be done in an appropriate manner and based upon sound reason (e.g. the patient is not benefitting from treatment, continuing treatment is no longer beneficial or appropriate, the neurotherapist can no longer provide treatment due to extenuating circumstances, or in order to avoid an ethical conflict or problem). It is unethical to abandon&nbsp; to neglect a patient in treatment; if a therapist is unable to continue providing treatment, they must attempt to provide their patient an alternative health care professional for their accommodation.</p><h2><a name=\"_Toc31009231\">Hygiene</a></h2><p>It is imperative that the neurotherapist maintains a clean and hygienic office for the protection of both clients and staff. This includes all equipment, sensors, pastes and gels used, preventing for cross contamination or any human byproduct (i.e. sweat, saliva, blood, etc.). Attached is a document concerning disinfecting in the time of COVID-19.</p><h3><a name=\"_Toc31009232\">Financial Concerns</a></h3><p>It is unethical for a therapist to maintain a client relationship solely for financial gain, nor is it ethical to terminate a patient relationship for non-payment of fees, unless the termination is handled in a clinically appropriate manner. All services billed by the practitioner must be for clinical services provided directly by the clinician or by their technician.</p><h2><a name=\"_Toc31009233\">At Home Training</a></h2><p>Neurotherapists recommending and enacting at home training are responsible for the patient’s (or patient’s care-takers) education and application of all neurofeedback modalities and their use. Since at home systems involve the neurotherapist not being present, the neurotherapist must take extra precautions to meet their responsibility to their patients.</p><p>Before implementing at home system use, a neurotherapist must consider the competence and capability of a patient or patient’s caretaker to administer treatments from an at home setting, and must be present via an online screen share for the initial training sessions to ensure the equipment and the set-up is appropriate. When at home training occurs, a neurotherapist must inform patients of the risk of at home training, consequences, limitations, and appropriate emergency responses, should a situation emerge. It is the neuerotherapist’s responsibility to ensure the patient signs all appropriate paperwork regarding at home training, its risks, consequences, and potential adverse effects before engaging in at home use.</p><h2><a name=\"_Toc31009234\">Intake</a></h2><p>During the initial intake, a neurotherapist will get written informed consent from their patients and clients when providing clinical services, including a form indicating the patient is aware of the QEEG procedure (if being done) as well as the neurotherapy procedures at hand.</p><h2><a name=\"_Toc31009235\">Disclosures</a></h2><p>A neurotherapist ought to provide clear information about the neurotherapy modalities used in easy to understand language so the patient can make an educated decision about partaking in neurotherapy. It is of paramount importance that the neurotherapist informas their patients of potential risks and benefits of therapy and any common side effects that occur from the treatment modalities they utilize.</p><p>It is strongly recommended that the neurotherapist informs their patient of their background, theoretical and professional orientation, education, training, and modalities of treatment.</p><h2><a name=\"_Toc31009236\">Non-Neurotherapist Roles</a></h2><p>When a neurotherapist acts in a professional role other than the role of a neurotherapy provider (be it psychologist, psychotherapist, nurse, nutritionist, acupuncturist, chiropractor) they are acting soley within that role and may clarify, when necessary, which role they are acting in in order to prevent confusion.</p><h2>Supervisor, Supervisee, Educator and Student Responsibilities</h2>Neurotherapists maintain professional roles and boundaries when in the role of student or supervisor/educator. The supervisor/educator takes seriously their impact on their students and supervisees and, thus, do not exploit the trust and dependency of their supervisees. A neurotherapist does not engage in romantic or sexual relationships with supervisees/students (over whom they exercise professional authority).&nbsp;&nbsp;Other unethical acts include: borrowing money from students, engaging in a close personal relationship with a supervisee, engaging in a businesses venture with a supervisee, barter with supervisees, or engaging in any of the aforementioned with the student’s spouse. It is mandatory that a supervisor maintain their professional skills with recurring courses and trainings.<br><h2>Competence of Supervisee</h2><p>Neurotherapists make sure their supervisees are addressed and taught at the level of their competence and are not providing services before they are clinically capable.</p><p>&nbsp;</p><h2><a name=\"_Toc31009237\">Consultation with Outside Parties and Referrals</a></h2><p>It is important that neurotherapists have access to professional communities of other clinicians doing similar work in the cases that they need to consult, collaborate with, and refer patients out to other professionals, physicians, and community resources. In cases where neurotherapy is not leading to desired results, neurotherapists ought to offer treatment alternatives that are appropriate for the patient’s symptoms.</p><h2>&nbsp;&nbsp;&nbsp;<a name=\"_Toc31009238\">Treatment Decisions and Case Notes</a></h2><p>All mental health care practitioners keep notes of their patient sessions, including the patients subjective state, their demeanor and reported changes or challenges since the last neurotherapy session, as well as the protocol given at the time of the appointment in as much detail as is necessary. This latter form of note keeping may be kept in electronic format, but it is paramount that the neurotherapist maintains a backup copy of the treatments undertaken in the case of computer failure.</p><p>&nbsp;</p><h1><a name=\"_Toc31009239\">Confidentiality</a></h1><p>A neurotherapist is held to the same levels of confidentiality as other mental health care practitioners: all information exchanged by the patient is confidential with these exceptions:</p><p>&nbsp;</p><p>1)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;if the patient is suicidal, in which case the neurotherapist has the obligation of staying with the patient until they can ensure their safety. The therapist may reach out to an emergency contact and ensure the patient is in the care of a close friend, spouse, or relative. If the patient seems unstable, it is the professional obligation of the neurotherapist to see that the patient is taken to the hospital, even if by an involuntary hold (a 5150 code). This may involve the police or calling 911 if the patient is resistant.</p><p>2)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;If the patient is abusing or knows of someone abusing an elderly person or a child (in which case it is the neurotherapists duty to reach out to the proper authorities (e.g. child protective services or the police);</p><p>3)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;If the patient is homicidal or threatening acting against another violently, in which case it is the neurotherapists duty to make sure all endangered parties are informed, by contacting the police.</p><p><b>&nbsp;</b></p><h2><a name=\"_Toc31009240\">Limits of Neurotherapist’s Role and Contact</a></h2><p>&nbsp;A neurotherapists will act solely within the provision of their role as a neurotherapist and within the role of their professional license, if applicable. A chiropractor is free to do chiropractic work, an acupuncturist is free to do acupuncture, a psychotherapist is free to do psychotherapy, etc., but no neurotherapist is allowed to reach beyond the bounds of the professional license with any neurotherapy client. For example, it would be unethical for someone without a license in mental health care to conduct psychotherapy with a patient while doing neurotherapy. The therapist will also purchase liability insurance that covers the extent of their neurotherapeutic work, including all forms of neurostimulation and neurofeedback.</p><h2><a name=\"_Toc31009241\">Competence</a></h2><p>A neurotherapist is expected to practice within the limits of their professional competence, based upon their experience, their education, and their training.&nbsp; It is also the therapist’s role to inform their patients about particular procedures and possible negative effects. A clinician who received the QEEG-D designation ought to have the competence of an intermediate practitioner and it is advised that they pursue their BCIA (Biofeedback Certification International Alliance) certificate before pursuing the QEEG-D or QEEG-T.</p><p>If a professional is serving in the role of a biofeedback or neurofeedback technician or assistant, they will engage in the practice only under the supervision of a qualified professional.&nbsp; Misrepresentation of one’s credentials, training, experience, degrees, or specialty is a violation of ethics and a violation of law in certain circumstances.</p><h2>&nbsp;<a name=\"_Toc31009242\">Treatment Alternatives and Referring Out</a></h2><p>Sometimes a client will seek neurotherapy who would be much better suited by another form of treatment. Sometimes a patient will seek neurotherapy who has a condition that is more severe than the neurotherapist can address or is foreign to the neurotherapist. In other situations a patient may come to a neurotherapist without knowing what is wrong with them, in dealing with a severe situation. In these situations it is the ethical duty of the neurotherapist to consider the client’s best interests and either refer to an appropriate specialist for a more suitable treatment or appropriate assessment and diagnosis.</p><h2><a name=\"_Toc31009243\">Complaints</a></h2><p>If a neurotherapist receives a filed complaint from a client, the board to which the complaint must first be presented is to the clinician’s professional licensure board, be it the American Psychological association, the American Nurses Association, the American Psychiatric Association, the American Medical Association, etc. The professional boards for the practice of neurotherapy, including the International Quantitative EEG Certification Board, The Biofeedback Certification International Alliance (BCIA) Board of Directors, and the Association of Applied Biofeedback and Psychophysiology (AAPB) will be the secondary board to determine whether or not the member failed to comply with either ethical and/or legal requisites.</p><h1><a name=\"_Toc31009244\">Core Professional Values of Neurofeedback Professionals</a></h1><p>&nbsp;</p><p>These core professional values are borrowed from the AAPB Code of Ethics:</p><p>a)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Enhancing human development and improvement through the life span</p><p>b)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Honoring diversity and embracing a multicultural approach in support of the worth, dignity, and uniqueness of people within their social and cultural context</p><p>c)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Promoting social justice</p><p>d)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Safeguarding the integrity of the provider/client relationship</p><p>e)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Practicing in a competent and ethical manner</p><p>&nbsp;</p><br><p></p>',1),(388,89,0,0,20,0,1,1,1590948344,0,'Basic','This module covers an overview of a program that allows you to record, artifact, and analyze EEG.\r\n\r\n<p style=\"text-align: center;\"><iframe src=\"https://player.vimeo.com/video/423291905\" width=\"640\" height=\"399\" frameborder=\"0\" allow=\"autoplay; fullscreen\" allowfullscreen=\"\"></iframe></p>',1),(389,90,0,0,20,0,1,1,1592261381,0,'Lecture on EEG101','<p><a href=\"https://www.youtube.com/watch?v=MTSQCligd4s&amp;feature=youtu.be\">EEG101</a><br></p>',1),(390,85,380,381,20,0,1,1,1593753485,0,'The Wisdom of Morphology and Montaging in EEG','<p><br></p><p><a href=\"https://www.youtube.com/watch?v=dpY2F_2nrAo\">The Wisdom of Morphology and Montaging </a><br></p><p><br></p><p><br></p>',1),(403,2,404,0,20,0,1,1,1614234598,0,'How do I Actually Read EEG? ','<p>This is the big question and, as you gain skill, you will forever find more and more information in the EEG content you are examining. However, first, we begin as green, newbie students. If this is you , embrace this time! Never again will you mind be as clean and uncorrupted when it comes to learning this stuff. A beginner\'s mind is a beautiful thing.&nbsp;</p><p>Here is a video to help you get your sea legs in Reading EEG.&nbsp;</p><p>Enjoy!&nbsp;</p><p><a href=\"https://vimeo.com/457888913\">Learning to Read EEG</a><br></p><p><img src=\"@@PLUGINFILE@@/Chalice.png\" alt=\"Chalice\" width=\"522\" height=\"720\" class=\"img-responsive atto_image_button_left\"><br></p>',1),(404,2,3,403,20,0,1,1,1614234598,0,'How do I Actually Read EEG? ','<p>This is the big question and, as you gain skill, you will forever find more and more information in the EEG content you are examining. However, first, we begin as green, newbie students. If this is you , embrace this time! Never again will you mind be as clean and uncorrupted when it comes to learning this stuff. A beginner\'s mind is a beautiful thing.&nbsp;</p><p>Here is a video to help you get your sea legs in Reading EEG.&nbsp;</p><p>Enjoy!&nbsp;</p><p><a href=\"https://vimeo.com/457888913\">Learning to Read EEG</a><br></p><p><img src=\"@@PLUGINFILE@@/Chalice.png\" alt=\"Chalice\" width=\"522\" height=\"720\" class=\"img-responsive atto_image_button_left\"><br></p>',1),(405,101,0,406,20,0,1,1,1564762933,1655386680,'Concepts of Drug Effects','<ul>\r\n    <li>Individuals may present unique individual effects in the EEG from drugs</li>\r\n    <li>Baseline brain function can either hide or reveal the effects of drugs on the EEG</li>\r\n    <li>Predicting Drug effects is difficult (some drugs produce effects that are inconsistent and variable), although there are response stereotypes to drugs</li>\r\n    <li>Recognizing drug effects is difficult</li>\r\n    <li>Patients taking more than one drug complicates the ease of seeing drug effects in the EEG. Mixtures of drugs become too complex to evaluate any one medication’s contribution, not to mention the synergistic combined effect of many meds</li></ul><p>Here is a video of Jay Gunkelman discussing medication and EEG</p><ul>\r\n  \r\n  <div style=\"padding:56.25% 0 0 0;position:relative;\"><iframe src=\"https://player.vimeo.com/video/438243445?h=4960790efa&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 Gunkelman on MEDICATION\"></iframe></div><script src=\"https://player.vimeo.com/api/player.js\"></script>\r\n</ul>\r\n<p><a href=\"https://vimeo.com/438243445\"><br></a></p>\r\n<p><br></p>',1),(406,101,405,0,20,0,1,1,1564763450,1591211642,'Generalities','Drugs (prescription and otherwise) can have a significant effect on the EEG. Not all brains respond to drugs similarly, however. Arousal level changes the EEG, but this is patient dependent. For example, a stimulation medication will increase alpha levels in an under aroused subject, but will decrease alpha in an over aroused (anxious) subject.<br><br>There is a reciprocal relationship between alpha and beta. If a drug stimulates the brain stem and alpha generators lose their synchronicity, beta appears in the EEG.\n\n\nThere are five classes of drugs that have effects on EEG:\n\n<br><br><ul><ul><li>Street Drugs</li><li>Anti-epileptic drugs/anti-convulsant drugs</li><li>Analgesics (includes opioids)</li><li>Anesthetics</li><li>Psychotropics</li></ul>\n\n\n\n\n</ul>\n\nGABAergic drugs create the greatest changes (benzodiazepines and barbiturates).&nbsp;<br>This will be discussed in the lesson you\'re embarking upon.<br>',1),(407,102,0,0,20,0,0,0,1564764546,1654214292,'Street Drugs','<p><br></p>\r\n<p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/WEED2.jpg\" alt=\"WEED\" width=\"280\" height=\"180\" class=\"atto_image_button_text-bottom\"><img src=\"@@PLUGINFILE@@/WEED3.jpg\" alt=\"WEED\" width=\"270\" height=\"180\" class=\"img-responsive atto_image_button_text-bottom\"><img src=\"@@PLUGINFILE@@/WEED.jpg\" alt=\"WEED\" width=\"270\" height=\"180\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n<p style=\"text-align: center;\"><br></p>\r\n    <p></p>\r\n    <h3><b>Marijuana/Hashish/THC</b></h3>\r\n    <h5>Marijuana and its sister drugs will Increase frontal alpha amplitude, with increased frontal coherence across the hemispheres, as well as phase synchrony.&nbsp; These findings are reported in chronic exposures.</h5>\r\n    <p>Effects on dampening reaction times in evoked potentials have been noted as well.</p>\r\n    <h4>Anteriorized Alpha in Raw EEG and in the QEEG</h4>\r\n    <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/anteriorized%20alpha.jpg\" alt=\"Anteriorized alpha\" width=\"500\" height=\"711\" class=\"img-responsive atto_image_button_middle\"></p>\r\n    <p style=\"text-align: center; \">&nbsp;</p>\r\n    <p><br><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">LSD (Lysergic Acid Diethylamide)</b><br></p>\r\n    <h3><span style=\"font-size: 1rem;\"><span><span><span><b><p><b><img src=\"@@PLUGINFILE@@/LSD%20%281%29.jpg\" alt=\"LSD Effects\" width=\"455\" height=\"300\" class=\"img-responsive atto_image_button_middle\"></b></p></b></span></span>\r\n        </span>\r\n        </span>\r\n    </h3><span style=\"font-size: 1rem;\">The effect of LSD on the EEG is dependent upon the baseline. If the EEG is normal, there is often a decrease in alpha and an increased in beta frequencies.</span><br><br><span style=\"font-size: 1rem;\">With slower EEG backgrounds, there is an\r\n     increase in alpha and beta activity.</span><br><br><span style=\"font-size: 1rem;\">The low voltage fast EEG phenotype shows little change in\r\n     spectral profile with exposure.<br><span style=\"font-size: 1rem;\"><br>An\r\n     increase in </span><i style=\"font-size: 1rem;\">conditioned inhibition is&nbsp;</i><span style=\"font-size: 1rem;\">seen with lower doses, as well as decreased paroxysmal activity.\r\n     The stimulant effects of this powerful drug may cause convulsions at higher doses, such as in the early government studies. In these studies, </span><i style=\"font-size: 1rem;\">milligram</i><span style=\"font-size: 1rem;\"> doses were supplanted for the </span>\r\n    <i style=\"font-size: 1rem;\">microgram</i><span style=\"font-size: 1rem;\"> recommendations from Switzerland, where the LSD was produced (Sandoz).<br></span></span><h3><b>PCP, Phencyclidine, or Angel Dust</b>&nbsp;</h3><span style=\"font-size: 1rem;\"><br>PCP causes a marked increase in slow activity, with paroxysmal activity and extreme voltages noted with increased dosage. Convulsions have been reported.</span>\r\n        <p></p>\r\n        <p><span style=\"font-size: 1rem;\"><br><img src=\"@@PLUGINFILE@@/pcp2.jpg\" alt=\"pcp\" width=\"455\" height=\"324\" style=\"text-align: center; \" class=\"atto_image_button_middle\"><br></span></p><h3><b>Morphine/Opiates/Heroin</b></h3><span style=\"font-size: 1rem;\">Shortly following administration, there is increased alpha, with slowing of alpha during the euphoric high.&nbsp; With increased dose, there is increased slowing, and like barbiturates, the EEG may go iso-electric. There is an increase in REM sleep noted with opiates.</span>\r\n        <p></p>\r\n        <p style=\"text-align: center; \"><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/heroin.jpg\" alt=\"Heroin\" width=\"500\" height=\"250\" class=\"img-responsive atto_image_button_middle\"><img src=\"@@PLUGINFILE@@/morphine.jpg\" alt=\"morphine\" width=\"250\" height=\"190\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"><br></span></p>\r\n        <p><br></p>\r\n        <h3><b style=\"font-size: 1.715rem;\">Isoelectric EEG</b><span style=\"font-size: 1.715rem;\">&nbsp;</span></h3>\r\n        <p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/isoelectric%20EEG.jpg\" alt=\"Isoelectric EEG\" width=\"500\" height=\"301\" class=\"atto_image_button_middle\"></span></p><p><span style=\"font-size: 1rem;\">An isoelectric EEG is defined as complete loss of cortical electrical activity with maximal amplification, if sustained for an hour or more under appropriate clinical circumstances, is highly suggestive of cerebral death.</span></p>\r\n        <p><span style=\"font-size: 1rem;\"></span></p>\r\n        <h2>Alcohol</h2>\r\n\r\n        <p><i><img src=\"@@PLUGINFILE@@/alcohol.png\" alt=\"Alcohol\" width=\"299\" height=\"200\" class=\"img-responsive atto_image_button_left\"><br></i></p><p><i><br></i></p><p><i><br></i></p><p><i><br></i></p><p><i><br></i></p><p><i><br></i></p><p><i>Ethanol</i>&nbsp;at higher levels causes slowing to occur, with the depressant effect seen behaviorally.&nbsp; In the low voltage fast type EEG (seen in anxious, nervous and in many chronic alcoholics and their family members), the initial\r\n            alcohol exposure causes the sudden occurrence of alpha. With severe chronic alcoholism, there can be an abnormal pattern&nbsp;<i>of periodic lateralized epileptiform\r\ndischarges (PLEDS)</i>&nbsp;seen with altered consciousness. This is not true underlying epilepsy, but rather disappears with the treatment of the alcoholism.</p><h4>Quantitative EEG of a Low Voltage Fast Profile, suggestive of excess GABA-A receptor sites&nbsp;</h4>\r\n            <p style=\"text-align: center;\"><br></p>\r\n            <p></p>\r\n            <p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/low%20voltage%20EEG.png\" alt=\"low voltage\" width=\"499\" height=\"427\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n            <p style=\"text-align: center; \"><span style=\"font-size: 1rem;\"><br></span></p>\r\n            <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">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 become over-aroused. This is a prominent 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 variant that is present in about 10% of the population. Typically, their alpha is fast and desynchronized.</span></p>\r\n            <h2 style=\"text-align: left;\">Cocaine&nbsp;</h2>\r\n                <p><img src=\"@@PLUGINFILE@@/coke.jpg\" alt=\"coke\" width=\"400\" height=\"300\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p>\r\n                <ul type=\"disc\">\r\n                    <li style=\"text-align: left;\">Cocaine decreases <i>synaptic\r\n     reuptake</i>, and amphetamines increase the release of the neurotransmitters in the <i>dopamine/norepinephrine</i> systems in the brain.</li>\r\n                    <li style=\"text-align: left;\">With lower to moderate doses, there is increased alpha and beta amplitudes.</li>\r\n                    <li style=\"text-align: left;\">With increased doses, there is a <i>desynchronization</i> of the EEG and faster activity predominates. There is an alpha increase frontally, seen during the euphoric phase of the subjective report.</li>\r\n                    <li style=\"text-align: left;\">Cocaine is a well-known <i>epileptic potentiator</i>.</li>\r\n                    <li style=\"text-align: left;\">Chronic abuse causes a “burned out” dopamine system, with delta decreases and slower alpha noted with little improvement even one year later in Prichep’s Phoenix House study.</li></ul>\r\n                <p></p>',1),(408,103,0,409,20,0,0,1,1588963808,1655386868,'Anti-Epileptic and Anti-Convulsant Drugs','<span style=\"font-size: 1rem;\">Anti-epileptic drugs (AED) and anti-convulsant drugs are most prescribed by neurologists for the treatment of seizures and epileptiform discharges.</span><span><br></span><p></p><h2>Negative/Bad Effects of AED Drugs on EEG</h2>\r\n\r\n<p></p><ul><li><span style=\"font-size: 1rem;\">Diffuse Slowing</span></li><li>Electro-cerebral Inactivity</li><li>Epileptiform Discharges (this is rare)</li></ul><!--[if !supportLists]--><p></p>\r\n\r\n\r\n\r\n\r\n\r\n<h3>Drugs that cause this:</h3>\r\n\r\n<p></p><ul><li>Phenobarbital</li><li>Benzodiazepines</li><li>Carbamazepine</li><li>Phenytoin</li><li>Ethosuximide</li></ul><p></p>\r\n\r\n<h2><a name=\"_Toc14686148\">Positive/Good Effects of AED Drugs on EEG</a></h2>\r\n\r\n<p></p><ul><li>In epilepsy, reduction in generalized Spike and\r\nWave (classic epileptiform EEG)</li><li>In epilepsy, decreased reactivity to\r\nphotoparoxysms with photic stimulation</li></ul><!--[if !supportLists]--><p></p>\r\n\r\n\r\n\r\n<h2>Other Effects of AEDs:</h2>\r\n\r\n<p></p><ul><li>May reduce alpha frequency and voltage</li><li>Diffuse slowing and depressed levels of\r\nconsciousness</li><li>Toxicity produces higher amplitude beta spindles<u style=\"font-size: 1rem;\">&nbsp;(t</u><span style=\"font-size: 1rem;\">his includes anything that induces sleep, anything ending in “azepam” or\r\n“albetol”)</span></li></ul><!--[if !supportLists]--><u></u><p></p>\r\n\r\n<p><u></u></p>\r\n\r\n<p><u></u></p>\r\n\r\n<p>Some types of anti-epileptic drugs for focal\r\nepileptiform discharges can cause seizures, agents that are gabaergic can\r\ninduce absence or myoclonic epilepsy.</p><p></p><h1>Generic AED names with&nbsp;brand names</h1><h4>Carbamazepine&nbsp;also available as&nbsp;Carbagen,&nbsp;Tegretol,&nbsp;Tegretol Prolonged Release</h4><p><br></p><h3>Image of Tegretol pills and chemical bond</h3><p><img src=\"@@PLUGINFILE@@/Carbamazepine%20%281%29.jpg\" alt=\"Carbamazepine\" width=\"500\" height=\"726\" class=\"img-responsive atto_image_button_left\"></p><p>Carbamazepine is a favorite partial seizure medicine in the developed world. Carbamazepine affects sodium channels, and inhibits rapid firing of brain cells. Long-acting forms such as Carbatrol or Tegretol-XR can be given once a day. Potential side effects include gastero-intestinal upset, weight gain, blurred vision, low blood counts, and low blood sodium (hyponatremia). Carbamazepine causes a rash rate of a few percent, sometimes even the dangerous rash called Stevens-Johnson syndrome. People of Asian descent with HLA-B*1502 antigen are more at risk. Typical adult dose is 400 mg tid.&nbsp;</p><p><br></p><p><br></p><p>This is a good choice of AED for slow alpha variants.</p><br><p></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><p><br></p><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4><br></h4><h4>Benzodiazepines and EEG Effects</h4><p>Benzodiazepines produce a spindling, sinusoidal hyper-rhythmic 18-25Hz pattern. They also decrease alpha.&nbsp;<span>Sometimes this pattern is more pronounced in the front of the head, but the pattern can be seen globally.&nbsp;</span><span>Dosing and systemic vascularity of the being will alter the expression of how the drug will appear.</span></p><p style=\"text-align: center; \"><span><audio controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/9796486011639889-audio.ogg\">@@PLUGINFILE@@/9796486011639889-audio.ogg</audio><br></span></p><p style=\"text-align: center; \"><span><br></span></p><p style=\"text-align: center; \"><span><a href=\"@@PLUGINFILE@@/Benzodiazepine%20EEG.mp4\">Benzodiazepine EEG.mp4</a><br></span></p><p><br></p><h3><span>&nbsp;Image of Benzodiazepine Pill Abuse Statistics</span></h3><h4><p style=\"text-align: center;\"><span style=\"font-size: 1.286rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Benzodiazepine%20Abuse%20Statistics.png\" alt=\"Benzodiazepine Abuse Statistics\" width=\"600\" height=\"331\" class=\"atto_image_button_middle\" style=\"font-size: 1.286rem; text-align: center;\"></p><p style=\"text-align: center;\"><br></p></h4><h4><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Image of Different Types of Benzodiazepine Pills</span></h4><p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/Benzodiazepine%20Pills.jpg\" alt=\"Benzodiazepine Pills\" width=\"600\" height=\"291\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: center;\"><br></p><h4><span style=\"font-size: 1.286rem;\"><br></span></h4><h4><span style=\"font-size: 1.286rem;\">Image of Benzodiazepine Toxicity in EEG</span><br></h4><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Benzodiazepines%20in%20the%20EEG.png\" alt=\"Benzodiazepines in the EEG\" width=\"700\" height=\"624\" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: center; \">·&nbsp; &nbsp; &nbsp;&nbsp;</p><h4>Image of Benzodiazepine Toxicity in a Linked Ears Montage. <i>Image generated from Neuroguide version 3.0.6.</i></h4><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/BENZODIAZEPINE%20QEEG.png\" alt=\"BENZODIAZEPINE QEEG\" width=\"700\" height=\"906\" class=\"img-responsive atto_image_button_middle\"><br></p><p></p><p>·&nbsp; &nbsp; &nbsp; &nbsp; &nbsp;</p><p></p><h3><span style=\"font-size: 1.286rem;\">Image of Benzodiazepine Toxicity in individual Hertz bins (linked ears montage). </span><i style=\"font-size: 1.286rem;\">Image generated from Neuroguide version 3.0.6.</i><br></h3><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Benzodiazepines%20in%20individual%20hertz%20bins.png\" alt=\"Benzodiazepines in individual hertz bins\" width=\"700\" height=\"354\" class=\"atto_image_button_middle\"><br></p><p style=\"text-align: center;\"><br></p><p style=\"text-align: center;\"><br></p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Benzodiazepines%20in%20individual%20hertz%20bins2.png\" alt=\"Benzodiazepines in individual hertz bins\" width=\"700\" height=\"351\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><h3>More Anti-Convulstants</h3><h4><br></h4><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\"><img src=\"@@PLUGINFILE@@/Neurontin.jpg\" alt=\"Neurontin Pills\" width=\"400\" height=\"290\" class=\"img-responsive atto_image_button_left\"></span></p><h4>Gabapentin&nbsp;also available as&nbsp;Neurontin</h4><p></p><p>This is often used as a secondary anticonvulsant to boost GABA.&nbsp;Gabapentin has the reputation of being a safe but not particularly powerful AED. The effectiveness criticism probably is because it is often prescribed at too low a dose. The drug probably works by influencing transport of GABA and effects on calcium channels. It has no drug interactions, is not metabolized in the liver and it does not bind to blood proteins. Side effects are unsteadiness, weight gain, fatigue, dizziness. Typical adult dose is 300-600 mg three times a day, but doses can be up to 1200 mg three times a day.</p><p><br></p><h4 style=\"text-align: center;\"><br></h4><p><br></p><p><br></p><h5><img src=\"@@PLUGINFILE@@/Vimpat.jpg\" alt=\"Vimpat\" width=\"401\" height=\"267\" class=\"img-responsive atto_image_button_left\"><span style=\"font-size: 1rem;\"><h4>Lacosamide<span>&nbsp;available as&nbsp;</span>Vimpat&nbsp; &nbsp; &nbsp; &nbsp;</h4></span></h5><p>Lacosamide is a new (2009) antiepileptic drug, for partial and secondarily generalized seizures. It is chemically related to the amino acid, serine. Vimpat blocks sodium channels (but in a different way from other seizure medicines), and this block reduces brain excitability. Side effects include dizziness, headache, nausea or vomiting, double vision, fatigue, memory or mood problems. Vimpat may affect the internal organs, blood counts or heart rhythm, but these potentially serious side effects are infrequent. The recommended starting dose is 50 mg twice daily, increased each week by an extra 100 mg, to the recommended maintenance dosage of 100-200 mg 2x/day.&nbsp; &nbsp;</p><p><br></p><p><br></p><p><br></p><p><br></p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><img src=\"@@PLUGINFILE@@/Lamictal.jpeg\" alt=\"Lamictal\" width=\"400\" height=\"300\" class=\"atto_image_button_left\"></span></p><h4><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Lamotrigine</span><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">&nbsp;also available as&nbsp;</span><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Lamitcal</span></h4><p></p><p>Lamotrigine is a broad-spectrum alternative to VPA, with a better side effect profile. However, lamotrigine may not be as effective for myoclonic seizures. Lamotrigine works by several mechanisms including blocking release of glutamate, the brain’s main excitatory neurotransmitter. It has the usual side effects of dizziness and fatigue, usually mild cognitive (thinking) impairment. Severe medical side effects are unusual. The practical side effect issue is rash, occurring in several percent of people who take it, especially if the dose is increased too fast. Therefore, it takes a couple of months to get up to the typical adult dose of 200 mg twice a day.&nbsp;</p><p>This is the best option for an EEG when the individual has a normal peak frequency alpha.</p><p><br></p><p><br></p><p><br></p><h4></h4><p></p><p><img src=\"https://schoolofneurotherapy.com/classroom/pluginfile.php/472/mod_lesson/page_contents/357/Keppra.jpg\" alt=\"Keppra\" width=\"300\" height=\"200\" class=\"img-responsive atto_image_button_left\"></p><h4><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Levetiracetam</span><span style=\"font-size: 1.286rem;\">&nbsp;also available as&nbsp;</span><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Desitrend</span><span style=\"font-size: 1.286rem;\">,&nbsp;</span><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Keppra</span><br></h4><p>Levetiracetam is one of the more used medicines in seizure clinics because it probably is effective for a broad-spectrum of seizures types, has a relatively low incidence of causing thinking/memory problems, and can be started at 500 mg twice a day, which is an effective dose. It has no drug interactions, is not metabolized in the liver.The most common side effects are dizziness, fatigue, insomnia, but the more troublesome problem can be irritability and mood changes. This may occur to some degree in up to a third of those taking the medicine. A typical adult dose is 500 - 1500 mg twice a day. This is best for epileptic findings that are temporal and generalized.<br></p><p><br></p><p><img src=\"@@PLUGINFILE@@/Ativan.jpg\" alt=\"Ativan\" width=\"400\" height=\"300\" class=\"atto_image_button_left\"></p><h4>Lorazepam (Ativan)</h4>Lorazepam is similar to clonazepam in dosage and action, but it is not as long-acting. It is usually used as a ‘rescue medication’ for patients who frequently have clusters of seizures. Best used&nbsp;for status epilepticus or very short-term management, as it is highly addictive and has dependency&nbsp;potential.&nbsp;It works reasonably quickly when taken orally and anti-seizure effect lasts for 2-6 hours. Typical adult dose is 0.5-2.0 mg orally or as needed.&nbsp;<p></p><h4><br></h4><p><br></p><p><br></p><p><br></p><p><br></p><h3><img src=\"@@PLUGINFILE@@/Oxcarbmazepine.jpg\" alt=\"Oxcarbazepine\" width=\"400\" height=\"300\" role=\"presentation\" class=\"atto_image_button_left\"></h3><h4>Oxcarbazepine<span>&nbsp;also available as&nbsp;</span>Trileptal<span>&nbsp; &nbsp;&nbsp;</span></h4><p>Slightly different from carbamazepine, it is at least as effective and may have fewer side effects, except for more risk for low blood sodium (hyponatremia). It is more expensive than generic carbamazepine. A typical adult dose is 600 mg twice a day. Ideal for people with slow alpha peak frequencies.&nbsp; &nbsp;&nbsp;<br></p><p><br></p><p><br></p><p><br></p><p><br></p><h4><br></h4><h4><br></h4><p><img src=\"@@PLUGINFILE@@/Phenobarbitol.jpg\" alt=\"Phenobarbitol\" width=\"401\" height=\"300\" class=\"img-responsive atto_image_button_left\"></p><h4>Phenobarbital&nbsp;also available as Luminal</h4>The old-timer: very inexpensive and effective in a single daily dose. Phenobarbital increases the effect of GABA, the main inhibitory neurotransmitter in the brain. Watch for sedation, thinking/memory problems and depression. Phenobarbital can cause long-term bone problems. Phenobarbital is mildly addictive and requires slow withdrawal. Phenobarbitol is used for infants.<p></p><h3><br></h3><p><br></p><h4>&nbsp;</h4><p><br></p><h4><br></h4><p><img src=\"@@PLUGINFILE@@/dilantin.jpg\" alt=\"Dilantin\" width=\"300\" height=\"300\" class=\"img-responsive atto_image_button_left\"></p><h4>Phenytoin&nbsp;also available as&nbsp;Epanutin,&nbsp;Phenytoin Sodium Flynn, Dilantin</h4><p></p><p>The most used AED by general physicians in the US, less so by epilepsy doctors, because of the side effects. Phenytoin alters brain cell sodium channels, which has the effect of limiting&nbsp;rapid firing of the brain cells. It is inexpensive. Common side effects are unsteadiness and moderate cognitive problems. There are long-term potential cosmetic (body/face hair growth, skin problems), and bone problems (osteoporosis). Phenytoin causes a rash rate of a few percent, sometimes even the dangerous rash called Stevens-Johnson syndrome. Typical adult dose is 300-400 mg per day, usually with 100 mg pills.</p><p><br></p><h3><br></h3><h3><br></h3><p><img src=\"@@PLUGINFILE@@/Lyrica.jpg\" alt=\"Lyrica\" width=\"400\" height=\"268\" class=\"img-responsive atto_image_button_left\"></p><h4>Pregabalin<span>&nbsp;also available as&nbsp;</span>Alzain<span>,&nbsp;</span>Axalid<span>,</span>&nbsp;Lecaent<span>,&nbsp;</span>Lyrica<span>,&nbsp;</span>Rewisca</h4><p></p><p>A relative of gabapentin, it may be better, and can be given twice a day. Some believe that it is more effective against seizures than is gabapentin. Pregabalin has no drug interactions, no liver metabolism, no protein binding, and similar side effects to gabapentin. Typical adult dose is 150 - 600 mg bid.&nbsp;</p><p><br></p><p><br></p><p><br></p><p><br></p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\"><img src=\"@@PLUGINFILE@@/Banzel.jpg\" alt=\"Banzel\" width=\"359\" height=\"300\" class=\"img-responsive atto_image_button_left\">Rufinamide<span>&nbsp;available as&nbsp;</span>Inovelon<span>, Banzel</span><br></span></p><p>Banzel is approved for add-on treatment of children age 4 and older and adults with&nbsp;Lennox Gastaut Syndrome. This syndrome can include seizure types such as atonic (drop) seizures, tonic (stiffening) seizures, myoclonic (brief jerking) seizures, or staring (absence) seizures, as well as partial seizures. Banzel works on sodium channels in brain cells, in a way to make them less excitable. Common side effects include headache, dizziness, fatigue and sleepiness, double vision and tremor (trembling). People who have the “short QT syndrome,” a rare heart rhythm irregularity, should not take Banzel. The drug comes as 200 and 400 mg tablets.</p><p></p><h4><br></h4><h4><br></h4><h4><br></h4><p><br></p><p><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/Topomax.jpg\" alt=\"Topomax\" width=\"259\" height=\"194\" class=\"img-responsive atto_image_button_left\">&nbsp;</span><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Topiramate</span><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">&nbsp;also available as&nbsp;</span><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Topamax</span></p>A good broad-spectrum AED (i.e., treats all types of seizures). Topiramate has several mechanisms, including blocking the enzyme carbonic anhydrase, which affects the acidity of brain tissue. More acidity (to a point) suppresses seizures. Side effects include thinking and memory problems in about 1/3rd, renal stones in 1-2%, rare cases of glaucoma (increased eye pressure) and weight loss. Typical adult dose is 150-200 mg twice a day.&nbsp;<p></p><h4><br></h4><h4><br></h4><h4><img src=\"@@PLUGINFILE@@/Depakote.jpg\" alt=\"Depakote\" width=\"270\" height=\"172\" class=\"img-responsive atto_image_button_left\"></h4><p></p><h4>Valproic acid&nbsp;available as&nbsp;Depakote, Convulex,&nbsp;Epilim Chrono,&nbsp;Epilim Chronosphere</h4>This is the standard broad-spectrum AED (treats all types of seizures) and no other AED is more effective for generalized seizure types. VPA has effects on GABA (at least in very high doses), and a neurotransmitter called NPY to block seizures, and maybe also on calcium channels. VPA has significant side effects: weight gain, tremor, hair loss, GI upset, blood count decreases, hepatic or pancreatic injury, bone weakness over time (osteoporosis), birth defects in up to 10% (folic acid can help to prevent them). Typical adult dose is 250 mg - 500 mg three times a day, but dose can be higher.&nbsp; This is best used on children\r\n(and for bipolar diagnoses with Lithium)<p></p><p><span style=\"font-size: 1rem;\">&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp;</span></p><p><img src=\"@@PLUGINFILE@@/Sabril.jpg\" alt=\"Sabril\" width=\"401\" height=\"156\" class=\"img-responsive atto_image_button_left\"><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Vigabatrin</span><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">&nbsp;available as&nbsp;</span><span style=\"font-size: 1.286rem; background-color: rgb(255, 255, 255);\">Sabril</span></p><p>At the time of this writing, vigabatrin is approved in the US, but official package insert information has not become available. Vigabatrin is a “designer drug,” made to block metabolism of GABA, the brain’s main inhibitory neurotransmitter. Sabril has been used for over a decade in many countries, and it is effective for partial seizures, with or without secondary generalization. It also may be very effective for infantile spasms, a serious type of seizures in young children. Release in the US was delayed because the drug is toxic to the retina of the eye in up to 30% of people who take it long-term. This toxicity can result in permanent loss of peripheral vision. Regular vision testing is recommended for all people on this drug. A typical regimen begins with 500 mg twice a day, and can increase over a month or two to 1500 mg twice a day.&nbsp;</p><br><br><p></p>',1),(409,103,408,0,20,0,0,1,1588963900,1654214874,'Barbiturates','<p></p><p></p><p>Barbiturates (ending in “barbitol”) are a class\r\nof drugs that were used extensively in the 1960s and 1970s as a treatment\r\nfor&nbsp;anxiety,&nbsp;insomnia, and\r\nseizure disorders. Apart from a few specific indications, they are not commonly\r\nprescribed these days, having been largely superseded by benzodiazepines.</p><p>Barbiturates are sedative drugs, which slow down the central nervous system in a similar way to alcohol. A small dose will make people feel relaxed, sociable and good-humoured. With larger doses hostility and anxiety are common effects and slurred speech, loss of co-ordination and difficulty staying awake may follow. Falling over and accidents become more likely. &nbsp;Injected into a vein barbiturates produce an almost immediate feeling of warmth and drowsiness.</p><p><br></p><p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/barbituates.jpg\" alt=\"Barbituates\" width=\"318\" height=\"239\" style=\"font-size: 1rem;\"></p><br></p><p><span style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.286rem;\">Effects</span><br></p>\r\n\r\n<p>In barbituates, high\r\namplitude rhythmic 18 to 26 Hz activity is noted, initially frontally,\r\nspreading with time to the entire cortex. With increased dose there is an\r\nincrease in slowing, with further increases the faster activity is decreased\r\nand the slowing predominates, progressing to a decreased voltage and even a\r\nrecoverable iso-electric pattern, in <u>barbiturate coma</u>.</p><p>Here are some of the EEG reactions to barbituates:</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Low voltage recording</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Electro cerebal inactivity</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Higher amplitude beta 1 and 2 bandwidth</p>\r\n\r\n<p><!--[if !supportLists]-->-&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Diffuse slowing</p><br><p></p>',1),(410,104,0,0,20,0,1,1,1589236641,1654215106,'Analgesics and Opioids','<p></p><p>An&nbsp;analgesic&nbsp;or&nbsp;painkiller&nbsp;is any member of the group of&nbsp;drugs&nbsp;used to achieve analgesia, relief from&nbsp;pain. Analgesic drugs act in various ways on the&nbsp;peripheral&nbsp;and&nbsp;central&nbsp;nervous systems. They are distinct from&nbsp;anesthetics, which temporarily affect, and in some instances completely eliminate,&nbsp;sensation.</p><p>Analgesics include acetaminophen, the&nbsp;nonsteroidal anti-inflammatory drugs&nbsp;(NSAIDs) such as the&nbsp;salicylates, and&nbsp;opioid&nbsp;drugs such as&nbsp;morphine&nbsp;and&nbsp;oxycodone. They can be highly addictive. Oxycontin, as seen below, was once a widely prescribed drug, but due to the opioid epidemic in America, it has become more regulated.</p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Oxycontin.jpg\" alt=\"Oxycontin\" width=\"420\" height=\"237\"></p><p>Tramadol (yellow and green pills below) is an opiate analgesic – one of the weaker opiate analgesics, it is used to treat moderate to moderate-severe pain.</p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/tramadol.jpg\" alt=\"tramadol\" width=\"300\" height=\"225\" class=\"img-responsive atto_image_button_text-bottom\"></p><h1><a name=\"_Toc14686155\">Opioids</a></h1><p>Opioids include tramadol, oxycodone, morphine, &nbsp;codeine,&nbsp;hydrocodone,&nbsp;dihydromorphine, and pethidine.&nbsp;&nbsp;These medications are known for their addictive properties. Tramadol is an opioid that acts as an SNRI, which occupies a serotonin transporter in the thalamus. This drug can produce a spike wave discharge (giving rise to seizure), however, the more common findings are less remarkable: greater alpha synchrony and somewhat heightened beta amplitudes.</p><p>Effects include:</p><p></p><ul><li>Slowing in the delta range</li><li>&nbsp;Greater alpha synchrony</li><li>Higher amplitde beta</li><li>&nbsp; Burst suppression pattern in neonates</li><li>&nbsp;Enhancement of epileptiform activity</li></ul><p>The below data is a patient with addiction to pain killers, namely tramadol, oxycontin, and hydrocodone.</p><h3><a name=\"_Toc14686156\">The 5 – 6Hz rhythm we see prominent at O2 and T6&nbsp; is a paroxysmal transient that occurs when the patient has closed eyes</a>, opiate addict.</h3><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/5-6hz.png\" alt=\"5-6Hz\" width=\"500\" height=\"732\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p></p><p><br></p><p></p><h5></h5><h3>The slow content that gives rise to seizure activity in an opiate addict is seen as quantified here.</h3><br><h5 style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Slow%20Content.png\" alt=\"Slow Content\" width=\"600\" height=\"383\" class=\"img-responsive atto_image_button_text-bottom\"><br></h5><h5><p>The figure below shows a fast spindling beta\r\nfrequency. This is a kindling frequency, which means that it is this fast\r\nspindling frequency that ultimately leads to the slow transient discharge that\r\nis ultimately the problem. In this case, the spindling beta represents an\r\nirritable cortex—one that is easily “kindled,” meaning that it easily sets off\r\nan epileptic event.</p></h5><h3><br>This fast spindling beta is a sign of an easily kindled cortex, which gives rise to epileptiform content (opioid addict)</h3><p></p><p><br>\r\n\r\n</p><p></p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/beta%20spindles.png\" alt=\"Beta Spindlse\" width=\"600\" height=\"957\" class=\"img-responsive atto_image_button_text-bottom\"></p><p><br></p><h3>Image of high amplitude spindling beta in an opiate addict</h3><p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/map.png\" alt=\"map\" width=\"600\" height=\"377\" class=\"img-responsive atto_image_button_text-bottom\"></p><p>The two figures above show a fast spindling beta frequency. This is a kindling frequency, which means that it is this fast spindling frequency that ultimately leads to the slow transient discharge that is ultimately the problem. In this case, the spindling beta represents an irritable cortex—one that is easily “kindled,” meaning that it easily sets off an event.</p><p><br>\r\n\r\n</p><br><p></p>',1),(411,105,0,0,20,0,1,1,1589237863,1655387086,'Types of Psychotropic Drugs','<p></p>\r\n<p><b>Types of Psychotropic Drugs</b></p>\r\n\r\n<ul type=\"disc\">\r\n    <li>Antidepressants</li>\r\n    <li>Antipsychotics</li>\r\n    <li>Anxiolytics</li>\r\n    <li>Hypnotics</li>\r\n    <li>Mood stabilizers</li>\r\n    <li>Stimulants</li>\r\n</ul>\r\n<p><b>Most Frequently\r\nPrescribed&nbsp;Psychotropic Drugs</b></p>\r\n\r\n<p></p><ul><li>Xanax (alprazolam), 48.5 million.</li><li>Zoloft (sertraline), 41.4 million.</li><li>Celexa (citalopram), 39.4 million.</li><li>Prozac (fluoxetine), 28.3 million.</li><li>Ativan (lorazepam), 27.9 million.</li><li>Desyrel (trazodone HCL), 26.2 million.</li><li>Lexapro (escitalopram), 24.9 million.</li></ul>\r\n    <!--[if !supportLists]--><p></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<h2><a name=\"_Toc14686158\">Anti-depressants</a></h2>\r\n\r\n<p>Antidepressants are grouped into&nbsp;classes&nbsp;based on how they affect the chemistry of the brain. While the antidepressants in a class will tend to have similar side effects and&nbsp;mechanisms of action, there are differences in their molecular\r\n    structures which can influence how well the drug is absorbed, disseminated, or tolerated in different people.</p>\r\n\r\n<p>There are three basic molecules, known chemically as monoamines, that are believed to be involved in mood regulation. These primarily work as neurotransmitters, which literally transmit nerve signals to their corresponding receptors in the brain. Antidepressants\r\n    work by influencing these neurotransmitters, which include:</p>\r\n\r\n<ul type=\"disc\">\r\n    <li><b>Serotonin</b>, the neurotransmitter whose role it is to regulate mood, appetite, sleep, memory, social behavior, and sexual desire</li>\r\n</ul>\r\n\r\n<h4><b>Image of the Chemical Bond of Serotonin</b></h4>\r\n<p></p>\r\n<p style=\"text-align: center;\"><span style=\"font-weight: bold; font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Serotonin.jpg\" alt=\"Serotonin\" width=\"350\" height=\"336\" class=\"img-responsive atto_image_button_middle\" style=\"font-weight: bold; font-size: 1rem; text-align: center;\"><span style=\"font-weight: bold; font-size: 1rem;\">&nbsp;</span></p><span><p style=\"text-align: center;\"><br></p></span>\r\n<p></p>\r\n\r\n<ul type=\"disc\">\r\n    <li><b>Norepinephrine</b>, which influences alertness and motor function and helps regulate blood pressure and heart rate in response to stress</li>\r\n</ul>\r\n<h4><b>Image of the Norepinephrine Chemical Bond</b></h4>\r\n<p></p>\r\n<p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Norepinephrine.jpg\" alt=\"Norepinephrine\" width=\"350\" height=\"294\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><span><p style=\"text-align: center;\"><br></p></span>\r\n<p></p>\r\n<h4><b>Image of the Dopamine Chemical Bond</b></h4>\r\n<p></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Dopamine.png\" alt=\"Dopamine\" width=\"500\" height=\"370\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><span><span style=\"font-weight: 600;\"><p style=\"text-align: center;\"><br></p></span></span><p></p><p><b style=\"font-size: 1rem;\"><b style=\"font-size: 1rem;\">Dopamine</b><span style=\"font-size: 1rem; font-weight: 400;\">, which plays a central role in decision-making, motivation, arousal, and the signaling of pleasure and reward</span></b><br></p>\r\n\r\n<p><br></p><p><u style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">There are five classes of anti-depressants; SSRIs,&nbsp; SNRIs, MAOs, TCAs, &amp; atypical\r\nantidepressants</u><br></p>\r\n\r\n<h3><a name=\"_Toc14686159\">Selective Serotonin Reuptake Inhibitors (SSRIs)</a></h3>\r\n\r\n<p>There are a number of antidepressants that work by preventing the reabsorption (reuptake) of neurotransmitters into the body. Collectively known as&nbsp;reuptake inhibitors, they prevent the reuptake of one or more neurotransmitters so that more are available\r\n    and active in the brain.\r\n</p>\r\n\r\n<p>Selective serotonin reuptake inhibitors&nbsp;(SSRIs) work by specifically inhibiting the reuptake of serotonin. SSRIs are a newer class of antidepressants first developed during the 1970s.</p>\r\n\r\n<p>Examples include:</p>\r\n\r\n<ul type=\"disc\">\r\n    <li>Prozac (fluoxetine)</li>\r\n    <li>Paxil (paroxetine)</li>\r\n    <li>Zoloft (sertraline)</li>\r\n    <li>Celexa (citalopram)</li>\r\n    <li>Luvox (fluvoxamine)</li>\r\n    <li>Lexapro (escitalopram)</li>\r\n    <li>Viibryd (vilazodone)</li>\r\n</ul>\r\n\r\n<p>SSRIs tend to have fewer side effects than older antidepressants but are still known to nausea, insomnia, nervousness, tremors, and sexual dysfunction.</p>\r\n\r\n<p>In addition to treating depressions, SSRIs are also sometimes used to treat obsessive-compulsive disorder (OCD), generalized anxiety disorder (GAD), eating disorders, and premature ejaculations. They have also proved helpful during stroke recovery.</p>\r\n\r\n<h4>Effects</h4>\r\n\r\n<p>These more modern antidepressants have fewer changes in the slow activity (associated with less viscero/autonomic side-effect), with a mild fronto-central beta increase in the range of 18-25 Hz and a decrease in alpha anteriorly.</p>\r\n<p>Here is a short video on SSRIs</p>\r\n<p>&nbsp;<a href=\"https://www.youtube.com/watch?v=uiXcAbrO8kU\">SSRI Video</a><br></p>\r\n\r\n<h3><a name=\"_Toc14686160\">Serotonin and\r\nNorepinephrine Reuptake Inhibitors (SNRIs)</a></h3>\r\n\r\n<p>Serotonin and norepinephrine reuptake inhibitors&nbsp;(SNRIs) work in a similar way to SSRIs except that they inhibit the reuptake of both norepinephrine and serotonin. The first SNRI was FDA-approved in December 1993.</p>\r\n\r\n<p>Increasing norepinephrine levels in tandem with serotonin levels can be particularly useful or people with&nbsp;psychomotor retardation&nbsp;(the slowing of physical movement and thought).\r\n</p>\r\n\r\n<p>Examples of SNRIs include:</p>\r\n\r\n<ul type=\"disc\">\r\n    <li>Effexor (venlafaxine)\r\n    </li>\r\n    <li>Cymbalta (duloxetine)\r\n    </li>\r\n    <li>Pristiq (desvenlafaxine)\r\n    </li>\r\n    <li>Savella (milnacipran)\r\n    </li>\r\n    <li>Fetzima (levomilnacipran)\r\n    </li>\r\n</ul>\r\n\r\n<p>Common side effects of SNRIs include nausea, drowsiness, fatigue, constipation, and dry mouth.</p>\r\n\r\n<p>Some SNRIs, like Cymbalta, can also be used to treat chronic pain, a condition closely linked to the development of depression. They have also proven useful in treating generalized anxiety, post-traumatic stress disorder (PTSD), social anxiety disorder\r\n    (SAD), panic disorder, and nerve pain associated with fibromyalgia.</p>\r\n\r\n<p>If the frontal lobe has regular frequency alpha seen in excess, especially with eyes-closed frontal alpha hypercoherence, then in our experience, an SSRI or an SNRI may be used to increase frontal function.</p>\r\n<p>Here\'s a video on how SNRIs work</p>\r\n<p><a href=\"https://www.youtube.com/watch?v=FrE7nfqlBjs\">SNRI Video</a><br></p>\r\n\r\n<h3><a name=\"_Toc14686161\">Tricyclic\r\nAntidepressants (TCAs)</a></h3>\r\n\r\n<p>Tricyclic antidepressants&nbsp;(TCAs) are an older class of drug first discovered in the 1950s. They were named after their chemical structure, which is composed of three interconnected rings of atoms.</p>\r\n\r\n<p>TCAs work similarly to reuptake inhibitors in that they block the absorption of serotonin and norepinephrine into nerve cells, as well as another neurotransmitter known as&nbsp;acetylcholine&nbsp;(which helps regulate the movement of skeletal muscles).</p>\r\n\r\n<p>Examples of TCAs include:</p>\r\n\r\n<ul type=\"disc\">\r\n    <li>Elavil (amitriptyline)**</li>\r\n    <li>Norpramin (desipramine)</li>\r\n    <li>Asendin (amoxapine)</li>\r\n    <li>Anafranil (clomipramine)</li>\r\n    <li>Pamelor (nortriptyline)</li>\r\n    <li>Tofranil (imipramine)*</li>\r\n    <li>Vivactil (protriptyline)</li>\r\n    <li>Surmontil (trimipramine)</li>\r\n    <li>Sinequan (doxepin)</li>\r\n</ul>\r\n\r\n<h4>Effects</h4>\r\n\r\n<p><b>*Imipramine</b></p>\r\n\r\n<p>This drug produces an increase in slow activity, a decrease in alpha 1 and 2 amplitude, and an increase in the faster beta frequencies in the mid to upper 20 Hz range and up.</p>\r\n\r\n<p>**<strong>Amitriptyline</strong></p>\r\n<p>This drug produces more slowing than imipramine, though the other effects are similar. This corresponds to an increased initial sedative effect and its use as a sleeping medication for sleep onset as well as the usual wakefulness effects of antidepressants.\r\n    In epileptics, there are increases in paroxysmal discharges, which can be controlled normally with adjustments to the anti-epileptic medications.</p>\r\n\r\n<p>In addition to their use in depression, tricyclic antidepressants can help treat chronic pain. They were also once commonly used in children with attention deficit hyperactivity (ADHD) but have since been replaced with more effective drug agents with\r\n    fewer side effects.</p>\r\n<p>Here\'s a video on Tricyclic antidepressants</p>\r\n<p><a href=\"https://www.youtube.com/watch?v=lzcYPKjjQvY\">Tricyclic Antidepressants</a><br></p>\r\n\r\n<h3><a name=\"_Toc14686162\">Monoamine\r\nOxidase Inhibitors (MAOIs)</a></h3>\r\n\r\n<p>One of the first classes of antidepressants developed were&nbsp;\r\n    <a href=\"https://www.verywellmind.com/monoamine-oxidase-inhibitors-maois-2584303\">monoamine\r\noxidase inhibitors</a>&nbsp;(MAOIs). This antidepressant class, first discovered in the 1950s, inhibits the action of an enzyme called monoamine oxidase, whose role it is to break down monoamines. By blocking this effect, more neurotransmitters are\r\n    available for use in mood regulation.\r\n</p>\r\n\r\n<p>Examples of MAOIs include:\r\n</p>\r\n\r\n<ul type=\"disc\">\r\n    <li>Nardil (phenelzine)</li>\r\n    <li>Parnate (tranylcypromine)</li>\r\n    <li>Marplan (isocarboxazid)</li>\r\n    <li>Emsam (selegiline)</li>\r\n</ul>\r\n\r\n<p>MAOIs have proven useful in treating&nbsp;agoraphobia, social phobia,&nbsp;bulimia, PTSD, borderline personality disorder, and bipolar depression. Even so, its use is usually reserved for when other antidepressant options have failed.</p>\r\n\r\n<h4>Effects</h4>\r\n\r\n<p>These medications have a wider variation of response than the other antidepressants.&nbsp;\r\n    <em>Isocarboxazide</em>&nbsp;increases 30-20 Hz and decreases slower and higher frequencies, similar to a stimulant profile.&nbsp;<em>Nialamide and Tranylcypromine\r\nproduce</em>&nbsp;a more typical profile, though with more variability.</p>\r\n\r\n<h3><a name=\"_Toc14686163\">Atypical\r\nAntidepressants</a></h3>\r\n\r\n<p>There are also other fairly new antidepressants that do not fit into any of the above-listed categories. Broadly described as atypical antidepressants, they affect serotonin, norepinephrine, and dopamine levels in unique ways.&nbsp;&nbsp;</p>\r\n\r\n<p>Examples of include:</p>\r\n\r\n<ul type=\"disc\">\r\n    <li>Wellbutrin (bupropion), classified as a&nbsp;\r\n        <strong>dopamine reuptake inhibitor</strong>, is used to treat depression and seasonal affective disorder as well as a smoking cessation aid.\r\n    </li>\r\n    <li>Remeron (mirtazapine) is a&nbsp;<strong>noradrenergic antagonist&nbsp;</strong>used for major depression, that blocks receptors of the stress hormone epinephrine (adrenaline) on the brain.</li>\r\n    <li>Oleptro (trazodone) and Brintellix (vortioxetine) are&nbsp;<strong>serotonin antagonist and reuptake\r\n     inhibitors&nbsp;</strong>(SARIs) used for major depression the both inhibit serotonin reuptake and block adrenergic receptors.</li>\r\n    <li>Symbax combines the SSRI fluoxetine with the antipsychotic drug fluoxetine to treat bipolar depression or treatment-resistant depression.</li>\r\n</ul>\r\n\r\n<p>Side effects can vary by drug type but may include dizziness, dry mouth, insomnia, nausea, vomiting, constipation, blurry vision, weight gain, and sexual dysfunction.</p>\r\n\r\n<h1><a name=\"_Toc14686165\">Anesthetic &amp; Sedative Medication</a> </h1>\r\n<p><a name=\"_Toc14686165\"></a></p>\r\n<p><a name=\"_Toc14686165\">An&nbsp;<b>anesthetic</b>&nbsp;(American English) or&nbsp;<b>anaesthetic</b>&nbsp;(British English;&nbsp;see spelling differences) is a&nbsp;drug&nbsp;used to induce&nbsp;anesthesia&nbsp;- in other words, to result in a temporary loss of&nbsp;sensation&nbsp;or&nbsp;awareness. They may be divided into two broad classes:&nbsp;general anesthetics, which result in a reversible loss of&nbsp;consciousness, and&nbsp;local anesthetics, which cause a reversible loss of sensation for a limited region of the body without necessarily affecting consciousness.</a></p>\r\n<p><a name=\"_Toc14686165\">A wide variety of drugs are used in modern anesthetic practice. Many are rarely used outside&nbsp;anesthesiology, but others are used commonly in various fields of healthcare. Combinations of anesthetics are sometimes used for their&nbsp;synergistic&nbsp;and&nbsp;additive&nbsp;therapeutic effects. Adverse effects, however, may also be increased.&nbsp;Anesthetics are distinct from&nbsp;analgesics, which block only sensation of&nbsp;painful&nbsp;stimuli.</a></p><h2><a name=\"_Toc14686166\">Effects (most volatile)</a></h2>\r\n\r\n<p></p><ul><li>Marked drop in gamma band activity (25 – 50Hz)</li><li>Increase in theta/delta frequencies&nbsp; (<u style=\"font-size: 1rem;\">Theta</u><span style=\"font-size: 1rem;\"> comes from inhibition of normal thalamic pacemaker cells, </span><u style=\"font-size: 1rem;\">Delta</u><span style=\"font-size: 1rem;\"> results from extreme depression of the thalamus). &nbsp;</span><b style=\"font-size: 1rem;\">Anesthetics</b><span style=\"font-size: 1rem;\">&nbsp;and their combinations which affect GABA</span><sub>A</sub><span style=\"font-size: 1rem;\">&nbsp;receptors\r\n    creates slowing that can mimic slow wave sleep, with burst suppression at higher concentrations</span></li><li>Increase in the power of the frontal electrodes (\r\n    <u style=\"font-size: 1rem;\">Beta</u><span style=\"font-size: 1rem;\">: is the result of sensory stimuli influencing the reticular activating system with desynchronization of thalamic pacemakers, maximal in the prefrontal regions)</span></li><li>Marked increase in hypercoherence/synchrony</li></ul>\r\n\r\n<p><span>Each anesthetic agent will have a different effect\r\non the EEG. Their profile will change the closer they get to isoelectric.\r\nIncreasing the dose of anesthetics will produce slowing, then burst\r\nsuppression, then electro-cerebral silence (isoelectric EEG) </span></p>\r\n\r\n<p><span>These maps are a patient who was in a car accident and\r\nwas taking a combination of pain management medications. The blending of\r\nsedatives and hypnotics tends to produce an excessive slowing in the EEG.</span></p>\r\n<a href=\"https://www.youtube.com/watch?v=T25jvLC6X0w\">\r\n    <h3><span><span style=\"\">Excessive slowing in the theta band as a result of combining\r\nhypnotics and sedatives</span>.<i> Image\r\ngenerated from Neuroguide version 3.0.6.</i></span>&nbsp;</h3></a><p style=\"text-align: center;\"><br></p><p style=\"text-align: center;\"><a href=\"https://www.youtube.com/watch?v=T25jvLC6X0w\" style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/sedatives.png\" alt=\"sedatives and hypnotics\" width=\"500\" height=\"662\" class=\"img-responsive atto_image_button_middle\"></a></p><br><br><span><span>Excessive slowing into the theta band as a result of\r\ncombining hypnotics and sedatives.</span>&nbsp;</span><i style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">Image generated from Neuroguide version 3.0.6.<br></i><br>\r\n    <p style=\"text-align: center;\"><br></p>\r\n    <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Meds2.png\" alt=\"Meds2\" width=\"500\" height=\"448\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_middle\"></p>\r\n    <h1><a name=\"_Toc14686167\">Stimulants</a> </h1><p><a name=\"_Toc14686167\"></a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;Used for ADHD disorders mainly</a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;Different ADHD profiles:</a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;High theta/beta ratio or theta/alpha ratio</a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;Higher relative theta</a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;Frontal spindling beta</a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;Mu rhythm</a></p><p><a name=\"_Toc14686167\">o&nbsp;&nbsp;&nbsp;Temporal lobe alpha</a></p><p></p>\r\n\r\n    <p><img src=\"@@PLUGINFILE@@/Adderall.jpg\" alt=\"Adderall\" width=\"400\" height=\"603\" class=\"atto_image_button_middle\"><br></p>\r\n\r\n    <h2><a name=\"_Toc14686168\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Effects of Stimulants</a><br></h2>\r\n\r\n    <p></p>\r\n    <ul>\r\n        <li>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Normalization of EEG</li>\r\n        <li>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; No change from baseline</li>\r\n        <li>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Decrease in theta, theta/alpha, and theta/beta ratios</li>\r\n        <li>&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; Increase in beta amplitudes</li>\r\n    </ul>\r\n    <p></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n    <p>Stimulants increase the activity in the RAS, with the Raphe nucleus releasing norepinephrine, decreasing the polarization in the reticular nucleus of the thalamus and thus increasing the “clocking” or peak frequency of the rhythmic alpha activity\r\n        and increasing faster activity.</p>\r\n\r\n    <p><strong>Amphetamines:</strong>&nbsp;Both&nbsp;<em>dextro and methamphetamines</em>&nbsp;like&nbsp;<em>Dextrostat or Adderal</em>&nbsp;are similar in effect, with decreased slower activity and increased beta from 12-26 Hz. There is a paradoxical increase\r\n        in alpha noted in the QEEG work of Itil (Itil et al., 1980). This is likely from the increased activation effect mentioned in the opening section.</p>\r\n\r\n    <p><strong>Methylphenidate:</strong>&nbsp;<em>Ritalin</em>&nbsp;produces a decrease in delta and theta, with a more pronounced posterior alpha increase and an increase in low beta, with effects delayed up to 6 hours, compared to the rapid effects of\r\n        the amphetamines.</p><br>\r\n    <p></p>',1),(412,106,0,0,20,0,1,1,1588619495,1654230219,'Part 1: Fundamentals of Neuroanatomy','<p></p>\r\n<h4 style=\"text-align: center; \">\r\n    <p style=\"text-align: left;\"><a style=\"color: rgb(55, 71, 79); background-color: rgb(255, 255, 255);\">The Central Nervous System (CNS)</a></p>\r\n    <p style=\"text-align: left;\"><span>The central nervous system includes the brain (contained within the skull), which weighs 1.3–1.4 kg in humans, and also the spinal cord, which extends into the vertebral canal. The brain is grossly divided into the brainstem, cerebellum, and cerebrum. The cerebrum is further divided into the basal ganglia, limbic system, and neocortex.</span></p>\r\n</h4>\r\n<h4 style=\"text-align: center; \"><br><img src=\"@@PLUGINFILE@@/CNS.jpg\" alt=\"Central Nervous System\" width=\"424\" height=\"839\" class=\"img-responsive atto_image_button_middle\">\r\n    <p style=\"text-align: left;\"><a style=\"color: rgb(55, 71, 79);   background-color: rgb(255, 255, 255);\"><b>Spinal cord</b></a></p>\r\n    <p style=\"text-align: left;\"><span style=\" text-align: center;\">The spinal cord descends from the brain stem down through the shielded tunnel of the vertebrae,  and transmits information from the body to the brain and from the brain to the body. Thus, the central nervous system is composed of nerves the are rooted to both the surface of the brain, as well as to the spinal cord. Most nerves are peripheral nerves, which extend and branch toward the surface of the body.</span></p>\r\n    <img src=\"@@PLUGINFILE@@/Spinal%20Cord.jpg\" alt=\"Spinal Cord Anatomy\" width=\"600\" height=\"760\" class=\"atto_image_button_middle\"><i><br></i><i><br></i><i><br></i><i><br></i><i><br></i><i><img src=\"@@PLUGINFILE@@/Peripheral%20Nervous%20System.jpg\" alt=\"Peripheral Nervous System\" width=\"723\" height=\"917\" class=\"img-responsive atto_image_button_middle\"></i></h4>\r\n<p>The brain grows, layer upon layer, like an onion. Brain cells generating grab onto a guidewire, which is a glial fiber, a glial highway, with the nucleus in the back. No other kind of cell has to do this.</p>\r\n<div>\r\n    <p><span>Neurons travel in waves, which scientists call <span>migration</span>.  In terms of the distances relative to their size, they are making an odyssey, without mistakes telling them where to go in the brain.</span></p>\r\n    <p>Here is a cool video made by the Pasterkamp lab, outlining the signaling events and molecular mechanisms involved in the formation of neuronal connections during development.<br></p>\r\n    <p><a href=\"https://www.youtube.com/watch?v=ZWACm6BkDVo\">Pasterkamp Labs</a><br></p>\r\n\r\n    <h2>The Triune Brain Theory</h2><br>\r\n    <p></p>\r\n    <p></p>\r\n    <p>The triune brain was first described by Maclean in 1990, as consisting of three layers that depict our evolution individually as a species.  The first layer is the reptilian brain (its core), responsible for activation, arousal, homeostasis,\r\n        and reproductive drives. This is the dinosaur brain, the same brain that has been around for 2,000,000 years. The reticular formation at the conjunction of the thalamus and the brainstem oscillates at 2Hz (delta) {Thatcher, 2015). At birth,\r\n        this structure is already in place and fully functional.</p>\r\n    <p><br></p>\r\n    <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/triune%20brain.jpg\" alt=\"Triune Brain\" width=\"699\" height=\"455\" style=\" \" class=\"img-responsive atto_image_button_middle\"></p>\r\n    <p></p>\r\n    <p></p>\r\n    <p>The reptilian brain controls the body’s most basic, involuntary actions, like a heartbeat, breathing, body temperature regulation, and balance. It consists of the brainstem and the cerebellum (which joins the limbic thalamus by the reticular activating\r\n        system). The cerebellum is the most densely packed area; surprisingly, this is where 80% of the brain’s neurons live (Herculano-Houzel, 2010). Used mostly for gross movements and balance, parts of the cerebellum are involved in the coordination\r\n        of language, memory, and reasoning (Schmahmann, 1997). Interestingly, new literature suggests that the cerebellum plays a significant role in regulating the cerebrum, both via white matter (sub-cortically) and via grey matter (cortically)\r\n        (Schmahmann, 1997, 1998, 2000; Teicher, Anderson, &amp; Polcari, 2012). This is the part of the brain that is cradled by the hand of a loving mother, and the part of the brain that also unconsciously senses the absence of her hand, in situations\r\n        of neglect (Fisher, 2014, p. 23).</p>\r\n    <p><br></p>\r\n    <h2><a name=\"_Toc28940388\"></a><a name=\"_Toc3535195\">Brainstem</a></h2>\r\n    <p>The brainstem is responsible for carrying all information from the body to the cerebrum and cerebellum (hindbrain) and from the brain to the body. The pathways ascending from the body to the brain are the sensory pathways and communicate to your brain\r\n        that which is going on with the body (pain, hunger, desires, temperature, sensations, etc). The descending pathways move from the brain to the body. The last job of the brain stem is its regulation of various systems, such as your cardiovascular\r\n        system, respiratory system, pain sensitivity controls, as well as alertness, and consciousness.</p>\r\n    <p><b>The medulla oblongata</b> or simply <b>medulla</b> is a long stem-like structure which makes up the lower part of the brainstem. It is anterior and partially inferior to the cerebellum. It is a cone-shaped neuronal mass\r\n        responsible for autonomic (inv<span style=\" \">oluntary) functions, ranging from </span><span style=\" \">vomiting</span><span style=\" \"> to </span><span style=\" \">sneezing</span>\r\n        <span style=\" \">.</span><span style=\" \"> The medulla contains the </span><span style=\" \">cardiac</span><span style=\" \">, </span><span style=\" \">respiratory</span>\r\n        <span style=\" \">, </span>\r\n            <span style=\" \">vomiting</span><span style=\" \"> and </span><span style=\" \">vasomotor</span><span style=\" \"> centers, and therefore deals with the autonomic functions of </span>\r\n            <span style=\" \">breathing</span>\r\n                <span style=\" \">, </span><span style=\" \">heart rate</span><span style=\" \"> and </span><span style=\" \">blood pressure</span><span style=\" \">. The sleep wake cycle is associated with the pons.</span></p>\r\n    <p><span style=\" \"><img src=\"@@PLUGINFILE@@/Medulla%20Oblongata.jpg\" alt=\"Medulla oblongata\" width=\"500\" height=\"378\" class=\"img-responsive atto_image_button_middle\"><br></span></p>\r\n    <p>The brainstem plays a primary role in conduit functions. That is, all information related from the body to the cerebrum and cerebellum and vice versa must traverse the brain stem. The ascending pathways coming from the body to the brain are the sensory\r\n        pathways. Descending tracts are upper motor neurons destined to synapses on lower motor neurons. The brain stem also has integrative functions. It is involved in cardiovascular system control, respiratory control, pain sensitivity control, alertness,\r\n        and consciousness.</p>Here is a short video on the anatomy of the brainstem.\r\n    <p></p>\r\n    <p> <a href=\"https://www.youtube.com/watch?v=T2zjlB4ctu4\">brainstem</a><br></p>\r\n    <p></p>\r\n    <h2><a name=\"_Toc28940390\">THE LIMBIC SYSTEM</a></h2>\r\n    <p>After the reptilian brain is formed, the next layer, the paleomammalian brain, better known as the limbic system, is primed and ready to be further developed by early life experiences. This area is largely responsible for the functions of memory,\r\n        learning, and emotion. This second layer is responsible for basic autonomic functioning, as well as reflexes, and basic survival (DeRidder, 2014). The proliferation of the limbic system created higher frequencies, such as theta and alpha. The\r\n        limbic structures include the amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus. These limbic structures are wrapped in the cerebral cortex, which is the outermost and third layer of the brain.</p>\r\n    <p><img src=\"@@PLUGINFILE@@/Limbic%20System.png\" alt=\"Limbic System\" width=\"600\" height=\"357\" class=\"atto_image_button_middle\"><br></p>\r\n    <p>From an evolutionary perspective, the reptilian brain is fully functional at birth and the second layer—the limbic system—is prepared for the organizational experiences of early life. The neuronal development of the brain’s first and second layers\r\n        are virtually complete at birth; the branching of dendrites that occurs thereafter is dubbed “wiring,” since the growth of neurons and dendrites resembles wires (Seung, 2012). The wiring and creation of oligodendrocytes (glia cells \r\n        <span style=\" \">responsible for myelination) now occurs from the limbic structures into the cortex. The self-reliance of the brain circuits has increased as we have evolved, and have moved to higher levels in the brain, ones that have less and less contact with\r\n            sensory inputs.</span>\r\n    </p>\r\n    <p>Most of our significant early emotional and intellectual experiences, those that shape our later perceptions and reactions, occur when the limbic and reptilian structures are in dominance (Cozolino, 2002, p. 9). That is to say, many of our social-emotional\r\n        reactions and behaviors are literally programmed beneath the surface of our consciousness. Indeed, empirical evidence suggests that processing emotion can occur without conscious awareness (Balconi &amp; Lucchiari, 2008; Bunce, Bernat, Wong, &amp;\r\n        Shevrin, 1999; LeDoux, 1998a). What you smell goes directly into the limbic system, smell is the only sense that is not mediated by the thalamus. Head damage or virus (such as COVID-19) can affect this system, preventing the capability of smell.\r\n        Severance of this connection is common in severe head trauma.</p>\r\n    <p>The sense of smell is tied directly to memory and emotion because the olfactory blub connect directly to the hippocampus, the seat of memory. Smells can create emotion because the olfactory projections link into the limbic system and the amygdala.</p>\r\n    <p> </p>\r\n    <h3><a name=\"_Toc28940391\">Neuroanatomy of the Limbic System</a></h3>\r\n    <p><b> </b>The amygdala is located within the temporal lobes. It is essential to the experience of fear responses and its primary function is arousal. This complex structure controls the autonomic responses associated with fear; emotional responses\r\n        {i.e. rage and anger) and Hormonal Secretions. The right-side amygdala is devoted to survival and reacts to threats, both real and perceived. The amygdala is an almond-shaped mass of nuclei located deep within the temporal lobes, medial to the\r\n        hypothalamus and adjacent to the hippocampus. This area of the brain is prone to kindling, which is essentially repetitive neuronal firing that gives rise to high amplitudes until the pattern collapses. Each kindling lowers the threshold of the\r\n        future ones, making them more likely.</p>\r\n    <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/amygdala.png\" alt=\"amygdala\" width=\"400\" height=\"513\" class=\"img-responsive atto_image_button_middle\" style=\" \"></p>\r\n</div>\r\n<div><span style=\" \"><br></span></div>\r\n<div><span style=\" \"><br></span></div>\r\n<div><span style=\" \"><br></span></div>\r\n<h4><span style=\" \"><h4>Amygdala</h4></span></h4>\r\n<div><span style=\" \">Check out this video of the Amygdala:</span><br></div>\r\n<div>\r\n    <p></p>\r\n    <p> <a href=\"https://www.youtube.com/watch?v=JVvMSwsOXPw\">Amygdala</a><br></p>\r\n    <p></p>\r\n    <h3><br></h3>\r\n    <h4>Basal Ganglia</h4>\r\n    <p>The Basal Ganglia are collections of nerve cells deep within the brain. Most of the basal ganglia are concerned with movement, though parts are devoted to language, thought, motivation and emotion. They include the caudate nucleus, the putamen, the\r\n        thalamus, the globus pallidus, and the tail of the caudate nucleus.</p>\r\n    <p><br></p>\r\n    <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Basal%20Ganglia.png\" alt=\"Basal Ganglia\" width=\"500\" height=\"350\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n    <p style=\"text-align: center; \"><br></p>\r\n    <p style=\"text-align: center; \"><br></p>\r\n    <div>\r\n        <h4>Diencephalon</h4>\r\n        <p>This is the division of the forebrain, the forward most portion of the brain in vertebrates, which controls temperature, reproductive functions, eating, sleeping, and the display of emotions. The diencephalon includes the thalamus, hypothalamus,\r\n            posterior portion of the pituitary gland and the pineal gland. The third ventricle is enclosed by the diencephalon. </p>\r\n        <p><br></p>\r\n        <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/diencephalon.jpg\" alt=\"diencephalon\" width=\"500\" height=\"376\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n        <p style=\"text-align: center; \"><br></p>\r\n        <h4>Hypothalamus</h4>\r\n        <p>The hypothalamus links the nervous system to the endocrine system via the pituitary gland (hypophysis). The hypothalamus controls body temperature, hunger, thirst, fatigue, anger, and circadian cycles. The hypothalamus is located below the thalamus,\r\n            just above the brain stem. The hypothalamus is responsible for certain metabolic processes and other activities of the autonomic nervous system. It synthesizes and secretes neurohormones, often called hypothalamic-releasing hormones, and these,\r\n            in turn, stimulate or inhibit the secretion of pituitary hormones.</p>\r\n        <p><br></p>\r\n        <p style=\"text-align: center; \"> <img src=\"@@PLUGINFILE@@/hypothtrlamus.jpg\" alt=\"hypothalamus\" width=\"500\" height=\"250\" class=\"img-responsive atto_image_button_text-bottom\"></p>\r\n        <p style=\"text-align: center; \"><br></p>\r\n        <p>For your viewing pleasure, a short video on the hypothalamus:</p>\r\n        <p> <a href=\"https://www.youtube.com/watch?v=TVhm2rBGhB0&amp;t=15s\">Hypothalamus</a> <br></p>\r\n        <p><br></p>\r\n        <h4>Hippocampus </h4>\r\n        <p> The hippocampus is a part of the forebrain, located in the medial temporal lobe. It belongs to the limbic system and plays major roles in short term memory and spatial navigation.</p>\r\n        <p> Here\'s a video on the hippocampus:  <a href=\"https://www.youtube.com/watch?v=5EyaGR8GGhs\">Hippocampus</a></p>\r\n        <p>This is a video about a famous person named \"HM\" and his life without a hippocampus.</p>\r\n        <p><a href=\"https://www.youtube.com/watch?v=KkaXNvzE4pk\">HM</a></p>\r\n        <p><br></p>\r\n        <h4>Pituitary</h4>\r\n        <p>The pituitary is a small pea-size master gland of the endocrine system that sits in a bony depression beneath the hypothalamus. Its job deals with directing chemical changes to regulate the entire organic system.</p>\r\n        <p>Here is a short video on the hormones that come from the pituitary gland:</p>\r\n        <p><a href=\"https://www.youtube.com/watch?v=7rWPKHFMqEU\">Pituitary</a><br></p>\r\n        <p> </p>\r\n        <h4>Reticular formation</h4>\r\n        <p>The reticular formation (also known as the reticular activating system) is at the core of the brainstem and plays a vital role in sleep, emotion, breathing, blood pressure, and heart rate. The reticular formation oscillates at 2 hz and is\r\n            the dinosaur brain, roughly <i>2,000,000 </i>years old in its evolutionary trajectory, is the same structure that we have.</p>\r\n        <p><br></p>\r\n        <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/RAS.jpg\" alt=\"RAS\" width=\"600\" height=\"600\"><br></p>\r\n    </div>\r\n    <h4>Thalamus</h4>\r\n    <p>The thalamus is an egg-shaped structure deep within the brain that acts as a relay station, receiving information from all senses (except olfactory)  processing the data and passing it between the spinal <i>cord,</i><i> </i>the medulla\r\n        oblongata and the cerebral cortex. It relays sensory signals like motor signals to the <i>cortex, </i>and it also plays in the regulation of sleep and arousal states. It is the beginning of the brain\'s formation at 5 weeks in utero.</p>\r\n    <p>The thalamus is composed of the thalamic nuclei, which aids in the processing of various stimuli. Here is a general video of the thalamus and the thalamic nuclei:</p>\r\n    <p> <a href=\"https://www.youtube.com/watch?v=Szt_OkcMPmM\">Thalamus</a></p>\r\n    <p>Here is a general video of the Basal Ganglia</p>\r\n    <p> <a href=\"https://www.youtube.com/watch?v=InJByqg1x-0\">Basal Nucleus</a><br></p>\r\n    <h4>Caudate Nucleus</h4>\r\n    <p>The caudate nucleus is one of the structures that makes up the dorsal striatum of the basal ganglia. This part of the brain plays important roles in various other nonmotor functions as well, including <a href=\"https://en.wikipedia.org/wiki/Procedural_learning\" title=\"Procedural learning\">procedural learning</a>, <a href=\"https://en.wikipedia.org/wiki/Associative_learning\" title=\"Associative learning\">associative learning</a> and <a href=\"https://en.wikipedia.org/wiki/Inhibitory_control\" title=\"Inhibitory control\">inhibitory control</a> of action,  among other functions. The caudate is also one of the brain structures which compose the <a href=\"https://en.wikipedia.org/wiki/Reward_system\" title=\"Reward system\">reward system</a> and\r\n        functions as part of the <a href=\"https://en.wikipedia.org/wiki/Prefrontal_cortex\" title=\"Prefrontal cortex\">cortico</a>–<a href=\"https://en.wikipedia.org/wiki/Basal_ganglia\" title=\"Basal ganglia\">basal ganglia</a>–<a href=\"https://en.wikipedia.org/wiki/Thalamus\" title=\"Thalamus\">thalamic</a> loop.</p>\r\n    <p>And here is a little video of the Caudate Nucleus (It\'s a little funky, but helps explain anatomy):</p>\r\n    <p> <a href=\"https://www.youtube.com/watch?v=GcB5_gXka2g&amp;t=4s\">Funky vid</a><br></p>\r\n    <p> </p>\r\n    <h4><a name=\"_Toc525053947\">Parahippocampal Gyrus</a></h4>\r\n    <p style=\"text-align: center; \"><a name=\"_Toc525053947\"><img src=\"@@PLUGINFILE@@/Parahippocampal%20gyrus.jpg\" alt=\"PArahippocampal gyrus\" width=\"700\" height=\"495\" class=\"img-responsive atto_image_button_middle\"></a></p>\r\n    <p><a name=\"_Toc525053947\"></a><a name=\"_Hlk525136529\">The parahippocampal gyrus is a region which is responsible for many functions, most notably for short-term working memory. The left-hand side is related to more verbal processes than the right, the right-hand side has more to do with forming associations. This area of the brain has much to do with the encoding and recognition of scenes; this area of the brain becomes active when taking in topographical scenes (images of cities, landscapes, and rooms—images of places).  Furthermore, this area is involved in procedural memory consolidation, recognition, and recall. It is a component part of the networks for autobiographical memory, embarrassment, and regret.</a><br></p>\r\n    <p><a name=\"_Hlk525136529\">The parahippocampal gyrus is a region which is responsible for many functions, most notably for short-term working memory. The left-hand side is related to more verbal processes than the right, the right-hand side has more to do with forming associations. This area of the brain has much to do with the encoding and recognition of scenes; this area of the brain becomes active when taking in topographical scenes (images of cities, landscapes, and rooms—images of places).  Furthermore, this area is involved in procedural memory consolidation, recognition, and recall. It is a component part of the networks for autobiographical memory, embarrassment, and regret.</a></p><br>\r\n    <p></p>\r\n    <p><img src=\"@@PLUGINFILE@@/parahippocampal%20gyrus.png\" alt=\"parahippocampal gyrus\" width=\"566\" height=\"651\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n    <h4>Tiff Thompson\'s Depth Theory of Neuroanatomy</h4>\r\n    <p></p>\r\n    <p>Proponents of the collective unconscious theory in neuroscience have suggested that neurobiological correlates to the collective unconscious are the subcortical areas of the brain, specifically the thalamus (which oscillates in delta, theta, and alpha\r\n        rhythms). The thalamus operates like a regulatory gateway, since all of the sensory input that comes into the brain, and all motor output, goes through the thalamus. The thalamus regulates what goes in and what goes out.  Because these structures\r\n        are located centrally, linking the brain with the rest of the nervous system, they are said to control vital processes, such as emotions and long-term memory (Hunt, 2012). Arousal occurs in the face of a threat, triggered by the amygdala, which\r\n        is an almond-shaped structure in the brain responsible for mediating the fear response. The amygdala locks down the hippocampus so as to react by shutting down this structure, the seat of the memory (LeDoux, 1998b). LeDoux speculates, however,\r\n        that psychoanalysis works by strengthening the cortical control of the amygdala. In fact, the face-to-face reciprocity between infant and mother is crucial for the development of the pre-frontal cortex, which serves to mediate the amygdala and\r\n        regulate affect (Schore, 1994, 2003; Siegel, 1999; Stern, 2013; Tronick, 2007).</p>\r\n    <p>Sigmund Freud, quite rightly, believed that mental activity was rooted in phylogenically­ old emotion and motivation systems, which were constructed in early mental development, and instantiated throughout later adult life (LeDoux, 1998a;Panskepp,\r\n        1998). Thus, affective reactivity, such as dissociation, can be seen as a return to nonverbal, largely unconscious parts of the brain. These are areas that can influence the higher-ordered new-mammalian brain (Cozolino, 2002, p. 6). Furthermore,\r\n        these older regions are innervated  by the vagus nerve, which literally means \"wandering nerve.\" The vagus nerve is also called the \"wandering nerve\" because it\'s the longest nerve in the human body and has countless branches that wind their\r\n        way from the brainstem all the way down to the lowest part of the intestines, touching most major organs along the way. The vagus nerve is the tenth cranial nerve and is the main afferent pathway connecting the gut to the brain. This nerve modulates\r\n        the parasympathetic nervous system, which counterbalances the fight, flight, or freezes stress response by eliciting the so­ called \"relaxation  response.\"</p>\r\n    <h4>The Vagus Nerve</h4>\r\n    <p> <img src=\"@@PLUGINFILE@@/Vagus%20Nerve.jpg\" alt=\"Vagus Nerve\" width=\"250\" height=\"731\" class=\"img-responsive atto_image_button_middle\"></p><p>A study released in June of 2015 noted the\r\n        discovery of vessels directly connecting the brain and the lymphatic system, a finding which will likely have continual substantial implications for major neurological diseases and also more common psychopathologies (Louveau et al., 2015). This\r\n        finding changes the way scientists perceive neuro-immune interaction and may make the link between the body and the brain/mind something beyond esotericism.</p>\r\n</div><br>Here\'s a short video pf Stephen Porges and his Theory on the Polyvagal Network:<br><a href=\"https://www.youtube.com/watch?v=ec3AUMDjtKQ\">Porges</a><br><br>\r\n<p></p>',1),(413,107,0,0,20,0,1,1,1588613308,1654022245,'The Neo Mammilian Brain: The Cortex','<p></p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/cortex2.png\" alt=\"cortex\" width=\"477\" height=\"348\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n<p>The cortex is the neomammalian brain, which is the grey matter. The cortex is the bark of the brain, “cortex” literally translating to bark in Latin. This part of the brain continues to develop and mature into the third decade of life, creating our learned\r\n    social-emotional behaviors, and emotions. Higher-level primates (including humans) oscillate at faster frequencies here.&nbsp;</p>\r\n<p>This layer of the brain is responsible for all conscious thought, learning, and self-awareness. Approximately 40,000 years ago, with the Cro-Magnon man, both hemispheres of the brain underwent a major functional reorganization. It was at this time that\r\n    the frontal lobes increased in size, bonding processes (sexual and social) became more complex, and the ability to communicate and express ideas began to emerge, notably in drawings, etchings, carvings, and sculpture. It is this third layer of the\r\n    cortex that allows for self-conscious awareness, among other qualities.</p>\r\n<p></p>\r\n<p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/cortex.jpg\" alt=\"cortex\" width=\"500\" height=\"307\" class=\"atto_image_button_middle\" style=\"font-size: 1rem;\"></p>\r\n<p style=\"text-align: left;\"><br></p>\r\n<p></p>\r\n\r\n<p><br></p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/evolution.png\" alt=\"evolution\" width=\"663\" height=\"391\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n<p>In a cortical organization, neurons are arranged in layers and the neurons in each layer are functionally alike and different from those in other layers. The crinkled sheet of nerve cells (grey matter) that is the cortex is 1/5” thick.&nbsp; This is the\r\n    house of the highest level of neural processing (e.g. language, memory, cognitive functioning). The cerebral cortex can be divided into areas concerned with particular functions. What lies underneath the cortex is considered white matter.<br></p><p></p><p>The cerebral cortex is the most complex structure of the human brain. It has a wide spectrum of functions, including planning and initiation of motor activity, perception and awareness of sensory information, learning, memory, conceptual thinking, awareness of emotions and many other.</p><p>In order to be able to perform all the above functions, the cerebral cortex has a unique, multilayered arrangement of the neurons. In the next paragraphs, we will analyze this arrangement as well as the different types of neurons that we find in the cerebral cortex.</p><p></p><h3>Cortical Cells in the Brain</h3><p>There are two primary types of brain cells: neurons and glia. Neurons are the nerve cells of the brain, and glia are the cells that surround the neurons. Glia were once thought to be merely the scaffolding that supported the neurons, but in recent times the variety of their functionality has been unovered. Glia are responsible for a whole host of things, including hemodynamics, the production of cerebral spinal fluid, inhibition and excitation, the removal of debris and dead cells, the metabolism of neurotransmitters, and many other functions.&nbsp;</p><p></p><p>Neurons are organized in layers, or laminas, parallel to the surface of the brain, and layers are differentiated between each other by the size and shape of the neuronal bodies.<br>&nbsp;<br><b>There are six layers of cerebral cortex:</b></p><ol><li>Molecular (plexiform) layer</li><li>External granular layer</li><li>External pyramidal layer</li><li>Internal granular layer</li><li>Internal pyramidal layer</li><li>Multiform (fusiform) layer</li></ol><p></p>\r\n<p style=\"text-align: center; \"><img src=\"http://neurones.co.uk/Neurosciences/Images/1/layers-of-cortex%20Kandel%20and%20pyramdal.jpg\" alt=\"Neurones.co.uk\"><br></p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/Pyramidal%203.jpg\" alt=\"\" width=\"600\" height=\"913\" role=\"presentation\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n<p>Different staining techniques reveal different cellular structures and different layers of cells.&nbsp;<br></p><p>The cerebral cortex consists of the hundreds of billions of neurons, and all of them are different variations of only three morphological shapes:&nbsp;<strong>pyramidal</strong>&nbsp;<strong>cells</strong>,&nbsp;<strong>fusiform cells</strong>&nbsp;and&nbsp;<strong>stellate (granular cells)</strong>. Other types of cells seen in the cortex are a modification&nbsp;one of those three. The other cells are&nbsp;<strong>horizontal</strong>&nbsp;<strong>cells</strong>&nbsp;<strong>of Cajal-Retzius</strong>&nbsp;and&nbsp;<strong>cells of Martinotti</strong>.<br></p><p><u>The first laye</u>r is the&nbsp;<strong>most superficial layer</strong>, laying directly under the pia mater.&nbsp;This layer is very poor with cellular component, which is represented by only a few&nbsp;<strong>horizontal cells of Cajal-Retzius</strong>. The major portion of this layer is actually the&nbsp;<strong>processes of the neurons</strong>&nbsp;lying within the deeper layers and their synapses</p><p><span><u>The second layer</u> is composed of mostly stellate cells.&nbsp;</span><strong>Stellate (granular) cells</strong>&nbsp;are usually small, and since their processes projects in all planes, they resemble a star. They are located all over the cortex, except for the most superficial layer. Their processes are very short and project locally in the cortex, with the role to modulate the activity of</p><p></p><p>The existence of these small cells in this layer gives that “granular” appearance to this layer, hence its name.&nbsp;</p><p>Cells of this second layer send their dendrites to various layers of the cortex, especially the molecular layer, whereas their axons travel deeper to the cortex, synapsing locally. Besides that intracortical synapsing, axons of this layer can be long enough to form the&nbsp;<strong>association</strong>&nbsp;<strong>fibers</strong>&nbsp;that travel through the white matter to finally end in the different structures of the CNS.</p><p></p><p>Based on whether or not the dendrites of stellate cells have dendritic spines (small cytoplasmic protrusions), they are referred to as spiny cells or aspiny cells.&nbsp;Dendrites of&nbsp;<strong>spiny</strong>&nbsp;<strong>cells</strong>&nbsp;do have spines and they are mostly placed within the layer IV where they release glutamate, which is an excitatory neurotransmitter, so they are functionally&nbsp;<strong>excitatory</strong>&nbsp;interneurons.&nbsp;<strong>Aspiny</strong>&nbsp;<strong>cells</strong>&nbsp;release gamma-aminobutyric acid (GABA) which is the most potent inhibitory neurotransmitter of the CNS, so they function as&nbsp;<strong>inhibitory</strong>&nbsp;interneurons.</p><p></p><p><u>The third layer </u>(the external pyramidal layer) consists predominantly of the&nbsp;<strong>pyramidal</strong>&nbsp;<strong>cells</strong>. The superficial cells of this layer are smaller than the deeper layer, that is very large.&nbsp;<span style=\"font-size: 1rem;\">The apical dendrites of these cells extend superficially and reach the molecular layer, whereas the basal processes join the subcortical white matter and then project again to the cortex, so they serve as both&nbsp;</span><strong style=\"font-size: 1rem;\">association</strong><span style=\"font-size: 1rem;\">&nbsp;and&nbsp;</span><strong style=\"font-size: 1rem;\">commissural</strong><span style=\"font-size: 1rem;\">&nbsp;corticocortical fibers.</span></p><p></p><p><strong>Pyramidal cells</strong>&nbsp;make up to 75% of the cellular component of the cortex and they are the main output neurons of the cerebral cortex. They vary in size, going from small to gigantic.&nbsp;&nbsp;Usually, they have one long axon that leaves the cortex and enters the subcortical white matter.&nbsp;<br></p><p><u>Layer four&nbsp;</u>is the&nbsp;<strong>main input</strong>&nbsp;cortical station (meaning that most of the stimuli from the periphery, arrive here), and for that reason, it is specially developed within the sensory areas.&nbsp;<span style=\"font-size: 1rem;\">It consists mostly of the&nbsp;</span><strong style=\"font-size: 1rem;\">stellate</strong><span style=\"font-size: 1rem;\">&nbsp;</span><strong style=\"font-size: 1rem;\">cells</strong><span style=\"font-size: 1rem;\">&nbsp;and a smaller portion of the&nbsp;</span><strong style=\"font-size: 1rem;\">pyramidal</strong><span style=\"font-size: 1rem;\">&nbsp;</span><strong style=\"font-size: 1rem;\">cells</strong><span style=\"font-size: 1rem;\">. The axons of the stellate cells remain in the cortex and synapse locally, whereas the axons of the pyramidal cells synapse deeper within the cortex, or they leave the cortex and join the white matter fibers.</span></p><p>Stellate cells, as the dominant cellular component, contribute to the formation of specific sensory cortical areas. Those areas receive fibers mostly from the thalamus in the following order:</p><ul><li>Stellate cells of the&nbsp;<strong>primary sensory cortex</strong>&nbsp;receive fibers from the&nbsp;<strong>ventral posterolateral (VPL)</strong>&nbsp;and&nbsp;<strong>ventral posteromedial (VPM) nuclei</strong>&nbsp;of the thalamus</li><li><strong>Primary visual cortex</strong>&nbsp;receives fibers from the&nbsp;<strong>lateral geniculate nucleus</strong></li><li><strong>Stellate</strong>&nbsp;<strong>cells</strong>&nbsp;from primary auditory cortex receive projections from the&nbsp;<strong>medial geniculate nucleus</strong></li></ul><p>When these sensory fibers “penetrate” the cortex, they turn horizontally so they can spread and diffusely synapse with the cells of the&nbsp;<strong>internal</strong>&nbsp;<strong>granular</strong>&nbsp;<strong>layer</strong>. Since these fibers are&nbsp;<a href=\"https://www.kenhub.com/en/library/anatomy/the-myelin-sheath-and-myelination\">myelinated</a>&nbsp;and therefore white, they are clearly seen in the environment of the gray matter. This stripe of the white matter is called the&nbsp;<strong>outer</strong>&nbsp;<strong>stripe</strong>&nbsp;<strong>of</strong>&nbsp;<strong>Baillarger</strong>. Since the stripe is grossly prominent in the primary visual cortex, it is referred to as the&nbsp;<strong>stripe of Gennari</strong>&nbsp;to make it distinctive.</p><p></p><p></p><section id=\"section13\"><p><u>The fifth layer</u> consists predominantly of the medium-sized and large&nbsp;<strong>pyramidal</strong>&nbsp;<strong>cells</strong>. It is the source of the&nbsp;<strong>output</strong>&nbsp;or corticofugal fibers. For that reason, it is most prominent within the motor cortex from which it sends fibers that mediate motor activity. The primary motor cortex contains a specific form of these cells, called the&nbsp;<strong>cells of Betz</strong>.<br></p><p>This layer also contains a horizontally oriented stripe of the white matter which is called the&nbsp;<strong>outer stripe of Baillarger</strong>. It is formed by the axons of the internal pyramidal layer that synapse locally within the layer, and also with the cells of the layers II and III.</p><p><u>The sixth layer</u> is the deepest layer of the cortex that directly overlies the subcortical white matter. It contains mostly&nbsp;<strong>fusiform</strong>&nbsp;<strong>cells</strong>&nbsp;with less dominant pyramidal cells and interneurons</p></section><section id=\"section14\"><h3><br></h3></section><br><p></p><p><img src=\"@@PLUGINFILE@@/Pyramidal%201.jpg\" alt=\"Pyramidal 1\" width=\"900\" height=\"1148\" class=\"img-responsive atto_image_button_text-bottom\"><br></p><p><img src=\"@@PLUGINFILE@@/Artistic%20Rendering%20of%20PN.png\" alt=\"Pyramidal Neurons\" width=\"752\" height=\"423\" class=\"img-responsive atto_image_button_left\"></p><p>Brain systems with “simple” computational demands evolved only a few neuron types. The thalamus, basal ganglia, and cerebellum possess a low degree of variability in their neuron types. In contrast, cortical structures have evolved not only five principle-cell types, but also numerous classes of GABAergic inhibitory neurons, also called cortical interneurons (Buszaki, 2006). One type is the aspiny cells, noted above.<br></p><p><b>Cortical interneurons</b> make up 1/5 of the cortical neuronal population and release the inhibitory neurotransmitter GABA (gamma-aminobutyric acid). Although they are outnumbered, interneurons innervate principle neurons at strategic places and with synaptic terminals, which allows for<b> Inhibitory Post Synaptic Potentials (IPSPs)&nbsp;</b> to approximately match the effects of <b>excitatory postsynaptic potentials (EPSPs).</b> It is through this dance that the balance of cortical activity is established.</p><p></p><p>A single neuron, when\r\nactive, produces an intracellular electric field (that must be measured inside the neuron) and\r\nan extracellular field. The extracellular field of neighboring neurons sum up to what is called\r\n<b>local field potential (LFP)</b></p><h3>Dipoles</h3><p>EEG fields result from the superposition of many synchronously firing and\r\nparallel-oriented neurons. Such bundles of active neurons can be approximated by a\r\ndipole. A dipole is defined by&nbsp;<span>its location (the dipole position)</span>&nbsp;and a vector that represents the strength and orientation of the flow of electric current (the dipole orientation). EEG and MEG field result from the superposition of many synchronously firing and\r\nparallel-oriented neurons (see image below). Such bundles of active neurons can be approximated by a\r\ndipole.<img src=\"@@PLUGINFILE@@/Dipole%20Image.png\" alt=\"Dipole Image\" width=\"700\" height=\"526\" class=\"img-responsive atto_image_button_left\"></p><p>The image below is of a dipole in the brain located in the dorsal anterior cingulate cortex, imaged in WinEEG. A dipole is most readily seen using a form of neuroimaging called \"independent Component Analysis,\" an advanced technique used by individuals in the neuroscience community to help them locate the position of the spectrally-independent component, or pattern, of EEG activity. This modality is most useful for determining the location of a pattern.</p><p></p><p>When many clusters of neurons point in the same direction (as is the case with dipoles), we can see synchronous activity in the EEG.&nbsp;<b>Synchrony</b>&nbsp;is the simultaneous appearance of rhythmic or morphologically distinct patterns over different regions of the head, either on the same side (unilateral) or both sides (bilateral). Synchrony in the EEG allows one to see patterns and rhythms in the data.&nbsp;</p><p>A brain with poor synchrony is a low voltage EEG; there are many reasons why someone may have a low voltage EEG, including a thick skull and excess GABA A receptor sites. We often see low voltage EEGs in alcoholics.</p><br><p></p><p><img src=\"@@PLUGINFILE@@/Dipole%20in%20WinEEG%20%281%29.png\" alt=\"Dipole\" width=\"600\" height=\"277\" class=\"atto_image_button_text-bottom\"><br></p><p><b>Low Voltage EEG</b></p><p><b><img src=\"@@PLUGINFILE@@/Low%20Voltage%20EEG.png\" alt=\"Low Voltage EEG\" width=\"500\" height=\"1297\" class=\"img-responsive atto_image_button_left\"></b></p><h3>Resonances</h3><p></p><p>Brain waves resonate back and forth in resonant loops. Lubar (1997) divided this activity into three categories of local, regional, and global resonant loops (Lubar, 1997).</p><p><b>Local resonant loops&nbsp;</b>take place between local cell columns, known as macro columns.&nbsp;</p><p>&nbsp;The resonances between these local cell columns usually occur at frequencies above 30 Hz (high beta and gamma frequencies). Gamma is an emergent property of the brain and does not have a generator, unlike the other rhythms of delta, theta, alpha, or beta.&nbsp;</p><p>Resonances that develop between cortical cell columns that are several centimeters apart are called<b>&nbsp;regional resonances.</b>&nbsp;The exchange of communication between cortico-cortico sites would also dominate this range as well as corticothalamic sites. These resonances result in alpha and low beta activity. These involve the idling and engagement of cell columns as they process information incoming as a result of attentional activities and conscious articulation.</p>Global resonances develop as a result of activity between distant sites of the cortex and fall into the theta and delta range. Many of the sites involved in this frequency range are believed to include subcortical functions. Hippocampal-septal activity in the limbic system is known to generate a significant amount of theta activity. Kirk and McKay (2003) have identified two separate theta ranges.<p></p><p></p><p><span style=\"font-size: 1.715rem; color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;;\"><br></span></p><p><span style=\"font-size: 1.715rem; color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;;\">Major Gyri and Sulci of the Brain</span><br></p>\r\n<p>MacLean noted the unconscious reptilian and limbic brain regions influence the higher-ordered neomammalian brain. The cortex consists of “bumps,” called gyri (“gyrus” is singular) and “grooves” called sulci (“sulcus” is singular). Some anatomists call\r\n    the deepest sulci “fissures” (Catani &amp; Thiebaut de Schotten, 2012, p. 8).\r\n    <br></p>\r\n<p><br></p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Gyrus.png\" alt=\"Gyrus\" width=\"477\" height=\"302\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n<p><br></p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/sulcus.png\" alt=\"sucus\" width=\"499\" height=\"183\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n<p><br></p>\r\n\r\n<h3>&nbsp;See here a map of all the major gyri and sulci in the brain.</h3>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/cortex.png\" alt=\"cortex\" width=\"700\" height=\"488\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n<p><br></p>\r\n<p>The Longitudinal fissure is the long sulcus that divides the left and right hemispheres of the brain. </p>\r\n\r\n<h3><a name=\"_Toc28940397\">Right hemisphere and Left\r\nHemisphere</a></h3>\r\n\r\n<p>There are differences between the functionality of the right and the left hemispheres of the brain.&nbsp; The right hemisphere of the brain is unique in that it is <b><i>not</i></b> temporally associated (unlike the left hemisphere, which uses the precedent\r\n    of the past to project into the future in anticipation). Whereas the left hemisphere is the side of our brain that speaks, read, writes, calculates, and takes care of numbers and facts (and some more specific responsibilities, such as making metaphors,\r\n    lexical ability, self-reflection, self-appraisal, and inferences during reading), the right-hand side plays the role of assimilating all of this information. The right-hand side of the brain does not distinguish where I end and you begin, nay, it\r\n    is an associational hemisphere that is more concerned with making meaning of all the component parts. It is the part of the brain that creates and draw similarity. It is the part of the brain that recognizes the connectivity of things, events, and\r\n    people. allows for us to connect with others, to understand the connectivity of things, to comprehend situations and data in a sensory way, even in a psi-phenomenological way.</p>\r\n<p>The Sulci that divides the hemispheres of the brain is called the Longitudinal Fissure</p>\r\n<h3>Longitudinal Fissure that Divides the Hemispheres\r\n</h3>\r\n<p><img src=\"@@PLUGINFILE@@/Longitudinal%20Fissure.png\" alt=\"Longitudinal Fissure\" width=\"448\" height=\"488\" class=\"img-responsive atto_image_button_left\"></p><p>The central sulcus (aka Rolandic Fissure) is the transverse sulci that separates the frontal lobes from the parietal lobes, as well as the sensory-motor strip into the motor cortex and the somatosensory cortex. </p>\r\n<p></p>\r\n<h4><a name=\"_Toc28940399\"><span>Central\r\nSulcus, aka Rolandic Fissure</span></a></h4>\r\n<p></p><img src=\"@@PLUGINFILE@@/Rolandic%20Sulcus.png\" alt=\"Rolandic Sulcus 1\" width=\"199\" height=\"127\" class=\"img-responsive atto_image_button_text-bottom\"><br>\r\n<p></p>\r\n<p><img src=\"@@PLUGINFILE@@/rolandic%203.png\" alt=\"rolandic 3\" width=\"319\" height=\"318\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n<h3>The Sylvian Fissure</h3>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Sylvian%20Fissure.png\" alt=\"Sylvian Fissure\" width=\"600\" height=\"436\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n<p style=\"text-align: center; \">The sylvian fissure is the meeting of the temporal nd the frontal lobes of the brain, which opens up into a pocket of cortical tissue called the insula.</p><br>\r\n<p></p>',1),(415,109,0,0,20,0,1,1,1588619686,1654022305,'The Lobes','<p></p><p>The basic division of each of the hemispheres is into four lobes: frontal, parietal, temporal, and occipital. Two prominent ﬁssures allow this subdivision to be made — the central ﬁssure and the lateral ﬁssure.</p><br><br><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp; &nbsp;</span><img src=\"@@PLUGINFILE@@/Lobes.png\" alt=\"Lobes\" width=\"557\" height=\"368\" style=\"font-size: 1rem;\"></p><p style=\"text-align: center;\"><br></p><p></p><p></p><h2><a name=\"_Toc28940412\">Pre-Frontal Cortex</a></h2><p style=\"text-align: left;\"><br></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/PFC.png\" alt=\"PFC\" width=\"300\" height=\"237\" class=\"atto_image_button_left\"><span style=\"font-size: 1rem;\"></span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">&nbsp;The prefrontal cortex&nbsp;makes up over 10% of the volume of the brain, The PFC contains the&nbsp;Brodmann areas 8, 9, 10, 11, 12, 13, 14, 24, 25, 44, 46 and 47.&nbsp;<sup>&nbsp;</sup>This brain region has been implicated in&nbsp;planning complex cognitive behavior, personality expression,&nbsp;decision&nbsp;<span>making, moderating social behavior, and&nbsp;</span>moderating certain aspects of speech and language.&nbsp;The basic activity of this brain region is considered to be orchestration of thoughts and actions in accordance with internal goals.</span><sup>&nbsp;</sup><span style=\"font-size: 1rem;\">The most typical&nbsp;psychological&nbsp;term for functions carried out by the prefrontal cortex area is&nbsp;executive function. Executive function relates to abilities to differentiate among conflicting thoughts, determine good and bad, better and best, same and different, future consequences of current activities, working toward a defined goal, prediction of outcomes, expectation based on actions, and social \"control\" (the ability to suppress urges that, if not suppressed, could lead to socially unacceptable outcomes). Patients with prefrontal cortex damage can experience blunted emotional responses, which may be another factor that negatively affects their ability to make decisions.</span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p><p></p><p><img src=\"@@PLUGINFILE@@/Frontal%20Lobes.png\" alt=\"Frontal Lobes\" width=\"300\" height=\"255\" class=\"img-responsive atto_image_button_left\"><br></p><p>Frontal lobes have the ability to regulate eye movement this is visual accommodation and convergence, the ability of the eyes to go left and right and focus and read.&nbsp; There is a physiological problem with ADD/ADHD kids—they have more difficulty keeping their eyes still.</p><p><br></p><p><br></p><p><br></p><p><br></p><p><a name=\"_Toc28940413\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\"><br></a></p><p><a name=\"_Toc28940413\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Dorso-Lateral Pre-Frontal Cortex</a><br></p><p>Between Brodmann areas 9, 10, 44 and 45 is the Dorso-Lateral Pre-Frontal Cortex (DLPFC).<a name=\"_Hlk494097976\">&nbsp;This area&nbsp;</a><a name=\"_Hlk520354468\">is the highest cortical area responsible for motor planning, organization and regulation. It has an important role in the integration of sensory and mnemonic information.</a></p><p style=\"text-align: center; \"><a name=\"_Hlk520354468\"><img src=\"@@PLUGINFILE@@/DLPFC.jpg\" alt=\"DLPFC\" width=\"300\" height=\"279\" class=\"img-responsive atto_image_button_middle\"><br></a></p><p>This area has cortical (surface) and sub cortical (under the surface—white matter) circuits for complex mental activity and executive functions. It plays a large role in executive memory (working memory, spatial memory, and short term memory), memory retrieval and encoding/recognition, as well as prospective memory, abstract thinking, intentionality and motivation.</p><p>In addition, this area is responsible for error processing and detection, processing emotional stimuli, self-reflection in decision making, pleasant and unpleasant emotions, inferential reasoning, decision weighing (conflict and reward), planning, and attribution of intention to others.</p><p>The sensory responsibilities of the dorsolateral pre-frontal cortex have to do with joint attention and autonomic nervous system regulation. The&nbsp;autonomic nervous system&nbsp;(ANS&nbsp;or&nbsp;visceral nervous system&nbsp;or&nbsp;involuntary nervous system) is the part of the&nbsp;peripheral nervous system&nbsp;that acts as a&nbsp;control system&nbsp;that functions largely below the level of&nbsp;consciousness&nbsp;to control&nbsp;visceral&nbsp;functions,&nbsp;including&nbsp;heart rate,&nbsp;digestion,&nbsp;respiratory rate,&nbsp;salivation,&nbsp;perspiration,&nbsp;pupillary dilation,&nbsp;micturition&nbsp;(urination),&nbsp;sexual arousal,&nbsp;breathing&nbsp;and&nbsp;swallowing. Most autonomous functions are involuntary but they can often work in conjunction with the&nbsp;somatic nervous system&nbsp;which provides voluntary control.</p><h2>Sensory motor Cortex</h2><p>The sensory-motor cortex registers sensation that is connected with specific body parts or body functions. The motor strip is part of the frontal lobe and is anterior to the sensory cortex, which is in the parietal lobe. Collectively, the sensory-motor cortex forms the central lobes of the brain. The primary motor cortex is Brodmann area 4, which works with other motor areas of the brain to plan and execute movements. The primary motor cortex receives thalamic inputs from different cell bodies within the thalamus. The nerve fibers that cast somatosensory information all over the body. &nbsp;The sensory-motor cortex is made up of Brodmann areas 1, 2, 3, 4, and 5.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/CENTRAL%20LOBE.png\" alt=\"CENTRAL LOBE\" width=\"300\" height=\"228\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_middle\"></p><h2><a name=\"_Toc28940415\">Homunculus</a></h2>\r\n\r\n<p>&nbsp;</p>\r\n\r\n<p>The homunculus is a neurological map that corresponds to the\r\nbrain’s territory for different body parts. Homunculus is a Latin term that\r\nliterally means “little man.”&nbsp; The\r\nanatomically correct homunculus demonstrates the brain area that is overly\r\nproportioned for the hands, mouth and tongue, second only to the ears, nose and\r\neyes.</p><p><br></p>\r\n\r\n<p style=\"text-align: left; \"><img src=\"@@PLUGINFILE@@/homunculus%201.png\" alt=\"homunculus 1\" width=\"600\" height=\"305\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"><img src=\"@@PLUGINFILE@@/Homunculus%202.png\" alt=\"homunculus 2\" width=\"260\" height=\"282\">&nbsp;<!--[endif]--></p><p style=\"text-align: right;\"><br></p><p></p><h3>Temporal Lobes</h3><p>The temporal lobe is so named\r\nbecause of its proximity to the temples. It is positioned toward the base of\r\nthe center of the cortex, just behind the temples. The&nbsp;temporal lobe&nbsp;is involved\r\nin&nbsp;primary&nbsp;auditory perception, such as hearing, and holds\r\nthe&nbsp;primary&nbsp;auditory cortex. <a name=\"_Hlk28772267\">The&nbsp;<b>primary</b>&nbsp;auditory\r\ncortex receives sensory information from the ears and secondary areas process\r\nthe information into meaningful units such as speech and words</a>. Much of the auditory work of the\r\ntemporal lobes is processed through the top of the temporal lobes—the superior\r\ntemporal gyrus. This region directly receives sound input from the ear. Some of\r\nthe other important functions of this brain region are:</p>\r\n\r\n<p><!--[if !supportLists]-->a.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->The formation of visual memories.\r\nIn coordination with the amygdala and the hippocampus, this region create long\r\nterm memories of conscious events. </p>\r\n\r\n<p><!--[if !supportLists]-->b.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->The interpretation of visual\r\nstimuli (this region recognizes faces and reads body language)</p>\r\n\r\n<p><!--[if !supportLists]-->c.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->The controlling of unconscious and\r\nautomatic relations, such as hunger and thirst</p>\r\n\r\n<p><!--[if !supportLists]-->d.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->The production of speech, which\r\ninvolves a conscious choice of what to say (this region is involved in “tip-of\r\nthe-tongue” phenomena.</p>\r\n\r\n<p><!--[if !supportLists]-->e.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->The recognition of language (both\r\nverbal and non-verbal).</p>\r\n\r\n\r\n\r\n<p><!--[if !supportLists]-->f.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n<!--[endif]-->Kolb &amp; Wishaw (1990) have\r\nidentified eight principle symptoms of temporal lobe damage: 1) disturbance of auditory\r\nsensation and perception, 2) disturbance of selective attention of auditory and\r\nvisual input, 3) disorders of visual perception, 4) impaired organization and\r\ncategorization of verbal material, 5) disturbance of language comprehension, 6)\r\nimpaired long-term memory, 7) altered personality and affective behavior, 8)\r\naltered sexual behavior. The temporal lobes includes the hippocampal formation and the\r\ninferior horn of the lateral ventricle.</p>\r\n\r\n<p>The temporal lobe is made up for Brodmann areas 20 21, 22, 28, 35,\r\n36, 37, 38, 41, 42, and 52.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Temporal%20Lobes.png\" alt=\"Temporal Lobes\" width=\"300\" height=\"242\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_middle\"></p><p></p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/temporal%20brodmann.png\" alt=\"temporal brodmann\" width=\"300\" height=\"224\" class=\"img-responsive atto_image_button_middle\"><br></p><p></p><h2><a name=\"_Toc28940417\">Parietal Lobes</a></h2>\r\n\r\n<p>The parietal\r\nlobes are divided into the superior and inferior parietal lobes. This region of\r\nthe brain is known largely for visuo-spatial attention, navigation, the\r\nintegration of senses and the major sensory inputs from the skin, which relay\r\nthrough the thalamus to the parietal lobes. The parietal lobe is abutted by the\r\nRolandic Fissure, which runs coronally through the brain, the Sylvian Fissure,\r\nwhich separates the temporal lobe from the parietal and the frontal lobe, and\r\nthe parieto-occipital sulcus.</p>\r\n\r\n<p>The posterior\r\nparietal cortex is made of the superior parietal lobe (Brodmann areas 5 and 7)\r\nand the inferior parietal lobes (Brodmann areas 39 and 40, which are separated\r\nby the intraparietal sulcus. This sulcus and the adjacent gyri are essential in\r\nlimb and eye movement. Each hemisphere rules the sensation of the skin on the\r\nopposite side of the body. The parietal lobes are used for the manipulation of\r\nobjects. The parietal lobe also includes the dorsal stream of vision, which is\r\nthe “where” in space an object appears. And the “how” stream, which has to do\r\nwith vision for action.</p>\r\n\r\n<h3><a name=\"_Toc28940418\"></a><a name=\"_Toc16242865\">Inferior Parietal Lobule</a> (BA 39 &amp; 40)</h3>\r\n\r\n<p>The inferior parietal lobule has been involved in the\r\nperception of emotions in facial stimuli,<sup> </sup>and interpretation of\r\nsensory information. The Inferior parietal lobule is concerned with language,\r\nmathematical operations, and body image, particularly the supramarginal gyrus\r\nand the angular gyrus. </p><p></p><p></p><h3><a name=\"_Toc28940419\">Superior Parietal Lobe (BA 5 &amp; 7)</a></h3>\r\n\r\n<p>There is a\r\ngreat deal of activity at the superior parietal lobe. This area is responsible\r\nfor spatial orientation, as well as sensory input from the hand.&nbsp; This region is also responsible for the\r\nintegration of sensory information in various modalities, including navigation\r\nand orienting oneself in space. It is the main sensory area as related to touch\r\nand sensory inputs from the skin (touch, temperature and pain receptors), which\r\nare relayed through the thalamus).&nbsp; </p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/parietal%20lobes.jpg\" alt=\"parietal lobes\" width=\"300\" height=\"281\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem;\"></p><p></p><p></p><h2><a name=\"_Toc28940420\">Occipital Lobe</a></h2>\r\n\r\n<p>The occipital\r\nlobe of the brain is divided into Brodmann areas 17, 18 and 19. This region is\r\nknown as the visual cortex of the brain. Visual nerves run straight from the\r\neye to the primary visual cortex to the visual association cortex. The lateral\r\noccipital sulcus divides the occipital gyrus into a superior and inferior part.\r\nThe cuneus is a smaller lobe in the occipital lobe of the brain. This region\r\nis bounded anteriorly by the parietao-occipital sulcus, and inferiorly by the\r\ncalcitrine sulcus. </p>\r\n\r\n<p>The occipital\r\nlobe is responsible for visual processing. This includes the perception of\r\nlight, intensity, motion, shapes, patterns, and color. Pattern recognition is\r\nimportant for piecing together words, reading sentences, and decoding visual\r\nstimuli in general.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Occipital%20Lobes.png\" alt=\"Occipital Lobes\" width=\"300\" height=\"235\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_middle\"></p><p></p><p></p><h2><a name=\"_Toc28940421\">Cerebellum</a></h2>\r\n\r\n<p><b>&nbsp;</b></p>\r\n\r\n<p>The\r\ncerebellum is the hindbrain structure that is connected to the brainstem by\r\nfibers that carry information into and out of its interior. The main function\r\nof the cerebellum is coordinating movement and planning motor activity\r\n(balance, muscle tension, joint position, and coordinated movements). It is\r\nfolded, like the cortex, which gives it high information processing power. </p>\r\n\r\n<p>Eighty per cent of the brain’s neurons are in the cerebellum (Herculano-Houzel, 2010)\r\nand emerging literature (Schmahmann, 1997; 1998, 2000; Teicher, Anderson, &amp;\r\nPolcari, 2012; Levin, 2009) suggests that the cerebellum plays a significant\r\nrole in regulating the cerebrum, both cortically and sub-cortically. This is\r\nthe part of the brain that remembers how to ride a bike, and remembers being\r\nrocked by mother.</p>\r\n\r\n<p>The cerebellum has strong connections with the brainstem and is\r\nsituated behind the brainstem (inside the skull) in humans. Because the\r\ncerebellum is a simpler form of cortex, it consists of only three layers&nbsp; (as opposed to the more evolved cerebral\r\ncortex, which has six layers). Parts of the cerebellum are quite old in the\r\nevolutionary sense, and parts are relatively newer. This “little brain” is\r\ninvolved in motor coordination and also in the planning of movements. The\r\ncerebellum is involved with motor control and is part of the motor system,\r\ninﬂuencing posture, gait, and voluntary movements. Many of the connections to\r\nthe cerebellum, including pathways and nuclei, are found in the brainstem.</p>\r\n\r\n<p>According to\r\nSebern Fisher (2014), Babies and young children learn through their senses and\r\nthe integration of sensory input. Sensory integration is the province of the\r\nparietal cortex and the cerebellum . . . . the development of the infant’s\r\ncerebellum depends mostly on the security, consistency, and rhythmicity of his\r\nparents’ holding. When there is a history of significant neglect, the mother\r\ndoes not hold her infant with intentionality or feeling. Many in fact report\r\nnever having been rocked or held, activities which promote the development of\r\nthe cerebellum (22). Some folks comment that they feel an emptiness at the back\r\nof their head, where a loving hand would normally cradle the baby (22).</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Cerebellum.png\" alt=\"Cdrebellum\" width=\"300\" height=\"241\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_middle\"></p><p></p>\r\n\r\n<p><br><!--[endif]--></p><br><p></p>',1),(416,110,0,0,20,0,1,1,1588657433,1654221715,'Brodmania!','<p></p>\r\n<h1><a name=\"_Toc28940422\">BRODMANN AREAS</a></h1>\r\n<p>The initial approach to understanding what part of the brain controlled what function was the legacy of Sir Charles Scott Sherrington (1857 – 1952) who found that different parts of the brain have different cellular architecture and control different functions and sensations. And in 1909, Korbinian Brodmann discovered that different regions of the brain had different cellular architecture, which he divided into numbered areas (today called “Brodmann areas”). &nbsp;He dissected the brain into 52\r\n    distinct regions. The cerebellar cortex is also subdivided into nearly a hundred areas. Currently, we know that each of these divisions is composed of characteristic neuronal circuits that consist of numerous neurons of diverse types interconnected with each other via synapses.</p>\r\n<h4>Sir Charles Scott Sherrington (Left) and Korbinian Brodmann (Right)</h4>\r\n<p><img src=\"@@PLUGINFILE@@/K%20Brodmann.jpg\" alt=\"K Brodmann\" width=\"400\" height=\"594\" class=\"img-responsive atto_image_button_text-bottom\"><img src=\"@@PLUGINFILE@@/Sherrington.jpg\" alt=\"Sherrington\" width=\"400\" height=\"594\" class=\"atto_image_button_right\"><br></p>\r\n<h3><a name=\"_Toc28940423\">Original Cortical Atlas by Brodmann, Colorized Lateral View of the left hemisphere</a></h3>\r\n<p style=\"text-align: left;\"><a name=\"_Toc28940423\"><img src=\"@@PLUGINFILE@@/Brodmann%201.png\" alt=\"Brodmann areas\" width=\"800\" height=\"561\" class=\"img-responsive atto_image_button_text-bottom\"><br></a></p>\r\n<h3><a name=\"_Toc28940424\">The 52 Brodmann areas of the brain</a></h3>\r\n<p></p>\r\n<p style=\"text-align: center;\"><a name=\"_Toc28940424\"><img src=\"@@PLUGINFILE@@/brodmann%202.png\" alt=\"brodmann 2\" width=\"621\" height=\"277\"><br></a></p>\r\n<p><a name=\"_Toc28940424\"></a></p>\r\n<h3><a name=\"_Toc28940424\">Brodmann area functions</a></h3>\r\n<a name=\"_Toc28940424\">\r\n    <p>8 sub-categories or groupings</p>\r\n    <p>Areas not in humans include: 14, 15, 27 and 49</p>\r\n    <p>1)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;executive functioning (9, 10, 44, 45, 46)</p>\r\n    <p>2)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;motor (4, 6, 8)</p>\r\n    <p>3)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;somatosensory (1, 2, 3, 5, 40, 31)</p>\r\n    <p>4)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;attention (7, 39)</p>\r\n    <p>5)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;visual (17, 18, 19, 15, 16)</p>\r\n    <p>6)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;memory (20, 21, 37, 28, 36)</p>\r\n    <p>7)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Emotional regulation (11, 38, 47, 13)</p>\r\n    <p>8)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sound (22, 41, 42)</p>\r\n    <p>9)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Primary Gustatory Area (43) Olfactory (34)</p>\r\n    <p>&nbsp;</p>\r\n</a>\r\n<h3><a name=\"_Toc28940425\">BAs 3, 1,and 2</a></h3>\r\n<h4><a name=\"_Toc28940424\"></a></h4>\r\n<p><a name=\"_Toc28940425\"></a></p>\r\n<p><a name=\"_Toc28940425\">This region is the primary somatosensotry cortex and is located at the post central gyrus of the brain (behind the Rolandic Fissure). It is divided into Brodmann areas 1, 2, 3a, and 3b. 3b is thought to be the primary somato-sensory cortex, and projects the outputs received from 3a to Brodmann areas 1 and 2. BA 3 mediates bodily sensations, because its wired to pathways bringing touch, pain, and temperature signals from the spinal cord, BA1 gets information on texture and Brodmann area 2 gets information on the size and the shape of an object. How cool is that?</a></p>\r\n<p></p>\r\n<h4>Brodmann areas 1, 2, and 3</h4><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA%20123.png\" alt=\"BA 123\" width=\"400\" height=\"375\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p>\r\n<p></p>\r\n<p style=\"text-align: center;\"><a name=\"_Toc28940424\"><img src=\"@@PLUGINFILE@@/BA123.png\" alt=\"BA 123\" width=\"625\" height=\"464\"><br></a></p>\r\n<p><a name=\"_Toc28940424\"></a></p>\r\n<h3><a name=\"_Toc28940424\">BA 4</a></h3>\r\n<p><a name=\"_Toc28940424\">Brodmann area 4 is the primary motor cortex of the brain and is located at the pre central sulcus.&nbsp; It is considered the most posterior part of the frontal lobe. BA 4 controls movements of the body and sends many axons to the spinal cord, which in turn is wired to the muscles of the body.</a></p>\r\n<p style=\"text-align: center;\"><a name=\"_Toc28940424\"><img src=\"@@PLUGINFILE@@/BA%204.png\" alt=\"BA 4\" width=\"498\" height=\"764\" class=\"img-responsive atto_image_button_middle\"><br></a></p><a name=\"_Toc28940424\">This region is the region of the motor homunculus, which is mainly involved in controlling voluntary dynamic, kinesthetic movements. It is responsible for motor (finger, hand wrist, lip tongue, face, mouth, and lower limb movement, as well as eye movements and blinking and learning motor sequences. This area is also responsible for somatosensory perception, such as finger moving and touch , and kinesthetic perception of limb movements. This region as the main motor center of the brain, initiates the onset of movements, mainly produced by contraction of skeletal muscle. These impulses pass via the internal capsule to the spinothalamic tract in the spinal cord, both parts of the pyramidal system.&nbsp;<br><br><br><br></a><a name=\"_Toc28940427\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">BA 5</a><br>\r\n<p>Brodmann area 5 is part of the parietal cortex, making up the superior parietal lobe as part of the post central gyrus. It is right behind Brodmann areas 1, 2, and 3, the primary somatosensory cortex. This area is involved with spatial orientation, and\r\n    receives a great deal of visual input as well as sensory input from one\'s hand. The postcentral gyrus is the principal somatic (of the body) sensory area. It is the end-point of sensory information from the skin (for touch, pain, pressure and temperature sensation) and from the spindle organs in the joints (for position sense).&nbsp;</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA5.png\" alt=\"BA5\" width=\"479\" height=\"764\" class=\"img-responsive atto_image_button_middle\"></p>\r\n<p>Comprehensively, this area is responsible for generating actions, moving hands, moving limbs, sensing of our fingers, experiencing softness and vibration, moving tongue and mouth, swallowing, voluntary breathing, imagining actions, blinking and eye movements,\r\n    the mirror neuron system, and verbal encoding. The slow Beta rhythm of 13-14 hz was once used in neurofeedback training as a means of reducing seizure and adding calm to patients otherwise stricken with anxiety. The lack of this particular bandwidth in this region suggests a lack of proprioceptive awareness and potentially a more anxious state.</p>\r\n<p><br></p>\r\n<h2><a name=\"_Toc28940428\">BA 6</a></h2>\r\n<p>BA 6 are part of the frontal lobe and lies anterior to the motor cortex (Brodmann area 4). The functions of Brodmann area 6 are the premotor cortex are diverse and project directly to the&nbsp;spinal cord.&nbsp;This region, therefore, may play a role in the direct control of behavior, with a relative emphasis on the&nbsp;trunk muscles&nbsp;of the body. It may also play a role in planning movement, in the spatial guidance of movement, in the sensory guidance of movement, in understanding the actions of others, and in using abstract rules to perform specific&nbsp;tasks. This area is also responsible for intention.</p>\r\n<p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Brodmann%20area%206.png\" alt=\"Brodmann area 6\" width=\"481\" height=\"764\" class=\"img-responsive atto_image_button_text-bottom\"></p>\r\n<h2><a name=\"_Toc28940429\"></a><a name=\"_Toc16242834\"></a><a name=\"_Toc525053908\">BA 7</a></h2>\r\n<p>Brodmann area 7 part of the parietal cortex of the brain and located posterior to the&nbsp;primary somatosensory cortex&nbsp;(Brodmann areas 3, 1 and 2), and superior to the&nbsp;occipital lobe. This region is believed to play a role in&nbsp;visuo-motor\r\n    coordination&nbsp;(e.g. tool use, reaching to grasp an object, handwriting, and visuospatial attention.&nbsp;(e.g., in reaching to grasp an object). In addition, area 7 along with&nbsp;area 5&nbsp;has been linked to a wide variety of high-level processing tasks, including activation in association with language use.<sup>[2]</sup>&nbsp;This function in language has been theorized to stem from how these two regions play a vital role in generating&nbsp;conscious&nbsp;constructs of objects in the world,\r\n    including self-reflection.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA7.png\" alt=\"Brodmann area 7\" width=\"480\" height=\"764\" style=\"font-size: 1rem;\" class=\"atto_image_button_text-bottom\"></p>\r\n<p></p>\r\n<h3><a name=\"_Toc28940430\">BA 8</a></h3>\r\n<p>Brodmann area 8 is anterior to Brodmann area 6 and is part of the frontal cortex. It includes the frontal eye fields (so that if one has a stroke on injury to the brain in this region, the eyes will drift towards the injury. It is involved in the management\r\n    of uncertainty, as well as the encoding of hope (a higher-order expectation positively correlated with uncertainty).</p>\r\n<h2><a name=\"_Toc28940431\"></a><br></h2><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA8.png\" alt=\"498\" width=\"480\" height=\"758\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_text-bottom\"></p>\r\n<h2><a name=\"_Toc525053909\">BA 9 and 10</a></h2>\r\n<p>Brodmann area 9 located in the pre-frontal cortex is responsible for executive memory, abstract thinking, intentionality and motivation, memory (working memory, spatial memory, short term memory, memory encoding and recognition, memory retrieval, forgetting),\r\n    motor skills, error detection, inductive reasoning, language skills (verbal fluency, metaphor comprehension, semantic categorization, verbal fluency, word-stem completion, generating sentences, etc). This area is underactive in individuals dealing\r\n    with bipolar depressive disorders. Left BA9 is responsible for empathy, processing pleasant and unpleasant emotional scenes, self-criticism, and attention to negative emotions.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA9.png\" alt=\"BA9\" width=\"480\" height=\"764\" class=\"atto_image_button_middle\"></p>\r\n<p>Right BA9 is responsible for attention to positive emotions, recognizing the emotions of others, attributing intention, suppressing sadness, theory of mind, working memory and spatial memory, as well as planning, calculation, and religiosity.</p>\r\n<p></p>\r\n<h2><a name=\"_Toc28940432\"></a><a name=\"_Toc16242836\"></a><a name=\"_Toc525053910\">BA 10</a></h2>\r\n<p><a name=\"_Hlk28777532\">Brodmann area 10 is the anterior-most portion of the pre-frontal cortex. Overall, this area of the brain governs working memory; spatial memory; recognition; recall; intentional forgetting; recognizing emotions; calculation; pain; organization, maintenance, and implementation of intentions, source monitoring (who said what information), logical inference, hypometabolism in bipolar disorder (with paralimbic, insula, and cingulate hypermetabolism).</a></p><p><a name=\"_Toc28940433\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\"><br></a></p><p><a name=\"_Toc28940433\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Brodmann area 10L</a><br></p>\r\n<p>Brodmann area 10L is responsible for self-reflection (about one\'s own abilities, traits and attitudes), Syntax, Metaphor, Lexical processing, Verbs, Self-reflection, Self-appraise, Inferences during reading,&nbsp; Forgiveability judgment (of a crime),\r\n    the integration of disparate relationships, dysfunction during remission in major depression, and the execution of delayed intentions.</p>\r\n<p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA10.png\" alt=\"BA10\" width=\"498\" height=\"764\" class=\"atto_image_button_middle\"><br></p>\r\n<h3><a name=\"_Toc28940434\">Brodmann area 10 R</a></h3>\r\n<p><a name=\"_Hlk28777561\">Brodmann area 10 is responsible for recalling episodes, nonspeech sounds,&nbsp; familiar odors, reward vs conflict, risk vs benefit, and carrying out delayed intentions.</a></p>\r\n<h2><a name=\"_Toc28940435\"><br></a></h2>\r\n<h2><a name=\"_Toc28940435\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">BA 11</a><br></h2>\r\n\r\n<p><a name=\"_Hlk28777582\"></a><a name=\"_Hlk522463468\">BA11 is the\r\norbito-frontal cortex, right above the eye sockets. It governs personal and\r\nsocial behavior, emotion, and decision making</a>, the formation and retrieval of temporal context of episodic information. In addition, this part of the brain is responsible for e<span style=\"font-size: 1rem;\">ncoding of new material, olfaction, nonspeech sounds, reward vs conflict.</span></p>\r\n<p style=\"text-align: center;\"><span style=\"font-size: 1rem;\"><img src=\"@@PLUGINFILE@@/BA11.png\" alt=\"BA11\" width=\"498\" height=\"764\" class=\"atto_image_button_middle\"></span></p>\r\n\r\n<h4>BA11 L is responsible for</h4>\r\n\r\n<p></p>\r\n<ul>\r\n    <li>Unexpected outcomes </li>\r\n    <li>Idioms </li>\r\n    <li>Face-name recognition</li>\r\n</ul>\r\n<p></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<h4>BA 11R is responsible for</h4>\r\n\r\n<p></p>\r\n<ul>\r\n    <li><a name=\"_Hlk28777602\">Experience of happiness </a></li>\r\n    <li>Self-calm </li>\r\n    <li>Conscious perception of odors </li>\r\n    <li>Empathy (Judge others\' emotional states) and forgiveness judgments </li>\r\n</ul>\r\n<p><br></p>\r\n<p><a name=\"_Toc28940436\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">BA 12</a><br></p>\r\n\r\n<p>Brodmann did not identify area 12 in humans, but it has been located as part of the orbito-frontal cortex, linked to taste perception, decision making and mental time travel. </p>\r\n<p style=\"text-align: center;\">&nbsp;<img src=\"@@PLUGINFILE@@/BA12.png\" alt=\"BA12\" width=\"480\" height=\"764\" style=\"text-align: center; \" class=\"atto_image_button_middle\"></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: center;\"></p><br><br>\r\n<p></p>\r\n<p></p>\r\n<h2><a name=\"_Toc28940437\">BA 13 and 16: The Insula</a></h2>\r\n\r\n<p>The lateral ﬁssure, when “opened,” reveals some buried cortical tissue; this area is called the insula. This area is responsible for receiving taste sensations, relayed from the brainstem, and olfactory sensation.</p>\r\n\r\n<p><img src=\"@@PLUGINFILE@@/BA13.png\" alt=\"BA13\" width=\"429\" height=\"287\" class=\"img-responsive atto_image_button_left\"><br>\r\n    <!--[endif]-->\r\n</p>\r\n\r\n<p><a name=\"_Hlk521876326\">The insula is also responsible for the processing of sensation,\r\nmotor movements and motor planning, verbal memory, motivational reasoning,\r\nvocal pitch, humor appreciation, risk taking, the expression of fear and\r\ndisgust. The right side is responsible for gating affect and impulse, including\r\nexplosivity, unreasonable responses, and the like. </a></p>\r\n\r\n<p>The anterior insula has been shown to play a part in the mental conditioning of pain perception—in a sense, the thought pattern associated with pain means that “the worse it gets the worse it gets.” The more the individual catastrophizes, ruminates, worries,\r\n    and focuses on the pain, the greater the expectation and manifestation of the pain.</p><p>The granular posterior insula processes tactile,\r\nauditory, and visual somatosensation. Craig (2004), found that there is\r\nexpansion of the right anterior insula and adjacent orbitofrontal cortices in\r\ntherapists and other folks who are empathically attuned.<br></p><p>The chemoarchitecture of the&nbsp;<b>insula</b>, especially the&nbsp;<b>anterior</b>, agranular&nbsp;<b>insula</b>, supports its role in motivation, emotion and addiction. The agranular&nbsp;<b>insula</b>&nbsp;receives strong&nbsp;<b>dopaminergic</b>&nbsp;innervation and contains a high density of D<sub>1</sub>&nbsp;<b>dopamine</b>&nbsp;receptors.<br></p>\r\n\r\n<p>The insular cortex is thought to connect to the sensory inputs from our internal organs. It serves interoception, the perception of information that arises from the center of the body and contributes to the felt sense of being. It also rules proprioception,\r\n    the sense of how one’s body feels.&nbsp; It also inhibits the firing of the amygdala. Early emotional trauma that interferes with the experience-dependent maturation of the insula and negatively impacts its role in generating an image of one’s physical\r\n    state (body image), a process that underlies the experiencing of basic emotions (Schore, 2003, p. 202).</p>\r\n\r\n<p>Craig (2004), found that there is expansion of the right anterior insula and adjacent orbitofrontal cortices in therapists and other folks who are empathically attuned.</p>\r\n<h5><a name=\"_Toc28940438\">BAs 14 and 15 do not exist in\r\nhumans.</a></h5><p><a name=\"_Toc28940438\"><br></a></p>\r\n\r\n<h2><a name=\"_Toc28940439\"></a><a name=\"_Toc16242837\"></a><a name=\"_Toc525053911\">BA 17, 18 and 19</a></h2>\r\n\r\n<p>These regions are located at the occipital lobe and visual nerves run straight from the visual cortex to the visual association cortex. </p><img src=\"@@PLUGINFILE@@/BA%2017%2018%2019.png\" alt=\"BA 17\" width=\"600\" height=\"212\" class=\"img-responsive atto_image_button_left\">\r\n<h2><a name=\"_Toc28940440\"></a><a name=\"_Toc16242838\"></a><a name=\"_Toc525053912\">BA 17</a></h2>\r\n\r\n<p>Brodmann area 17 is important in the perception of light intensity, distinguishing visual patterns, contours, colors and motion. It is involved in spatial orientation and transmits information to the dorsal stream and the ventral stream. The dorsal stream\r\n    is the “where pathway” which is associated with motion, representation of object locations, and control of the eyes and arms. The ventral stream is the “what pathway” and is associated with form recognition and object representation. It is associated\r\n    with the storage of long-term memory. This area is involved with the discrimination of shapes, textures, objects and faces.</p>\r\n\r\n<h2><a name=\"_Toc28940441\"></a><a name=\"_Toc16242839\"></a><a name=\"_Toc525053913\">BA 18</a></h2>\r\n\r\n<p>Brodmann area 18 is important for the perception of light intensity, motion, and in the monitoring of color, shape, and visual patterns. Face-name association and word-face encoding are related to this area. If visual agnosia is present, the ability to\r\n    track visual motion patterns and discriminate finger gestures may be compromised, as may be orientation and selective attention (another possibility is that these things may be heightened).</p>\r\n\r\n<p>&nbsp;</p>\r\n\r\n<h2><a name=\"_Toc28940442\"></a><a name=\"_Toc16242840\"></a><a name=\"_Toc525053914\">BA 19</a></h2>\r\n\r\n<p>Brodmann area 19 is the associative visual area. It is also used for light intensity and pattern detection. This region comprises parts of the lingual gyrus, the cuneus, the middle occipital gyrus, and the superior occipital gyrus. This area is important\r\n    in the spatial orientation of the stimulus.&nbsp; This area is also implicated in the focusing of attention and the phonological properties of written words. &nbsp;</p>\r\n\r\n<p>The cuneus is responsible for the evaluation of stimuli. It is also implicated in the recall of episodic memory and has a role in pain perception. It is important in attention comprehension and visual processing. (Choo et al., 2012; Choo et al., 2009).\r\n    It also plays a key role in the integration and synthesis of almost all sensory input.&nbsp; This area is also implicated in the distinction of self from other (Thompson &amp; Thompson, 2015). There is the possibility that one may feel anterograde\r\n    amnesia when it is damaged. This area, lastly, is involved in the identification of pain and has connections to the hippocampus, the posterior parietal cortex, the posterior parahippocampal gyrus, and the dorsal striatum (all implicated in memory)\r\n    (Thompson &amp; Thompson, 2015).</p>\r\n<p></p><h2><a name=\"_Toc525053914\"><br></a></h2><h2><a name=\"_Toc525053914\">BA 20</a></h2><br>Brodmann area 20 is the inferior temporal lobe. This region is implicated in the higher levels of the ventral stream of visual processing and the representation of complex object features. It also contains the fusiform gyrus and is thought to be involved\r\n    in face perception. The most common symptom of inferior temporal lobe damage is&nbsp;visual agnosia, which involves impairment in the identification of familiar objects.&nbsp;\r\n<p></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA%2020.png\" alt=\"BA13\" width=\"476\" height=\"764\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem;\"></p><h2><a name=\"_Toc28940444\"></a><a name=\"_Toc16242841\"></a><a name=\"_Toc525053915\">BA 21 and BA 22</a></h2>\r\n\r\n<p>Brodmann areas 21 is over the temporal lobe, encompassing most of the lateral temporal cortex. This region is also referred to as the middle temporal cortex. This region is linked to sentence generation and word processing, specifically:</p>\r\n\r\n<p></p>\r\n<ul>\r\n    <li>Word generation </li>\r\n    <li>Monitor speech </li>\r\n    <li>Repeating words </li>\r\n    <li>Complex sounds </li>\r\n    <li>Deductive reasoning </li>\r\n    <li>Categorization </li>\r\n    <li>Observe motion </li>\r\n    <li>Complex sounds</li>\r\n    <li>Mirror neuron system</li>\r\n</ul>\r\n<p></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<p style=\"text-align: left;\">BA 21 is vital for long term memory, like facts and events. The structures in the medial temporal gyrus include the hippocampus, the amygdala, brainstems and other regions critical for memory formation and storage.</p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA21.png\" alt=\"BA21\" width=\"480\" height=\"764\" class=\"atto_image_button_middle\"></p><p style=\"text-align: left;\"><br></p>\r\n\r\n<p>This area also holds the primary auditory cortex which is involved in high level auditory processing, and the processing of speech and words. This is an area where auditory signals from the cochlea reach the cerebral cortex and are processed by the primary\r\n    auditory cortex. The ventral part of the temporal cortices are involved in high-level visual processing of complex stimuli such as faces and scenes, and the anterior parts are for object perception and recognition. <sup></sup></p>\r\n\r\n<p>Damage in this areas would lead to disturbance of auditory sensation and perception, disturbance of selective attention of auditory and visual input, disorders of visual perception, impaired organization and categorization of verbal material, disturbance\r\n    of language comprehension, impaired long-term memory, and altered personality and affective behavior (Kolb &amp; Wilshaw, 1990).</p>\r\n<p></p>\r\n<h2><a name=\"_Toc28940445\"></a><a name=\"_Toc16242843\"></a><a name=\"_Toc525053917\">BA\r\n22</a></h2>\r\n<p style=\"text-align: center;\"><a name=\"_Toc525053917\"><img src=\"@@PLUGINFILE@@/BA22.png\" alt=\"BA22\" width=\"480\" height=\"701\" class=\"img-responsive atto_image_button_middle\"><br></a></p>\r\n\r\n<p>Brodmann area 22 is also known as Wernicke’s area, which is essential for auditory working memory. Responsible for auditory perception and processing, this is responsible for high-level auditory processing. It is possible that damage to this area would\r\n    show a lack of discrimination for auditory detail, as well as difficulty in sentence generation. The left&nbsp;hemisphere&nbsp;helps with generation and understanding of individual words. On the right side of the brain it helps to discriminate&nbsp;pitch&nbsp;and\r\n    sound&nbsp;intensity, both of which are necessary to perceive&nbsp;melody&nbsp;and&nbsp;prosody. This part of the brain is active in&nbsp;processing language&nbsp;and is part of&nbsp;Wernicke\'s area. The other main region included in Wernicke\'s area\r\n    is&nbsp;Brodmann area 40, the&nbsp;supramarginal gyrus.</p>\r\n<h2>BA 23</h2>\r\n\r\n<p>Brodmann area 23 is part of the posterior cingulate cortex (PCC). This area is also known as&nbsp;ventral posterior cingulate area 23. <a name=\"_Hlk529261768\">The PCC is a highly connected node in the brain. This is a fundamental\r\narea of intersection for all of the networks in the brain to convene and converge\r\ninto what is called the rich club. </a>The name “rich club” is analogous to social systems, where highly central individuals— being rich in connections—form a highly interconnected club (Zhou &amp; Mondragon, 2004). Rich clubs are very similar to the\r\n    substation system in power grids. The substations are there to facilitate the transmission of power, disseminating loads at appropriate intervals to conjoining substations, allowing for the ease of transmission and the prevention of system failure.\r\n</p>\r\n<p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA23.png\" alt=\"BA23\" width=\"498\" height=\"761\" class=\"atto_image_button_middle\"></p>\r\n<p><span style=\"font-size: 1rem;\">The posterior cingulate cortex\r\nmediates the person\'s&nbsp;</span><span style=\"font-size: 1rem;\">recognition &nbsp;of the existence\r\nin space. The precuneus is here and it may hold a good deal of a\r\nperson\'s autobiographical &nbsp;memory, and in that, her sense of identity.\r\nThis area is poorly infused with blood\r\nin fMRI studies of the DMN in patients with developmental trauma.\r\n</span><b style=\"font-size: 1rem;\">The precuneus &nbsp;is</b><span style=\"font-size: 1rem;\">\r\n</span><b style=\"font-size: 1rem;\">suggested\r\nto be the \'core node\' or \'hub\' of the default mode network, a web of&nbsp;</b><span style=\"font-size: 1rem;\">connections that are activated during\r\n\"resting consciousness\" in which people\r\ndo not engage intentionally in sensory or motor &nbsp;activity. This involvement in the default network &nbsp;is suggested to underlie its role in self-consciousness. It is one of the areas of the brain most deactivated\r\nduring slow-wave sleep and rapid eye\r\nmovement sleep and &nbsp;is involved in memory tasks, including episodic memory, source memory,\r\nand contextual associations. lastly, it is also, together &nbsp;with the dorsal premotor cortex, involved in visuospatial mental operations. &nbsp;While the\r\npremotor area engages in the mental\r\noperation, the precuneus aids monitoring the success of that operation in terms of internally represented visual images.</span></p><p><span style=\"font-size: 1rem;\"><br></span></p>\r\n<h2><span>BA24</span></h2>\r\n<p></p>\r\n<p><span style=\"font-size: 1rem;\"></span></p>\r\n<p>This Brodmann area occupies most of the&nbsp;anterior cingulate gyrus&nbsp;in an arc around the&nbsp;genu of the corpus callosum. Its outer border corresponds approximately to the&nbsp;cingulate sulcus.&nbsp;Broadmann area 24 is responsible for several\r\n    types of attention, arousal and inhibition of responses, and memory (like episodic and those related to odor and taste). It is involved in learning the value of actions (performance monitoring with adjustments made by orbital frontal cortex and the\r\n    dorso lateral pre frontal cortex, and detecting uncertainty. It play a major role in the Intention Network (9R, 47R, 20R, 38L, 24LR, 21LR, cerebellum), and verbal initiation. This region deals with mood swings, worry, self-other overlap and novelty\r\n    seeking personality. Francis Crick&nbsp;listed area 24 as the seat of free will because of its centrality in amotivational syndromes.</p>\r\n\r\n<p><br></p>\r\n<p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA24.png\" alt=\"BA24\" width=\"481\" height=\"764\" class=\"img-responsive atto_image_button_middle\"></p>\r\n\r\n<h2><a name=\"_Toc28940448\">Anterior Cingulate Cortex</a></h2>\r\n\r\n<p>&nbsp;<a name=\"_Hlk28777674\">The anterior cingulate cortex is a collar of\r\nwhite matter that surrounds the corpus callosum (the bundle of fibers that\r\nconnects the hemispheres of the brain. This is a major network hub of the\r\nbrain, responsible for the integration of network activity of all sorts.&nbsp; The anterior cingulate cortex is responsible\r\nfor much of our autonomic functioning, including heart rate, decision making,\r\nempathy, impulse control and emotion. &nbsp;</a></p>\r\n\r\n<p>Mood Disorders are often seen stemming from a dysregulation in this area and can manifest as depression, amotivational, and angry behaviors. The ACC can also be disorganized if one was predispositioned towards developmental trauma.</p>\r\n\r\n<p>Studies on meditators of various disciplines (notably transcendental meditation) show the anterior cingulate gyrus as activated by alpha when in deep states.&nbsp; This has been linked to a surge in dopamine, in honing of attention (and expertise in attention),\r\n    and in the ability to self-regulate easily. &nbsp;The ACC is disorganized in developmental trauma. Hyperreactivity of the anterior cingulate is also the brain signature of OCD (also in substance abuse).</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/ACC.jpg\" alt=\"BA24\" width=\"504\" height=\"490\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span></p><h2 style=\"text-align: left;\"><a name=\"_Toc525053920\"><br></a></h2><h2 style=\"text-align: left;\"><a name=\"_Toc28940449\"></a><a name=\"_Toc16242846\"></a><a name=\"_Toc525053920\">BA 25</a></h2>\r\n\r\n<p style=\"text-align: left;\">This area of the brain, Brodmann area 25, is called the subgenual area because it is “below the knee” of the corpus callosum. This area is very deep in the midline cortex and has an very important link to the affect network. It is this area that is considered\r\n    to be of key intervention to people who have intractable depression. It is rich in serotonin transporters and is influential in many networks. This area governs personality and social behavior, such as moral reasoning and the evaluation of emotional\r\n    words. It influences the hypothalamus and the brain stem, which are involved in sleep and appetite, as well as the hippocampus, which is essential for memory formation and self-esteem. </p>\r\n\r\n<p></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;&nbsp;</span><img src=\"@@PLUGINFILE@@/BA25.png\" alt=\"BA25\" width=\"498\" height=\"734\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">Irregular independent components at the subgenual anterior cingulate\r\n    affect the function of the brains’ Error Detection and Correction processes.&nbsp; This system which can be stuck in the “off position” as much as it can get stuck “on.” Usually if you are getting a lot of error codes (“that’s wrong,” “did you forget\r\n    to lock the door,” etc.) a significant marker here could signify an obsessive compulsive or oppositional defiant disorders. The anterior midline holds a model of what is going on in the world at the Subgenual Anterior Cingulate location. When that\r\n    spot is not working properly, you end up having error codes.</span></p><p></p>\r\n<p style=\"text-align: left;\"><br></p>\r\n<p style=\"text-align: left;\"><br></p>\r\n<p></p>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940450\"></a><a name=\"_Toc16242847\"></a><a name=\"_Toc525053921\">BA 2</a>6</h2>\r\n\r\n<p style=\"text-align: left;\">Brodmann area 26 is located at the isthmus of the posterior cingulate gyrus. Its role is not well defined.</p>\r\n<p></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp; &nbsp;</span><img src=\"@@PLUGINFILE@@/BA26.png\" alt=\"BA26\" width=\"498\" height=\"743\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: left;\"><br></p><p></p>\r\n\r\n<h2 style=\"text-align: left;\"><br></h2><h2 style=\"text-align: left;\"><a name=\"_Toc28940451\">BAs 27 &amp; 28</a> </h2>\r\n\r\n<p style=\"text-align: left;\">Brodmann area 27 is a &nbsp;cortical&nbsp;area that is a&nbsp;rostral&nbsp;part of the&nbsp;parahippocampal gyrus&nbsp;of the&nbsp;guenon. Brodmann areas 27, 28, 36 and 37 exist in the parahippocampal or fusiform gyrus of the ventral temporal lobe in\r\n    humans. These regions of the brain are responsible for representing space, such as those involving head-direction cells or grid cells, in areas 27 (the parasubicular cortex) and 28 (the ventral entorhinal cortex).</p><img src=\"@@PLUGINFILE@@/BA27.png\" alt=\"BA27\" width=\"400\" height=\"606\" style=\"text-align: left;\" class=\"atto_image_button_left\"><img src=\"@@PLUGINFILE@@/BA28.png\" alt=\"BA26\" width=\"400\" height=\"609\" class=\"img-responsive atto_image_button_right\" style=\"text-align: left;\">\r\n<h2></h2><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p>\r\n<p style=\"text-align: center;\">&nbsp;<img src=\"@@PLUGINFILE@@/BA29.png\" alt=\"BA29\" width=\"495\" height=\"764\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p>\r\n<h2 style=\"text-align: left;\"><br></h2>\r\n<h2></h2>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940452\">BA 29</a></h2>\r\n<p style=\"text-align: left;\">Brodmann area 29 is the medial area of the cortex that is part of the paralimbic cortex, involved in semantic associations (not conscious) and novelty. It is one of the less studied areas of the brain. &nbsp;It lies between the posterior cingulate are\r\n    the hippocampal areas and may be integral to the synthesization and integration of new information (i.e. memory).</p>\r\n<h2 style=\"text-align: left;\"><br></h2>\r\n<h2 style=\"text-align: left;\">BA 30</h2>\r\n<p style=\"text-align: left;\">Brodmann area 30 is the retrosplenial region and is part of the cingulate cortex and cuneus. This area is implicated in the affect, memory, and default mode network. It has a role in attending to speech, listening to sentences and understanding the emotional\r\n    aspects of words. It has connection to limbic areas and is implicated in mood regulation. It is one of the central midline structures, is involved in the default mode network, and has a role in appraisal of one’s self (insight) (Thompson &amp; Thompson,\r\n    2015).\r\n</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/BA30.png\" alt=\"BA29\" width=\"400\" height=\"764\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p><p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\"><br></p>\r\n<p></p>\r\n\r\n<h2 style=\"text-align: left;\">BA 31</h2>\r\n\r\n<p></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">Brodmann area 31, also known as&nbsp;dorsal posterior cingulate area 31, is a subdivision of the&nbsp;cytoarchitecturally&nbsp;defined&nbsp;cingulate region&nbsp;of the&nbsp;cerebral cortex. In the human it occupies portions of the&nbsp;posterior cingulate\r\n    gyrus&nbsp;and medial aspect of the&nbsp;parietal lobe. The region is typically discussed as having a unitary function because of a common pattern of relative deactivation observed during attentionally demanding tasks. One influential hypothesis is\r\n    that the posterior cingulate cortex has a central role in supporting internally-directed cognition. It is a key node in the default mode network and shows increased activity when individuals retrieve autobiographical memories or plan for the future,\r\n    as well as during unconstrained ‘rest’ when activity in the brain is mind wandering.</span></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/BA%2031.png\" alt=\"BA31\" width=\"479\" height=\"761\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n<h2 style=\"text-align: left;\">BA 32</h2>\r\n\r\n<p style=\"text-align: left;\">This area is also known i<span>n the&nbsp;human&nbsp;brain&nbsp;as the&nbsp;<span style=\"\">dorsal anterior cingulate area 32</span>,&nbsp;which controls self-monitoring of current emotional or somatic states, such as the anticipation and detection of\r\n    targets (indicating novelty), the influence of motor responses, and the cognitive control of action selection, </span>such as detecting errors when reward was expected for an action, but did not materialize.&nbsp; Involved in reward-based decision\r\n    making and activated by active distress.</p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/BA32.png\" alt=\"BA32\" width=\"436\" height=\"681\" style=\"text-align: left;\" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: left;\"><br></p><p></p>\r\n\r\n<p style=\"text-align: left;\">The ACC functions to inhibit the firing of the amygdala. It is often referred to as the transitional limbic cortex because it lies at the transition between the cortical and the subcortical regions. Joseph (1996) describes the ACC as “a supra-modal area\r\n    that is involved in the integration of motor tactile, autonomic, and emotional stimuli, as well as in the production of emotional sounds and the capacity to experience psychological pain and misery (p.243). In some abuse cases, this area has little\r\n    blood flow; no blood flow means little neuronal activation, which likely correlates directly to the sense of the self as a black hole—as non-existent.</p>\r\n\r\n<h4 style=\"text-align: left;\"><b><a name=\"_Toc525053924\">Brodmann area 32L</a> controls</b></h4><h3 style=\"text-align: left;\"><a name=\"_Toc28940456\"></a></h3>\r\n\r\n<p style=\"text-align: left;\"><ul><li>Visual uncertainty </li><li>Mood regulation </li><li>Evaluate emotional words </li></ul>\r\n    <!--[if !supportLists]--></p>\r\n\r\n\r\n\r\n\r\n\r\n<h4 style=\"text-align: left;\"><span><b>Brodmann area 32 Right controls</b></span></h4>\r\n\r\n<p style=\"text-align: left;\"><ul><li>Sustain response set </li><li>Identify pain </li><li>Self-insight </li><li>Reward </li><li>Reappraise negative emotions </li></ul>\r\n    <!--[if !supportLists]--></p>\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n\r\n<p></p>\r\n<h2 style=\"text-align: left;\"><br></h2><h2 style=\"text-align: left;\"><a name=\"_Toc28940457\">BA 33</a> </h2>\r\n\r\n<p style=\"text-align: left;\">Brodmann area 33 is <b>part of anterior cingulate cortex</b>&nbsp;is a subdivision of the&nbsp;cytoarchitecturally&nbsp;defined&nbsp;cingulate region&nbsp;of&nbsp;cerebral cortex. It is a narrow band located in the&nbsp;anterior cingulate gyrus&nbsp;adjacent\r\n    to thesupracallosal gyrus&nbsp;in the depth of the&nbsp;callosal sulcus, near the genu of the&nbsp;corpus callosum.</p><p style=\"text-align: center;\">&nbsp;<img src=\"@@PLUGINFILE@@/BA33.png\" alt=\"Ba33\" width=\"400\" height=\"764\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"></p>\r\n<p></p>\r\n<p style=\"text-align: left;\">&nbsp;</p>\r\n<p style=\"text-align: left;\"><br></p>\r\n\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940458\">BA 34</a></h2>\r\n\r\n<p style=\"text-align: left;\">&nbsp;</p>\r\n\r\n<p style=\"text-align: left;\">Area 34 of Brodmann&nbsp;refers to a subdivision of the cytoarchitecturally defined&nbsp;hippocampal region&nbsp;of the&nbsp;human&nbsp;cerebral cortex. It is located in the&nbsp;entorhinal area&nbsp;on the&nbsp;medial&nbsp;aspect of the&nbsp;temporal\r\n    lobe.\r\n</p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/BA34.png\" alt=\"BA34\" width=\"481\" height=\"764\" style=\"text-align: left;\" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: left;\"><br></p><p></p>\r\n<h3 style=\"text-align: left;\">BA 35</h3><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">Brodmann area 35 is </span><b style=\"font-size: 1rem;\">perirhinal area 35</b><span style=\"font-size: 1rem;\">. It is a subdivision of the&nbsp;cytoarchitecturally&nbsp;defined&nbsp;hippocampal region&nbsp;of the&nbsp;cerebral cortex. In the human it is located along the&nbsp;rhinal sulcus. Cytoarchitectually\r\nit is bounded medially by the&nbsp;entorhinal area 28&nbsp;and laterally by the&nbsp;ectorhinal area 36.</span></p><p></p>\r\n\r\n\r\n\r\n<p style=\"text-align: left;\">The hippocampus is responsible for synthesizing short term into long term memory, episodic memory, autonomic processes, response inhibition, and spatial cognition. Hippocampus damage can lead to anxiety disorders and an inability to suppress responses\r\n    that have been conditioned. It also encodes emotional responses from the amygdala. Damage to the hippocampus will result in the inability to form new memories. This is also an area that is responsible for conflict detection and approach-avoidance\r\n    behaviors, linking it to some anxiety conditions.\r\n</p>\r\n\r\n<p style=\"text-align: left;\">There are two hippocampi—one for each hemisphere. Each has a different role in memory. The RH hippocampus records memory in spatial and temporal fields and the LH holds verbal memory. The RH hippocampus is central to implicit, non verbal memory—in a sense,\r\n    unremembered memory. When RH memory begins to return, it is often in felt experiences and in pictures and in spatial contexts. The LH hippocampus is involved in declarative or explicit memory, also called semantic memory (i.e. related to words), and\r\n    gives us the ability to used words to communicate emotional states. Sustained stress and high levels of circulating cortisol and other stress hormones (i.e. glucocorticoids) lead to a smaller hippocampus, structurally, and as a result, to impaired\r\n    memory. “ A likely explanation is that the shrinkage in the hippocampus is due to the effects of heightened cortisol, which is known to be toxic to the hippocampus” (van der Kolk, 2007, p. 233).</p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/BA%2035.png\" alt=\"BA 35\" width=\"480\" height=\"763\" style=\"text-align: left;\" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: left;\"><br></p><p></p>\r\n\r\n<p style=\"text-align: left;\">The hippocampus is responsible for synthesizing short term into long term memory, episodic memory, autonomic processes, response inhibition, and spatial cognition. Hippocampus damage can lead to anxiety disorders and an inability to suppress responses\r\n    that have been conditioned. It also encodes emotional responses from the amygdala. Damage to the hippocampus will result in the inability to form new memories. This is also an area that is responsible for conflict detection and approach-avoidance\r\n    behaviors, linking it to some anxiety conditions. The flow of information in the hippocampus is mostly unidirectional, or so called feed forward&nbsp; (Buszaki. 70).</p>\r\n\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940460\"></a><a name=\"_Toc16242851\"></a><a name=\"_Toc525053925\">BA 36 &amp; 37</a></h2>\r\n<p style=\"text-align: center; \"><a name=\"_Toc525053925\"><img src=\"@@PLUGINFILE@@/Ba36.png\" alt=\"BA36\" width=\"480\" height=\"727\" style=\"text-align: left;\" class=\"img-responsive atto_image_button_middle\"></a></p><p style=\"text-align: left;\"><a name=\"_Toc525053925\"><br></a></p><p></p>\r\n\r\n<p style=\"text-align: left;\">Ectorhinal area 36 is a subdivision of the cytoarchitecturally defined temporal region of cerebral cortex. With its medial boundary corresponding approximately to the rhinal sulcus it is located primarily in the fusiform gyrus, which is responsible for\r\n    the recognition of faces. Cytoarchitecturally it is bounded laterally and caudally by the inferior temporal area 20, medially by the perirhinal area 35 and rostrally by the temporopolar area 38</p>\r\n\r\n<p style=\"text-align: left;\">Area 36 (the lateral perirhinal cortex) is crucial for various types of associative learning. Earlier human neuroimaging studies have also indicated that faces, bodies and visual word forms are represented in different regions of area 37 in the posterior\r\n    fusiform gyrus. Recent neuroimaging studies in humans have shown substantial functional differentiation between face-related regions in areas 37 and 36, which is similar to that seen in macaque monkeys, as shown through their face patches. This implies\r\n    the crucial involvement of both areas in face processing. </p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA37.png\" alt=\"BA37\" width=\"400\" height=\"625\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p>\r\n<p></p>\r\n<p></p>\r\n\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940462\">BA38</a></h2>\r\n\r\n<p style=\"text-align: left;\">BA 38 is part of the temporal cortex. The temporal pole is a paralimbic region involved in high level semantic representation and socio-emotional processing. The&nbsp;uncinate fasciculus&nbsp;provides a direct bidirectional path to the orbitofrontal cortex,\r\n    allowing mnemonic representations stored in the temporal pole to bias decision making in the frontal lobe. The temporal pole appears to be a convergence zone where semantic memories that are stored in the ventral anterior temporal lobe are imbued\r\n    with emotional significance and personal meaning.&nbsp; In addition, concepts of individual people, abstracted away from the perceptual representations, are stored in a “face patch” in the temporal pole. This face patch is found in both non-human\r\n    primates and humans.&nbsp;&nbsp;This relates to early work showing that damage to the temporal pole can cause an amnestic prosopanosia in which knowledge of familiar people is lost.&nbsp; Bilateral damage to the temporal poles, though rare, can cause\r\n    dramatic changes in personality.&nbsp;Kluver-Bucy syndrome&nbsp;involves damage to the greater temporal pole as well as the&nbsp;amygdala. In this disorder, individuals demonstrate fearlessness, hyper sexuality, and hyper orality.</p>\r\n\r\n<p></p><p style=\"text-align: left;\"><span style=\"font-size: 10.5px; vertical-align: super;\">&nbsp;</span></p><sup><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA38.png\" alt=\"BA38\" width=\"500\" height=\"787\" class=\"img-responsive atto_image_button_middle\" style=\"vertical-align: super;\"></p></sup><p></p>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940463\">BA 39</a></h2>\r\n\r\n<p style=\"text-align: left;\">BA39 encompasses the&nbsp;angular gyrus, lying near to the junction of&nbsp;temporal,&nbsp;occipital&nbsp;and&nbsp;parietal lobes. This region is thought to have correlation with the visual representation of words and phonemes, damage to Brodmann area\r\n    39 may result in dyslexia&nbsp;or in semantic&nbsp;aphasia.&nbsp;Albert Einstein&nbsp;had more glia in this region than the normal person and it has been hypothesized this is why he had remarkable mathematical genius.</p>\r\n<p></p>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940464\">BA 40</a> </h2>\r\n\r\n<p style=\"text-align: left;\">Brodmann area 40 is located the inferior parietal lobule. This region of the brain is responsible for: attention to phonemes, categorization, verbal creativity, aversiveness, emotional working memory, conscious recollection, visual grasping, gesture imitation,\r\n    visuomotor planning, intention/conflict detection, deduction, empathy, and goals.</p>\r\n<p style=\"text-align: center;\">&nbsp;<img src=\"@@PLUGINFILE@@/BA40.png\" alt=\"BA40\" width=\"480\" height=\"720\" class=\"img-responsive atto_image_button_text-bottom\"><br></p>\r\n\r\n<p style=\"text-align: left;\">Brodmann area 40 is responsible for attendance to calculation, phonemes, categorization, verbal creativity, aversiveness, emotional working memory, conscious recollection, visual grasping, gesture imitation, visuomotor planning, Repetitive passive movements,\r\n    intention/conflict detection, deduction, empathy , music performance, goals, imitation of novel actions.</p>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940465\"></a><br></h2>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/ba41.png\" alt=\"ba41\" width=\"480\" height=\"743\" style=\"text-align: left;\" class=\"img-responsive atto_image_button_middle\"></p>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc525053928\">BA 41, 42</a></h2>\r\n<p style=\"text-align: left;\">Brodmann areas 41, and 42 are all parts of the auditory cortex. In extreme cases, damage here will show loss in the conscious awareness of sound, 41 and 42 are areas that comprise Herschel’s gyrus, an area that is known for picking up and recognizing\r\n    the paralinguistics of speech (including prosody, tone, gait, tenor, timbre, tempo, volume, and patterns). This area is responsible for how we decode what the other is saying. Herschl’s gyrus and has a direct corollary to the densely packed cochlear\r\n    nucleus, which is responsible for the processing of sounds. In this region of the brain words and sounds are decoded through the heteromodal association cortex and are given meaning through the angular gyrus, where they are then related to other words\r\n    and meanings encountered in the past.</p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/ba42.png\" alt=\"ba41\" width=\"487\" height=\"784\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p>\r\n<p></p>\r\n<h3 style=\"text-align: left;\">BA 43</h3>\r\n\r\n<p style=\"text-align: left;\">Brodmann Area 43 responds to pressure on the eardrum &nbsp;and to oral intake (eating and drinking). Because eating and drinking change pressure on the middle ear and eardrum, Brodmann Area 43 may be the primary somatosensory cortex of the eardrum.</p>\r\n\r\n<p style=\"text-align: left;\">Additionally, Brodmann Area 43 was found to be functionally active in a study differentiating the roles of the left-frontal and right-cerebellar regions during semantic analysis. Brodmann Area 43 showed a major increase in functional activation by fMRI,\r\n    when study participants &nbsp;were asked to complete tasks which involved the selection of a verbal response from many possible responses, rather than a sustained search for a verbal response from few possible responses.\r\n</p>\r\n<p style=\"text-align: center;\">&nbsp;<img src=\"@@PLUGINFILE@@/ba43.png\" alt=\"bA43\" width=\"500\" height=\"764\" style=\"text-align: center; \" class=\"atto_image_button_middle\"></p><p style=\"text-align: left;\"><br></p><h3 style=\"text-align: left;\"><a name=\"_Toc28940468\"><br></a></h3><h3 style=\"text-align: left;\"><a name=\"_Toc28940468\">BA 44 and 45</a></h3>\r\n\r\n<p style=\"text-align: left;\"><a name=\"_Hlk26903308\">Brodmann\r\nareas 44 and 45 are the pars opercularis and the pars triangularis, respectively.\r\nThese areas are part of Broca’s area and cover the insula. Broca’s area was\r\ndiscovered in a patient who was unable to produce speech. This area is\r\nimportance for semantics, phonetics, as well as verbal understanding, speech\r\narticulation, grammatical processing, and speech fluency. Boiled down, this is\r\nthe area that enables us to speak. When compromised, we may see difficulty\r\nproducing speech, stuttering, and other symptoms of difficulty producing words.\r\nThis area is also important for internal speech and the internal rehearsal of\r\ninformation. </a></p>\r\n\r\n\r\n\r\n<p style=\"text-align: left;\">The pars traingularis (Brodmann area 45) is important in memory networks, particularly episodic, syntactic, semantic, and declarative memory encoding. When reading aloud, this area allows for the decoding and correct pronunciation of speech&nbsp; (Thompson\r\n    &amp; Thompson, 2015, p. 51-52).</p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA%2044%20and%2045.png\" alt=\"BA 44 \" width=\"538\" height=\"700\" class=\"img-responsive atto_image_button_text-bottom\"></p><p style=\"text-align: center;\"><br></p>\r\n<p></p>\r\n<h2 style=\"text-align: left;\"><a name=\"_Toc28940469\"></a><a name=\"_Toc16242856\"></a><a name=\"_Toc525053930\">BA 46</a></h2>\r\n\r\n<p style=\"text-align: left;\">Brodmannn area 46 is intimately connected to areas 8 and 9, all the executive regions of the brain.&nbsp; These are the areas of the prefrontal dorsolateral cortex, which are implicated in making judgments, planning, monitoring, revising, sustaining attention,\r\n    working memory, inhibition of responses, willed actions and verbal and episodic memory retrieval.&nbsp; Mirror neurons are located here. Spatial information is also processed here (Thompson &amp; Thompson, 2015).</p>\r\n\r\n<p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/BA46.png\" alt=\"BA46\" width=\"480\" height=\"753\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></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: left;\"><a name=\"_Toc525053931\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 2.143rem; background-color: rgb(255, 255, 255);\">BA 47</a><br></p>\r\n\r\n<p style=\"text-align: left;\">Brodmann area 47 is part of the frontal cortex that curves from the lateral surface of the brain to into the orbital frontal cortex. This area is implicated in deductive reasoning, language and emotions. It is located in the pre-frontal cortex near Brodmann\r\n    areas 9 and 10, parallel to Brodmann area 11.&nbsp; This area is part of the executive network and is important in processing syntax and semantics of language (oral and sign language) categorization and aspects of language and speech. It is also important\r\n    for episodic and working memory. It is one of the key areas for deductive reasoning and is important in making inferences, as well as monitoring actions and incoming information and behavior. Lastly, it is important in the temporal coherence of processing\r\n    music (Thompson &amp; Thompson, 2015, p. 54).\r\n    </p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/BA47.png\" alt=\"BA47\" width=\"400\" height=\"603\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem;\"></p>\r\n<p></p><p style=\"text-align: center;\"><br></p>\r\n<p></p>',1),(417,111,0,418,20,0,1,1,1588712741,1654021956,'History, Anatomy and Function','<p></p>\r\n<p>The discovery of neurotransmitters and the firing of the EEG were different discoveries. Hans Berger was not the first electroencephalographer (Caton was), but Berger was the first to dedicate time to studying the firing of the brain. Berger was excessively\r\n    self-conscious about his initial findings on EEG, so much so that he undertook 5 years of testing and surveying the results of his studies on EEG before he released it to the public in report form.&nbsp;</p>\r\n<h3>Richard Caton (Left) and Hans Berger (Right)</h3>\r\n<p>&nbsp;<img src=\"@@PLUGINFILE@@/berger.jpeg\" alt=\"berger\" width=\"444\" height=\"333\" class=\"img-responsive atto_image_button_middle\"><img src=\"@@PLUGINFILE@@/caton.jpg\" alt=\"caton\" width=\"250\" height=\"319\" class=\"img-responsive atto_image_button_left\"></p>\r\n\r\n<p><br></p>\r\n<h3>Otto Loewi</h3><img src=\"@@PLUGINFILE@@/Loewi.jpg\" alt=\"loewi\" width=\"180\" height=\"255\" class=\"img-responsive atto_image_button_left\">\r\n<p>Otto Loewi was the first neuroscientist to prove that neurotransmistters are released in the junction (synapse) between the vagus nerve and the heart muscle. He received a Nobel Prize with Henry Hallett Dale from Cambridge England in 1936 for their discoveries.\r\n    Loewi wrote:</p>\r\n\r\n<p><i>The night\r\nbefore Easter Sunday of that year, I awoke, turned on the light, and jotted\r\ndown a few notes on a tiny slip of thin paper. Then I fell asleep again. It\r\noccurred to me at six o’clock in the morning that I had written down something\r\nmost important, but I was unable to decipher the scrawl. The next night, at\r\nthree o’clock, the idea returned. It was the experiment to determine whether or\r\nnot the hypothesis of chemical transmission that I had thought about years ago\r\nwas correct. I got up immediately, went of&nbsp;\r\nthe laboratory, and performed a simple experiment on a frog heart\r\naccording to the nocturnal design.</i> (Loewi, 1960, 15).</p>\r\n<h2><a name=\"_Toc3535192\"><br></a></h2>\r\n<p><br></p><h3><a name=\"_Toc3535192\">Ramon y Cajal and The Discovery of the Neuron</a></h3>\r\n<p><a name=\"_Toc3535192\">The neuron is considered to be the fundamental structural and functional unit of the nervous\r\nsystem. While other organs of the body were fairly well understood morphologically during the\r\nlast few centuries, the understanding of what the neuron \"looks like\" was not well known until\r\nearly 1900. Before this time scientists could not \"see\" the structure of the brain and it appeared as\r\na tangled net of various fibers. In fact, several theories until the late 1800s held that the brain was\r\ncomposed of a series of tiny tubes through which certain secretions flowed. Ill health was\r\nthought to be the result of an imbalance of the flow of these secretions through these tubes.&nbsp;</a></p>\r\n<p><a name=\"_Toc3535192\"><img src=\"@@PLUGINFILE@@/cajal.png\" alt=\"Cajal\" width=\"300\" height=\"370\" class=\"img-responsive atto_image_button_left\">Who first identified the structure of the neuron?\r\nDuring the early years of 1900, a well known Spanish anatomist Santiago Ramon\r\ny Cajal changed all that. Using a new staining method, silver chromate, recently\r\ndeveloped by his Italian colleague, Camillo Golgi, Cajal was able to identify the\r\nstructure and boundaries of individual neurons. It became evident to him that the\r\nbrain was composed of individual cells of varying morphologies and that these\r\ncells were unique in several ways. First, neurons are not necessarily spherical\r\nshaped as are cells of other body tissue. Indeed, there are several different forms\r\nor morphologies to the neuronal cell structure. Second, whatever the form of the neuron, Cajal\r\nnoted that each neuron consisted of a cell body and three other morphologically defined areas.<br></a></p>\r\n<p><a name=\"_Toc3535192\"><br></a></p>\r\n<p><a name=\"_Toc3535192\"><br></a></p>\r\n<p><a name=\"_Toc3535192\"><br></a></p>\r\n<p><a name=\"_Toc3535192\"><br></a></p>\r\n<h2><a name=\"_Toc3535192\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\"><br></a></h2><h2><a name=\"_Toc3535192\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\"><br></a></h2><h2><a name=\"_Toc3535192\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Intricate Neuroanatomy: The Neuron</a><br></h2>\r\n\r\n<p>The major cell of the central nervous system is the <b><u>neuron</u></b>. Neurons are pretty much the most basic unit of the brain, as well as the most complicated cell in the human body. The brain has about 100 billion neurons with an estimated 200 trillion\r\n    connections between them (Buszaki, 2006) or 50 dendrites per neuron. A neuron has a cell body (also called soma, or perikaryon); dendrites, which are the branched<b>&nbsp; </b>projections of a neuron that act to conduct the electrical stimulation\r\n    received from other neural cells to the cell body, or soma, of the neuron from which the dendrites project. Dendrites extend a short distance from the soma (each of them having spines that absorb neurotransmitter); and an axon (also called fiber),\r\n    which connects one neuron with others. The fibrous axons occupy more space in the brain than neurons, dendrites, and spines combined. In short, axons take information away from the cell (longer axons are covered in the myelin sheath, which provides\r\n    faster transmission.</p>\r\n\r\n<p>Neuronal membranes are specialized for electro-chemical events, the firing of action potentials and the release/reception of neurostransmitters. This is how neurons communicate to one another. The dendrites and cell bodies of the neurons receive information,\r\n    and the axons transmit the ﬁring pattern of the cell to the next neuron. Generally, each neuron receives synaptic input from hundreds or perhaps thousands of other neurons, and its axon distributes this information via collaterals (branches) to hundreds\r\n    of other neurons. The overwhelming majority of neurons are used for the processing of information and are called interneurons. The more dramatic the level of processing, the more the interneurons are involved.</p>\r\n<p><br></p>\r\n<p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/neuron.png\" alt=\"Neuron\" width=\"432\" height=\"330\" class=\"img-responsive atto_image_button_middle\"></p>\r\n\r\n<p>Neurons prefer to take the shortest paths with their surrounding peers. They receive most of their information from their immediate neighbors and act locally (p. 45). In order to communicate with distant neurons, it requires the use of costly connections\r\n    metabolic resources and connections to transporting electrical pulses over long distances (Buzsaki, 2006).</p>\r\n<h3><span style=\"font-size: 1.715rem;\"><br></span></h3>\r\n<h3><span style=\"font-size: 1.715rem;\">Anatomy of a Neuron</span><br></h3>\r\n<p>Watch this video on the anatomy of a neuron:</p>\r\n<p><a href=\"https://www.youtube.com/watch?v=HZh0A-lWSmY\">neuron</a><br></p>\r\n<p></p>\r\n<p>Communication between neurons occurs almost exclusively at specialized junctions called <b>&nbsp;<u>synapse</u>s</b>, using biological molecules called <b><u>neurotransmitters</u></b>. Neurotransmitters modify ion movements across the neuronal membranes\r\n    of the synapse and alter neurotransmission (with each action potential neurotransmitters travel across the synaptic gap) — neurotransmitters can be excitatory or inhibitory in their action, or modulate synaptic excitability. The post-synaptic neuron\r\n    will modify its ﬁring pattern depending on the summative effect of all the synapses acting upon it at any moment in time. The action of neurotransmitters depends also on the speciﬁc receptor type; there is an ever-increasing number of receptor subtypes\r\n    allowing for even more complexity of information processing within the CNS. Drugs are being designed to act on those receptors for therapeutic purposes.\r\n</p>\r\n\r\n<p>&nbsp;Here is a short video of the function of the synapse:</p>\r\n<p><a href=\"https://www.youtube.com/watch?v=WhowH0kb7n0\">synapse</a><br></p>\r\n<p>And here is a video with a little more info:</p>\r\n<p><a href=\"https://www.youtube.com/watch?v=i-XwPjN3ZtI\">synapse</a><br></p>\r\n<p><br></p>\r\n<h3>Anatomy of an Axon</h3>\r\n<p><img src=\"@@PLUGINFILE@@/axon.png\" alt=\"axon\" width=\"670\" height=\"374\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n<p>When measuring EEG—we are measuring “action potentials” along the axon. An action potential is a firing—bam!—that is the swapping of potassium and sodium along the border of the axon. Much of the substance of the brain consists of <b>a<u>xons</u></b>,\r\n    also called ﬁbers, which connect one part of the brain with other areas. Low frequency oscillations (i.e., delta and theta) coordinate long-range communications, between lobes of the brain (von Stein, Chiang, &amp; Konig, 2000). </p>\r\n\r\n<p>This stage of wiring the brain happens in utero, with the long connections being the most fundamental (Grubin, 2011). It is these long fibrous white matter tracks that theta and delta traverse. Many of the axons are myelinated by oligodendrocites (a type\r\n    of glial cell), this “insulation,”&nbsp; serve to increase the speed of axonal conduction; the thicker the <b>myelin sheath</b>, the faster the conduction. Axons originating from one area (cortex or nucleus) and destined for another area usually group\r\n    together and form a tract, also called a pathway (or fasciculus).</p>\r\n<p><br></p>\r\n\r\n<h3>&nbsp;A Neuron and an Axon</h3>\r\n<p><img src=\"@@PLUGINFILE@@/Neuron%20and%20Axon.png\" alt=\"Neuron and Axon\" width=\"679\" height=\"419\" class=\"img-responsive atto_image_button_left\"></p>\r\n<p></p>\r\n<p></p>\r\n<p>Moreover, there are even more numerous glial cells and finely branch blood vessels that support and nourish the neurons. The neuronal circuits in each subdivision constitute local networks, which are further integrated to form global neural systems across\r\n    subdivisions or divisions. Current neuroscience is based on the belief that these networks and systems operate through specific mechanisms and play specific functional roles in the living body.</p>\r\n\r\n<p><br></p>\r\n<p><br></p>\r\n<p><b style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem;\">What are neurotransmitters and how do they work?</b><br></p>\r\n\r\n<p>Neurotransmitter substances are biochemical enzymes which, when released from the presynaptic cell, cross the synaptic cleft and bind with receptors on the membrane of the post synaptic cell.&nbsp;</p>\r\n<p>Many neurotransmitter substances have been identified in the CNS and are divided into two general classes:&nbsp;\r\n</p>\r\n<p>1. Substances of low molecular weight such as: noradrenaline, dopamine, serotonin, 5HTP, histamine, glutamate, GABA, glycine&nbsp;</p>\r\n<p>2. Neuroactive peptides (which have large molecular weight): i.e. vasopressin, substance P, somatostatin. </p>\r\n<p><img src=\"@@PLUGINFILE@@/neurotransmitters%201.png\" alt=\"Neurotransmitters\" width=\"900\" height=\"545\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><img src=\"@@PLUGINFILE@@/neurotransmitters%202.png\" alt=\"neurotransmitters 2\" width=\"900\" height=\"772\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n<p><img src=\"@@PLUGINFILE@@/neurotransmitters%203.png\" alt=\"neurotreanmitters 3\" width=\"900\" height=\"277\" class=\"img-responsive atto_image_button_left\"><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><br></p>\r\n<p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\"><br></span></p><p><span style=\"font-size: 1rem;\">All transmitter substances meet certain criteria. They must be able to:</span><br></p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->1)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->be synthesized in the pre-synaptic neuron </p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->2)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->be stored in vesicles in the pre-synaptic neuron\r\n</p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->3)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->be released by neuronal activity bind with receptors on the post synaptic cell </p>\r\n\r\n<p>\r\n    <!--[if !supportLists]-->4)&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;\r\n    <!--[endif]-->be removed from the synaptic cleft </p>\r\n\r\n<p>After propagation, the action potential proceeds to the terminal end of the axon. Depolarization of the terminal membrane causes changes in voltage gated channels that allow calcium to enter. As Ca+ enters the cell, synaptic vesicles containing transmitter\r\n    substance migrate toward the cell membrane where they fuse with the membrane. The contents of the vesicle then releases thousands of transmitter molecules into the extracellular synaptic cleft.\r\n</p>\r\n\r\n<p>Transmitter molecules cross the cleft and bind receptors on the post synaptic membrane in a \"lock and key\" fashion producing changes which ultimately act to excite or inhibit the cell. Whether the post synaptic cell moves toward threshold (excitatory)\r\n    or away from threshold (inhibitory) is a function of transmitter action on the receptor of the post synaptic membrane. Some transmitter substances such as glutamate cause excitatory changes, i.e. they move the resting membrane potential toward threshold.\r\n    Such a synaptic potential is referred to as an excitatory post synaptic potential or EPSP. Other transmitters such as GABA and dopamine are inhibitory moving the Resting Membrane Potentials away from threshold and this post synaptic potential is called\r\n    an IPSP. However, the action of a specific chemical transmitter substance on the post synaptic membrane does not depend on the molecular make-up of the transmitter, but rather on the properties of the receptor with which the transmitter binds. </p>\r\n\r\nMore about neurotransmitters: Acetylcholinestrase (ACh-ase) Once in the synaptic cleft the transmitter signaling must be turned \"off\' or stopped. This is carried out by an enzyme that is present in the synaptic space. In the case of acetylcholine, this\r\nenzyme is called acetylcholinesterase (ACh- ase). ACh -ase acts to catalyze the acetylcholine and breaks it into acetate and choline which is reabsorbed into the presynaptic cell for re- synthesis. This series of events is demonstrated using the transmitter\r\nsubstance acetylcholine as a model. Many transmitters work in the same way as acetylcholine. However, a second type of neural transmission may occur in some synapses. This is by way of so-called second messenger transmission. In second messenger transmission\r\na transmitter substance binds with a receptor that then causes metabolic activity inside the cell to produce indirect changes in ionic conductances and thus voltage changes. Second messenger activation usually lasts longer than that of chemically gated\r\ntransmission. Inhibition in neural signaling may also be produced before the action potential reaches the presynaptic terminal. Specific to axo-axonic synapses, presynaptic inhibition occurs when the excitatory action of a presynaptic neuron produces\r\nchanges in a post synaptic axon to the extent that it inhibits release of the transmitter.\r\n<p></p>\r\n\r\n<h2>Post Synaptic Potentials</h2>\r\n<p><b>Postsynaptic potentials</b>&nbsp;are changes in the&nbsp;membrane potential&nbsp;of the postsynaptic terminal of a&nbsp;chemical synapse. Postsynaptic potentials are&nbsp;graded potentials, and should not be confused with&nbsp;action potentials&nbsp;although\r\n    their function is to initiate or inhibit action potentials. They are caused by the presynaptic neuron releasing&nbsp;neurotransmitters&nbsp;from the terminal bouton at the end of an&nbsp;axon&nbsp;into the&nbsp;synaptic cleft. The neurotransmitters\r\n    bind to&nbsp;receptors&nbsp;on the postsynaptic terminal.<br></p>\r\n<p>\r\n    </p><p>Neurons have a&nbsp;resting potential&nbsp;of about −70&nbsp;mV. If the opening of the ion channel results in a net gain of positive charge across the membrane, the membrane is said to be&nbsp;depolarized, as the potential comes closer to zero. This\r\n        is an&nbsp;<b>excitatory postsynaptic potential&nbsp;(EPSP)</b>, as it brings the neuron\'s potential closer to its firing threshold (about −55&nbsp;mV).</p>\r\n    <p>If, on the other hand, the opening of the ion channel results in a net gain of negative charge, this moves the potential further from zero and is referred to as&nbsp;hyperpolarization. This is an&nbsp;<b>inhibitory postsynaptic potential&nbsp;(IPSP)</b>,\r\n        as it changes the charge across the membrane to be further from the firing threshold.</p>\r\n    <p>Neurotransmitters are not inherently excitatory or inhibitory: different receptors for the same neurotransmitter may open different types of ion channels.</p>\r\n    <p>EPSPs and IPSPs are transient changes in the membrane potential, and EPSPs resulting from transmitter release at a single synapse are generally far too small to trigger a spike in the postsynaptic neuron. However, a neuron may receive synaptic inputs\r\n        from hundreds, if not thousands, of other neurons, with varying amounts of simultaneous input, so the combined activity of afferent neurons can cause large fluctuations in membrane potential or&nbsp;subthreshold membrane potential oscillations.\r\n        If the postsynaptic cell is sufficiently depolarized, an&nbsp;action potential&nbsp;will occur.&nbsp;</p>Curious to better understand? This video should help explicate this interesting dynamic.<p></p>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/B92rsa1is_k\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n<h2>Long Term Potentiation and Long Term Depression</h2>\r\n<p></p>\r\n<p>In&nbsp;neuroscience,&nbsp;<b>long-term potentiation</b>&nbsp;(<b>LTP</b>) is a persistent strengthening of&nbsp;synapses&nbsp;based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal\r\n    transmission between two&nbsp;neurons.<span style=\"font-size: 10.5px;\"> </span>The opposite of LTP is&nbsp;<b>long-term depression (LTD)</b>, which produces a long-lasting decrease in synaptic strength.</p>\r\n<p>Here is a video on long term potentiation</p>\r\n<iframe width=\"560\" height=\"315\" src=\"https://www.youtube.com/embed/T8e1yH_z-8s\" title=\"YouTube video player\" frameborder=\"0\" allow=\"accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture\" allowfullscreen=\"\"></iframe>\r\n<p><br></p>\r\n<p><br></p>\r\n<p>Long term potentiation is one of several phenomena underlying&nbsp;synaptic plasticity, the ability of&nbsp;chemical synapses&nbsp;to change their strength. As memories are thought to be encoded by modification of&nbsp;synaptic strength,&nbsp;LTP is widely\r\n    considered one of the major cellular mechanisms that underlies&nbsp;learning&nbsp;and&nbsp;memory.</p>\r\n<p>LTP was discovered in the rabbit&nbsp;hippocampus&nbsp;by&nbsp;Terje Lømo&nbsp;in 1966 and has remained a popular subject of research since. Many modern LTP studies seek to better understand its basic biology, while others aim to draw a causal link between\r\n    LTP and behavioral learning. Still others try to develop methods, pharmacologic or otherwise, of enhancing LTP to improve learning and memory. LTP is also a subject of&nbsp;clinical research, for example, in the areas of&nbsp;Alzheimer\'s disease&nbsp;and&nbsp;addiction\r\n    medicine.</p><br>\r\n<p></p>\r\n<p></p>\r\n<p></p>',1),(418,111,417,419,20,0,1,1,1588818115,1596822752,'Blood Supply, Glia, and Ventricles','<p></p><h2><a name=\"_Toc28940476\">Blood Supply</a></h2><p>&nbsp;The blood supply to the brain takes up to 20% of the total oxygen consumption of the body. A lack of oxygen to the brain results in ischemia, hypoxia (partial restriction of oxygen) and anoxia (total deprivation of oxygen to the brain). In the image of the arterial supply of blood to the central nervous system are the larger pair of the left and right carotid artery and the smaller pair of the vertebral arteries.</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Vertebral%20Arteries.png\" alt=\"Vertebral Arteries\" width=\"600\" height=\"352\" class=\"atto_image_button_middle\" style=\"font-size: 1rem; text-align: center;\"><br><span style=\"font-size: 1rem; text-align: left;\"><br></span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">This is a great video on blood flow in the brain:</span></p><p></p><p></p><p style=\"text-align: center;\"><a href=\"https://www.youtube.com/watch?v=Pl2tYwx7o5w\">Blood Flow</a><br></p><p style=\"text-align: center;\">And here is a video on the up-close dynamics of blood flow in the brain:&nbsp;<a href=\"https://www.youtube.com/watch?v=9hhfM7rQHiM\">Blood Flow Part 2</a></p><p></p><p style=\"text-align: left;\">The left and right carotid\narteries bifurcate at the fourth vertebrae and form the internal\ncarotid &nbsp;arteries,\nentering the brain through\nthe carotid canal of the temporal bone. These internal&nbsp;<span style=\"font-size: 1rem;\">carotid &nbsp;arteries form the circle\nof Willis, as well as the ophthalmic arteries (supplies\nthe structures of the orbit), the posterior communicating artery (the \"connecting vessel: in\nthe circle of willis), the anterior choroidal\nartery (supplies the areas of the brain\nimportant for&nbsp;</span><span style=\"font-size: 1rem;\">motor &nbsp;control and vision, and the anterior &nbsp;cerebral artery (which supplies\nthe cerebrum).</span></p><p style=\"text-align: left;\"><br></p><p></p><h3 style=\"text-align: left;\">Carotid Canal</h3><p></p><p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/Carotid%20Canal.png\" alt=\"Carotid Canal\" width=\"474\" height=\"398\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p><h2 style=\"text-align: center; \"><br></h2><h2 style=\"text-align: left;\"><a name=\"_Toc28940477\" style=\"color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);\">Glia</a><br></h2>\n\n<p style=\"text-align: left;\">Other than neurons,\nthe other major\ncells of the central nervous\nsystem are glia, in fact, glial cells\nare the most abundant cells in the central nervous\nsystem. Glia is Latin for \"glue/\'&nbsp; and glia\nsurround the neurons and provide support and insulation for them. The extensive brain vessel\nsystem needs the support&nbsp; of glial cells because glia feed neurons\nand the brain is supplied\nby the highest density of blood vessels\nin the entire body.</p>\n\n<p style=\"text-align: left;\">Glia can be divided into two classes, macroglia and microglia.&nbsp;</p><p style=\"text-align: left;\">1) Microglia are glial cells that are scavengers of the central nervous\nsystem, removing pathogens, debris, bacteira, damaged cells, and other\nforeign substances.&nbsp; They have a spider-like shape.</p><p style=\"text-align: left;\">The other types of glial cells are macroglia, including:</p><p style=\"text-align: left;\">1) <b>Astrocytes</b>, which are involved in supportive\n&nbsp;structural and metabolic &nbsp;events, as well as repairing damaged\ncells, regulating neuronal communication and maintaining the blood-brain barrier (keeping blood from entering the brain).&nbsp;</p><p style=\"text-align: left;\"><ul><li><span style=\"font-size: 1rem;\">They are the most abundant&nbsp;</span></li><li><span style=\"font-size: 1rem;\">Numerous star-shaped projections that anchor\nneurons to their\ncapillaries (nutrient supply)&nbsp;</span></li><li><span style=\"font-size: 1rem;\">Form a living barrier\n(blood-brain barrier) between\ncapillaries and neurons\nto protect against\nharmful substances in\nthe blood.&nbsp;</span></li><li><span style=\"font-size: 1rem;\">Help control the\nchemical environment</span><span style=\"font-size: 1rem;\">&nbsp;</span></li></ul><span style=\"font-size: 1rem;\">2) <b>Oligodendrocytes,</b> which are responsible for the formation\nand maintenance &nbsp;of the <span><u>myelin sheath</u></span> that ensheaths\nthe axons, allowing for efficient communication\nbetween &nbsp;neurons,&nbsp;</span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">3) <b>Schwann cells</b>,\nwhich are the myelinating glia of the spinal\ncord and peripheral nervous system,&nbsp;</span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">4) <b>Ependymal cells</b>, which are found in the walls of the ventricles,\nwhere they produce\ncerebrospinal fluid; their cilia circulates the CSF around the brain removing waste products, washing\nit over at night, and protecting the brain from injury&nbsp;</span></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">5) <b>Satellite cells</b>, which are also part of the peripheral nervous system and playing\nboth a supportive and protective role of regulating the neural environmental for the peripheral nerves and 6) radial glia, which are fundamental for neurogenesis and neural migration (the movement of\nnew neurons through the brain).</span><br></p><p style=\"text-align: left;\"><br></p><h3 style=\"text-align: left;\">Types of Glia</h3><p></p><p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/Glia.png\" alt=\"Glia\" width=\"474\" height=\"374\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: center;\"><br></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: center; \">In his book, \"The Other Brain,\" R. Douglas Fields talks all about glia. It\'s a pretty fascinating read, surprisingly.&nbsp; I recommend it.</p><p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/The%20Other%20Brain.jpg\" alt=\"The Other Brain\" width=\"300\" height=\"453\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: center;\"><br></p><p></p><p style=\"text-align: center; \"><br></p><p style=\"text-align: left;\"><br></p><div><h2 style=\"text-align: left;\"><a name=\"_Toc28940478\">Ventricles</a></h2>\n\n<p style=\"text-align: center; \">&nbsp;<img src=\"@@PLUGINFILE@@/ventricles.png\" alt=\"ventricles\" width=\"549\" height=\"331\" class=\"img-responsive atto_image_button_text-bottom\"></p>\n\n<p style=\"text-align: left;\">The ventricles are a network of cavities that are filled with cerebrospinal fluid. The main role\n&nbsp;of the &nbsp;ventricles is\nthe creation and circulation of the cerebrospinal fluid; this clear, colorless liquid surrounds and\nprotects the brain, suspending it in fluid. This fluid removes toxins\n&nbsp;and washes over the brain. There are the two C-shaped lateral ventricles, the third ventricle,\nwhich &nbsp;is formed when the &nbsp;diencephalon is formed in\nthe first &nbsp;5 weeks of life, the cerebral aqueduct (which connects the third and the fourth ventricles), the intraventricular foramen and the fourth ventricle. In the third ventricle is a connection of the thalami, called the interthalamic\nadhesion. The fourth ventricle&nbsp; is shaped like a tent &nbsp;and lives between\nthe brainstem and the cerebellum. The cerebrospinal fluid leaves the brain through\n&nbsp;the fourth ventricle &nbsp;and moves into the cerebral aqueduct\ninto the central\ncanal, which travels\nthe spinal cord. The ventricles\nare surrounded by the choroid\n&nbsp;plexus, which is composed\nof glial cells, called ependymal\ncells</p>\n\n<p style=\"text-align: left;\">(it is these cells that secrete\ncerebrospinal fluid throughout the ventricles and around the\nbrain).</p>\n\n</div><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">Watch a little video about ventricles here:&nbsp;</span></p><p style=\"text-align: center;\"><a href=\"https://www.youtube.com/watch?v=9e9Lo0OPON4\" style=\"font-size: 1rem;\">Ventricles</a></p><p></p>',1),(419,111,418,0,20,0,1,1,1588823054,1655229248,'Networks','<p></p>\r\n<p><span style=\"font-size: 1rem;\">Networks are built of nodes and connections;\r\nnodes are highly connected and highly central neocortical regions in the brain that are responsible for the integration of\r\ninformation, globally (across many networks) &nbsp;(Van\r\nden Heuvel &amp; Sporns,\r\n2011). Some nodes are more densely connected than others, some less. Rubinov and Sporns (2010) identified different\r\nnodes as different kinds of hubs, based upon their level of participation in th</span><span style=\"font-size: 1rem;\">eir respective networks, or communities, as well as their level of connectedness to other modules.&nbsp;</span><br></p>\r\n<p><span>Networks self-organize in such a way that allows a dynamic homeostasis between &nbsp;excitatory and inhibitory states, this is called \"self-organized criticality\" in physics.</span></p>\r\n<p><span>We have many brain imaging modalities, of which EEG is the primary tool for neurotherapists and neurologists. However, its important you know all the other modalities, how they are used, and the mechanism of action they are tracking in the brain.&nbsp;</span></p>\r\n<p><span>Here is an explaner video that covers, PET scan, CAT scans, MRI, and fMRI.</span></p>\r\n<p><span><a href=\"https://www.youtube.com/watch?v=N2apCx1rlIQ\">Neuro Imaging</a><br></span></p>\r\n<p>And here is a video on how we came to understand networks via EEG</p>\r\n<p><br></p>\r\n<iframe src=\"https://player.vimeo.com/video/443180276?h=96188cfc15&amp;color=13979b&amp;title=0&amp;portrait=0\" width=\"640\" height=\"360\" frameborder=\"0\" allow=\"autoplay; fullscreen; picture-in-picture\" allowfullscreen=\"\"></iframe><br>\r\n<h3><a name=\"_Toc28940480\">Resting State Networks</a></h3>\r\n\r\n<p>There are thought &nbsp;to be 20 fundamental &nbsp;networks in the brain (Laird, et al, 2010}, which made of \"brain hubs.\" &nbsp;Hubs, or high density nodes, are highly connected and highly central neocortical &nbsp;hub regions in the brain that are responsible\r\n    for the integration of information, globally (across many networks). &nbsp;\"Rich clubs\" are the most densely connected hubs. There are at least 12 highly connected, bi-hemispheric &nbsp;hubs, which lie in the precuneus, superior frontal&nbsp; and\r\n    superior parietal cortex, as well as the subcortical hippocampus, putamen, and thalamus.</p>\r\n\r\n<p>\"[T]hese brain regions play a central role in the overall network &nbsp;organization. These nodes participate &nbsp;in multiple &nbsp;communications &nbsp;and are central, densely connected, and of short paths to one another (Sporns et al., 2007; van\r\n    den Heuvel et al., 2010}.</p>\r\n\r\n<p>Rich clubs are very similar to the substation system in power grids. The subs are there to facilitate the transmission of power, disseminating loads at appropriate &nbsp;intervals to conjoining substations, allowing for the ease of transmission and the\r\n    prevention &nbsp;of system failure. Whether or not a rich club is present in a network&nbsp; can provide details about that network, in terms of the level of resilience, hierarchical ordering, and specialization. The fewer rich clubs as nodes would\r\n    reflect a more specialized network.</p>\r\n\r\n<p>Disturbances in the hubs connectivity &nbsp;and structure &nbsp;is partly responsible for neuropathology. Failure of a hub can have a severe effect on the level of global communication efficiency of a network, due to its central role in the network (Albert\r\n    et al., 2000; Callaway et al., 2000; Zhou and Mondragon, 2004). Studies have suggested connectome &nbsp;abnormalities in a wide range of neurological and psychiatric brain disorders, for example, Alzheimer\'s disease, amyotrophic lateral sclerosis,\r\n    Parkinson\'s disease, schizophrenia, and autism, with each disorder affecting brain communication efficiency and capacity in a different manner (Bosboom et al.,&nbsp;<span style=\"font-size: 1rem;\">2009; Stam et al., 2009;\r\nLynall et al., 2010; van den Heuvel et al., 2010; Verstraete et al., 2010; Zalesky et\r\nal., 2011).</span></p>\r\n<h4><span style=\"font-size: 1rem;\"><a name=\"_Toc28940481\"><b>Module decomposition of provincial and connector hubs and the major networks of the brain. Images from Van del Heuvet M.P. &amp; Sporns, 0. (2011). Rich club organization of the human connectome. The journal of neurosciences, 3(144). 15775-15786.</b></a></span></h4>\r\n<p style=\"text-align: center; \"><span style=\"font-size: 1rem;\">&nbsp;<img src=\"@@PLUGINFILE@@/Networks.png\" alt=\"NETWORKS\" width=\"700\" height=\"729\" style=\"text-align: center; \" class=\"img-responsive atto_image_button_middle\"></span></p>\r\n<p><span style=\"font-size: 1rem;\"><a name=\"_Toc28940481\" style=\"color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; background-color: rgb(255, 255, 255);\"><br></a></span>&nbsp;</p>\r\n<p></p>\r\n\r\n<br>\r\n<p></p>\r\n<p></p>\r\n<p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp; &nbsp;&nbsp;</span><img src=\"@@PLUGINFILE@@/NETWORKS%20.jpg\" alt=\"Resting Networks\" width=\"600\" height=\"441\" 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<h3>\r\n    <div>\r\n        <h3><a name=\"_Toc28940482\" style=\"color: rgb(55, 71, 79); font-size: 1.715rem; background-color: rgb(255, 255, 255);\">Resting State Networks</a><br></h3>\r\n\r\n        <p></p>\r\n        <p><br></p>\r\n        <h5>\r\n            <div>\r\n\r\n                <p>The resting-state networks are built &nbsp;on the long fibrous white &nbsp;matter tracts &nbsp;that &nbsp;create the fundamental structures of the brain. There are 14 major &nbsp;resting-state networks, these are the default mode network\r\n                    (DMN), &nbsp;dorsal atten-tion network (DAN), ventral &nbsp;attention network (VAN), right &nbsp;frontoparietal network (rFPN), left &nbsp;frontoparietal net- work &nbsp;(IFPN), language network (LN}, cingula-opercular network (CON),\r\n                    auditory network (AN), ventral &nbsp;somata- &nbsp;motor network (VSN), dorsal somatomotor network (DSN), visual foveal network (VFN), visual peripheral net- work (VPN), medial &nbsp;prefrontal network (MPN), and lateral prefrontal\r\n                    network (LPN).</p>\r\n\r\n                <p>&nbsp;<span>Within resting state networks, low&nbsp;\r\nfrequency oscillations coordinate long-range&nbsp;</span><span>communications (von Stein et al., 2000)\r\nand gamma &nbsp;oscillations (40-150) coordinate local&nbsp;</span><span>communication (Buzsaki and Draguhn, 2004;\r\nvon Stein et al., 2000).&nbsp;</span><span>Cross-frequency coupling,\r\nin particular phase-amplitude coupling, has been attributed an important role\r\nfor communication between brain &nbsp;areas (Canolty &nbsp;and Knight, 2010;\r\nCanolty et al., 2006; Jensen and Colgin, 2007). Phase-amplitude coupling\r\nprovides a mechanism for&nbsp;</span><span>brain network information,\r\nwhich reconciles previous findings and theories &nbsp;on long-range\r\ncommunications between neural populations.</span></p>\r\n\r\n                <p>The communication of low-frequency oscillations\' phase needs to be time locked with no phase delay, since cortical and subcortical hubs facilitate synchronization of distant oscillatory activity &nbsp;with zero lag (Haider er al., 2006).\r\n                    The hubs act as dynamic relays of long- distance cortico-cortical information. Excitability &nbsp;cycles of local neural populations &nbsp;need to be synchronized to form a network. High frequency bursts (i.e. gamma) are preferentially\r\n                    occurring about the trough &nbsp;of the low frequency phase cycles of local field potentials &nbsp;(Canolty et al., 2006). If low-frequency phases are asynchronous (e.g. occurring at different &nbsp;frequencies and/or &nbsp;with &nbsp;a\r\n                    phase delay), the \"gate is closed\", &nbsp;and consequentially, coherent high-frequency oscillations &nbsp;and/or &nbsp;synchronous&nbsp; cell firing are less likely to occur, leading to suboptimal communication /coactivations between\r\n                    two brain regions (Florin &amp; Baillet, 2015).</p>\r\n\r\n                <h3><a name=\"_Toc28940483\"><b>Default Mode Network</b></a></h3>\r\n\r\n                <p>The most well-known of the resting state networks&nbsp; is the default mode network, which is an area of the brain that&nbsp; is active when the brain is in wakeful rest. Generally speaking,the DMN is online when we are not doing anything\r\n                    in particular, but are instead simply \"being.\" When we see hypo phase lag, as we do here, there is a possibility&nbsp; that the DMN is off balance, and that the process of resting in a present state is off balance.</p>\r\n\r\n                <p>Observations of the default mode network (DMN) during sleep show, just as during the DMN activity in mind wandering, that portions of the pre-frontal cortex are active during dreaming, as are the medial temporal lobe structures and the\r\n                    posterior &nbsp;cingulate (all of these points are nodes that make up the network of the DMN). Conversely, other studies show that,&nbsp;<span>in REM sleep,\r\nexecutive-processing regions of the pre-frontal cortex are mostly deactivated,&nbsp;</span><span>beyond levels seen during waking mind\r\nwandering, which suggests that &nbsp;dreaming may be an \"intensified\"\r\nversion of waking mind wandering (Fox, Nijeboer, Solomonova, Domhoff, &amp;\r\nChristoff., 2015). Rizzolatti, Semi, &amp; Fabbri-Destro (2013) contend that\r\nthe activation ofthe DMN might &nbsp;correspond to the psychoanalytic\r\n&nbsp;unconscious (p. 5).</span></p>\r\n                <p><span>Here is an interesting video on the Default Mode Network</span></p>\r\n                <p><span><a href=\"https://www.youtube.com/watch?v=QdPhkP9D2-A\">DMN video</a><br></span></p>\r\n                <p><span><br></span></p>\r\n\r\n                <h2><a name=\"_Toc28940484\"><b>Fasiculli</b></a></h2>\r\n\r\n                <p>Fasiculus means \"little bundle\" in Greek. These are cortical-cortical, intrahemispheric connections. They are nerve fibers in the central nervous system. Most&nbsp; projection pathways run dorso-ventral (descending) or vento- dorsal (ascending).\r\n                    Most association tracts run longitudinally along and antero-posterior axis from the frontal lobes to the projection areas and vice versa and connect cortical areas within the fasiculi. Arcurate fasiculli connect the frontal cortex\r\n                    to the temporal lobe.</p>\r\n                <p>Damaged fasiculli can reflect dementia, as well as learning disabilities (which can also be the result of wiring differences from normal demographic).&nbsp;<span style=\"font-size: 1rem;\">&nbsp;</span></p>\r\n                <p>Here is a video on the Fiber Pathways of the Cerebrum</p>\r\n                <p><a href=\"https://www.youtube.com/watch?v=LVasm5bqn-Y\">Fiber Pathways of the Cerebrum</a></p>\r\n                <p></p>\r\n                <h3>Short Fasiculi: Also known as U-Fibers, shaped like a bow, which interconnect cortical regions.</h3>\r\n\r\n            </div>\r\n\r\n            <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/short%20fasiculi.png\" alt=\"Short Fasiculi\" width=\"500\" height=\"311\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1rem;\"></p>\r\n            <br clear=\"all\"></h5>\r\n        <p><br></p>\r\n        <p></p>\r\n        <p><span style=\"font-size: 1.715rem;\">Superior Longitudinal Fasiculus: Connects the frontal, temporal,\r\nparietal and occipital lobes</span><br></p>\r\n        <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Superior%20Longitudinal%20Fasiculus.png\" alt=\"Superior Longitudinal Fasiculi\" width=\"501\" height=\"342\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1.715rem;\"></p>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p></p>\r\n        <p>Arcuate Fasiculus: Subset of the Superior Longitudinal Fasiculus, connects Broca’s to Wernicke’s Areas</p>\r\n        <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Arcuate%20Fasiculus.png\" alt=\"Arcuate Fasiculus\" width=\"499\" height=\"339\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1.715rem;\"></p>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p></p>\r\n        <p>Inferior Longitudinal Fasiculus: Connects Occipital and Temporal Lobes\r\n        </p>\r\n        <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Inferior%20Longitudinal%20Fasiculus.png\" alt=\"Inferior Longitudinal Fasiculus\" width=\"500\" height=\"334\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p></p>\r\n        <p>Uncinate Fasiculus: Connects Anterior Temporal and Inferior frontal Lobes</p>\r\n        <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/uncinate%20Fasiculus.png\" alt=\"Uncinate Fasiculus\" width=\"500\" height=\"321\" class=\"img-responsive atto_image_button_middle\"><br></p>\r\n        <p><br></p>\r\n        <p></p>\r\n        <p><span style=\"font-size: 1.715rem;\">Cingulum (C-shaped) fasiculus: Connects the hemispheres and runs\r\nparallel with the cingulate and the parahippocampal gyrus</span><br></p>\r\n        <p style=\"text-align: center; \"><span style=\"font-size: 1.715rem;\"><img src=\"@@PLUGINFILE@@/fasicului.png\" alt=\"fasicului\" width=\"600\" height=\"368\" class=\"atto_image_button_middle\"><br></span></p><br>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p>Perpendicular Fasiculus: Runs up and down, intralobular in the occipital lobe</p>\r\n        <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Perpendicular.png\" alt=\"Perpendicular\" width=\"500\" height=\"351\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1.715rem;\"></p>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p><span style=\"font-size: 1.715rem;\">Corpus Callosum: Bundle of fibers that connects the hemipsheres of\r\nthe brain</span><br></p>\r\n        <p style=\"text-align: center;\"><span style=\"font-size: 1.715rem;\">&nbsp;</span><img src=\"@@PLUGINFILE@@/Corpus%20Callosum.png\" alt=\"Corpus Callosum\" width=\"435\" height=\"335\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1.715rem; text-align: center;\"></p>\r\n        <p style=\"text-align: center;\"><br></p>\r\n        <p></p>\r\n        <p><span style=\"font-size: 1.715rem;\">Anterior Commisure: connects the anterior temporal lobes and the\r\nolfactory bulbs</span><br></p>\r\n        <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Anterior%20Commisure.png\" alt=\"Anterior commisure\" width=\"501\" height=\"347\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1.715rem;\"></p>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p><span style=\"font-size: 1.715rem;\">Corona Radiata: Connects the cortex to the subcortical structures,\r\nsuch as the thalamus, the brainstem, etc.</span><br></p>\r\n        <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Corona%20Radiata.png\" alt=\"Corona Radiata\" width=\"500\" height=\"401\" class=\"atto_image_button_middle\" style=\"font-size: 1.715rem;\"></p>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p></p>\r\n        <h3><a name=\"_Toc28940485\">Internal Capsule:</a> </h3>\r\n\r\n        <h5>\r\n            <p><br>The&nbsp;<a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/internal-capsule\" title=\"Learn more about Internal Capsule from ScienceDirect\'s AI-generated Topic Pages\">internal capsule</a>&nbsp;is a thick sheet of white\r\n                matter consisting of&nbsp;<b>projection fibres</b>&nbsp;passing to and from the cerebral cortex. It makes a sharp ‘knee-bend’ or&nbsp;<b>genu</b>&nbsp;around the apex of the lentiform nucleus (Latin: genu, knee). This gives it a V-shape\r\n                when viewed in axial (horizontal) section (Fig. 3.22). There is therefore an&nbsp;<b>anterior limb</b>&nbsp;(between the lentiform nucleus and the head of the caudate nucleus) and a&nbsp;<b>posterior limb</b>&nbsp;(between the lentiform\r\n                nucleus and the thalamus).</p><br></h5>\r\n        <p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/internal%20capsule.png\" alt=\"fasiculi\" width=\"500\" height=\"426\" class=\"img-responsive atto_image_button_middle\" style=\"font-size: 1.715rem;\"></p>\r\n        <p></p>\r\n        <p><br></p>\r\n        <p><br></p>\r\n        <p><a name=\"_Toc28940486\">Fornix</a></p>\r\n        <h5><a name=\"_Toc28940486\">The&nbsp;<b>fornix</b>&nbsp;(meaning\r\n\"arch\" in Latin) is a C-shaped bundle of nerve fibers in the brain\r\nthat acts as the major output tract of the hippocampus. The&nbsp;<b>fornix</b>&nbsp;also carries\r\nsome afferent fibres to the hippocampus from structures in the diencephalon and\r\nbasal forebrain. The&nbsp;<b>fornix</b>&nbsp;is part of\r\nthe limbic system.</a></h5>\r\n        <p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Fornix.png\" alt=\"Fornix\" width=\"501\" height=\"323\" class=\"img-responsive atto_image_button_middle\"><br></p><br>\r\n        <p></p>\r\n        <p></p>\r\n        <p></p>\r\n    </div>\r\n</h3>\r\n<p></p>',1),(420,112,0,421,20,0,1,1,1564057663,1654211118,'Collecting EEG Data','The first item of importance is understanding what the Electroencephalogram is, in a general sense.&nbsp;<br>Here is a very basic explainer video of what an EEG is:<br><a href=\"https://www.youtube.com/watch?v=tZcKT4l_JZk\">Basic EEG Video</a><br>Here is\r\na brief video that covers some fundamentals. Details of what\'s covered here will be further described&nbsp; in the lessons to come.<br><br><a href=\"https://youtu.be/86zIa3pGM50\">Fundamentals of EEG</a><br><br>\r\n<p>There are several software programs that will allow you to collect 19+ channel EEG data. A few of them include EEGStudio, Neuroguide, and NeuroField. This section will cover two platforms for recording EEG: NeuroField and Neuroguide.</p><br>\r\n<h3><b>The 10–20 System and Electrode Placement</b></h3>\r\n<p><span><span>To begin, we first cap up. At present (2019), caps with electrodes placed using the international 10-20 system are popular in clinical neurotherapy. The 10-20 system is an internationally recognized way of placing electrodes on a head that is replicable and verified scientifically. The electrodes pick up the EEG from the cerebral cortex underneath the electrode location.</span></span>\r\n</p>\r\n<p><span><span><img src=\"@@PLUGINFILE@@/10-20%20cap.png\" alt=\"10-20 cap\" width=\"500\" height=\"456\" class=\"img-responsive atto_image_button_left\" style=\"text-align: center;\"></span></span></p><p style=\"text-align: center;\"><br></p>\r\n<p></p><br>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b><br></b></p>\r\n<p><b>See in this short video the process of capping in EEG Acquisition.</b></p><p><b><iframe src=\"https://drive.google.com/file/d/1RSdnorKxJlnC7khht3UWW83QWpxbGoEn/preview\" width=\"640\" height=\"480\" allow=\"autoplay\"></iframe></b></p><br>\r\n<p><span style=\"font-size: 1rem;\">The “10” and “20” refer to the distances between electrodes, which are either 10% or 20% of the total diameter or radius (transverse and sagittal) of the skull (Figure 1a). The landmarks that are used sagittal are the nasion (the depressed area between\r\n        the eyes on the ridge of the nose) and the inion (the bump at the back of the skull, which can be felt with mild palpitation); landmarks that are used transversely (aka coronally) are the ears (often the tragus of the ear) (Figure 1b).</span></p>\r\n<ol>\r\n    <br>\r\n    <div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/electrode-placement.png\" alt=\"Figure 1b: The locations of the nasion, inion, and tragus points for measurement purposes.\" width=\"600\" height=\"570\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></div>\r\n    <p style=\"text-align: center; \"><i>Figure 1a. The International 10-20 system of electrode placements.</i></p>\r\n    <p style=\"text-align: center;\"><br></p>\r\n    <div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/tragus-points.png\" alt=\"Figure 1b: The locations of the nasion, inion, and tragus points for measurement purposes.\" width=\"600\" height=\"350\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></div>\r\n    <p style=\"text-align: center; \"><i>Figure 1b: The locations of the nasion, inion, and tragus points for measurement purposes.</i></p>\r\n    <p style=\"text-align: center; \"><i><br></i></p>\r\n    <p style=\"text-align: center; \"><i><img src=\"@@PLUGINFILE@@/Landmarks%20on%20the%20head.jpg\" alt=\"Landmarks on the Head\" width=\"598\" height=\"502\" class=\"img-responsive atto_image_button_left\"><br></i></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\"><br></span></p>\r\n    <p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">On an EEG cap there are 19 active electrodes, two reference ear electrodes, and one ground electrode.</span></p></ol>\r\n<ol style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/EEG%2019%20CH%20CAP.jpg\" alt=\"19 Channel EEG Cap\" width=\"300\" height=\"204\" role=\"presentation\" class=\"atto_image_button_middle\"></ol>\r\n<ol>The above image is of a 19 channel cap and the below image is of a 64 channel cap. The more electrodes in a cap the higher spatial resolution of the EEG findings.&nbsp;</ol>\r\n<ol style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/32%20channel%20cap.jpg\" alt=\"64 channel cap\" width=\"300\" height=\"208\" class=\"img-responsive atto_image_button_middle\"><br></ol>\r\n<ol><br>\r\n    <h5><b>Electrode Labels</b></h5>\r\n    <p>Each electrode is labeled by a letter or pair of letters.</p><p><img src=\"@@PLUGINFILE@@/Electrode%20labels.jpg\" alt=\"Electrode Labels\" width=\"728\" height=\"493\" class=\"img-responsive atto_image_button_text-bottom\" style=\"font-size: 1rem;\"></p>\r\n    <br>\r\n    <p>We will reference 19 channel placements because this, as of 2020, is the most commonly used electrode arrangement in the field of neurotherapy.&nbsp;</p>\r\n    <p>In a 19-channel placement, there are 19 electrodes, the ground, and the reference electrodes (Figure 1c). In a 32, 64, or 128 channel system, there are more electrode names. The additional electrodes are initially placed between the 20% marks and\r\n        are of the “Modified Combinatorial Nomenclature” (MCN) system (Figure 1d). The MCN system adds the following acronyms to designate areas (FC, FT, AF, TP, CP). The MCN system also renames four electrodes in the 10-20 system:</p>\r\n    <ul>\r\n        <li>T3 becomes T7</li>\r\n        <li>T4 becomes T8</li>\r\n        <li>T5 becomes P7</li>\r\n        <li>T6 becomes P8</li>\r\n    </ul>\r\n    <br>\r\n    <p>Even numbered electrodes (2, 4, 6, 8) are on the right hemisphere of the head and odd numbered electrodes (1, 3, 5, 7) are on the left hemisphere of the head.</p>\r\n    <p>A1 and A2 refer to the ear references and M1 and M2 refer to mastoid references.</p>\r\n    <br>\r\n    <div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/inion.png\" alt=\"\" width=\"600\" height=\"473\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\r\n    <p style=\"text-align: center; \"><i>Figure 1c: 19 active electrodes and reference electrodes (A1 and A2).</i></p>\r\n    <p style=\"text-align: center;\"><br></p>\r\n    <div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/mnc-system.png\" alt=\"\" width=\"600\" height=\"567\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></div>\r\n    <p style=\"text-align: center; \"><i>Figure 1d: The electrodes active in the MCN System</i></p>\r\n</ol>\r\n<p><br></p>',1),(421,112,420,422,20,0,1,1,1564077340,1655300274,'Prep and Hygiene','<h3><b>HOW DO I INSTRUCT PATIENTS TO PREPARE FOR AN EEG?</b></h3><br>\r\n<p>Before your client comes in for their EEG, you will want to remind them of a few hygiene and self-care tips to ensure you get the best recording possible:</p>\r\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/prep-hygiene.png\" alt=\"\" width=\"800\" height=\"372\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></div>\r\n<div><br></div>\r\n<br>\r\n<ul>\r\n    <li>Don\'t drink alcohol the night before.</li>\r\n    <li>Limit caffeine intake to zero or at most, one cup of coffee.</li>\r\n    <li>Don\'t come in hungry.</li>\r\n    <li>Don\'t come in drowsy.</li>\r\n    <li>Limit hair products.</li>\r\n    <li>Get a good night\'s sleep.<br></li>\r\n</ul>\r\nIt is important that the clinician or neurotherapy technician is in good standing health when working with patients, we never want to work with another if harboring a cold or other illness. In addition, be sure to sanitize all equipment that is used on clients (i.e. electrodes) inbetween patients and do not reuse EEG caps between patients unless sanitized.&nbsp;<br><br>\r\n<p>The products you will need to prepare your client for EEG acquisition include Nuprep, an alcohol pad or cotton ball + 70% alcohol rubbing alcohol, a blunt tip syringe (you will want to dispose of these inbetween clients), and Electrogel. You will need an electrocap, dropped ears (this depend on the amplifier),\r\n    and sponge discs for acquisition.&nbsp;</p>\r\n<p>You can find the links directing you to the prices and descriptions to all these products here:</p>\r\n<br>\r\n<table width=\"100%\">\r\n    <tbody>\r\n        <tr>\r\n            <td align=\"center\"><a href=\"https://bio-medical.com/nuprep-eegecg-skin-prep-gel-3-pack-of-4oz-tubes.html\" target=\"new\"><img src=\"@@PLUGINFILE@@/nu-prep.jpg\" alt=\"\" width=\"200\" height=\"134\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>NuPrep</a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><br><a href=\"https://electro-cap.com/index.cfm/supplies/\" target=\"new\"><img src=\"@@PLUGINFILE@@/blunt.png\" alt=\"\" width=\"400\" height=\"387\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>Blunt-tipped needles and syringes</a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><br><a href=\"https://electro-cap.com/index.cfm/supplies/\" target=\"new\"><img src=\"@@PLUGINFILE@@/electro-gel.png\" alt=\"\" width=\"165\" height=\"200\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>Electrogel </a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><br><a href=\"https://electro-cap.com/index.cfm/supplies/\" target=\"new\"><img src=\"@@PLUGINFILE@@/sponge-disks.png\" alt=\"\" width=\"176\" height=\"200\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>Sponge Disks </a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><br><a href=\"https://electro-cap.com/index.cfm/caps/\" target=\"new\"><img src=\"@@PLUGINFILE@@/electrocaps.png?time=1564078364483\" alt=\"\" width=\"200\" height=\"255\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>Electrocaps E1-LEX with drop references </a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><br><a href=\"https://bio-medical.com/ear-drop-clips.html\" target=\"new\"><img src=\"@@PLUGINFILE@@/electrocaps-2.png\" alt=\"\" width=\"200\" height=\"202\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>Electro-Cap 3 1/2\" DIN Ear Clips </a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><br><a href=\"https://www.amazon.com/gp/product/B001IKKHFO/ref=ppx_yo_dt_b_asin_title_o09_s00?ie=UTF8&amp;psc=1\" target=\"new\"><img src=\"@@PLUGINFILE@@/db-alcohol-swabs.png\" alt=\"\" width=\"480\" height=\"450\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"><br>BD Alcohol Swabs 100 Each (Pack of 12) </a></td>\r\n        </tr>\r\n    </tbody>\r\n</table>\r\n<p><br></p>\r\n<p>Each hardware/software system differs in the steps you need to take to record. However, whichever system you use, you will need to ensure low impedance. This can be done with a QCheck with the NeuroField System, a Checktrode system, or any built-in impedance\r\n    system, such as EEGStudio’s impedance meter.</p>\r\n<p>To learn how to record in the NeuroField system, watch this short video.</p>\r\n<p style=\"text-align: center; \"><a href=\"@@PLUGINFILE@@/Recording%20in%20Neurofield.mp4?time=1588279301862\">&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\"><source src=\"@@PLUGINFILE@@/recording%20in%20Neurofield.mp4?time=1588279357311\">@@PLUGINFILE@@/recording%20in%20Neurofield.mp4?time=1588279357311</video>&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</a><br></p>\r\n<p>To learn how to record in the NeuroGuide system, watch this short video.</p>\r\n<p style=\"text-align: center; \">&nbsp;&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\"><source src=\"@@PLUGINFILE@@/Recording%20and%20EEG%20in%20Neuroguide.mp4\">@@PLUGINFILE@@/Recording%20and%20EEG%20in%20Neuroguide.mp4</video>&nbsp;&nbsp;&nbsp;<br></p>\r\n<br>\r\n<table width=\"100%\">\r\n    <tbody>\r\n        <tr>\r\n            <td align=\"center\"><a href=\"https://bio-medical.com/catalogsearch/result/?q=checktrode\" target=\"new\"><img src=\"@@PLUGINFILE@@/ufi.jpg\" alt=\"\" width=\"400\" height=\"280\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></a></td>\r\n            <td>1089NP Checktrode EEG &amp; qEEG Impedance Meter\r\n                <br> Use the 1089NP to rapidly check applied electrode contact impedance of multiple EEG electrode configurations. Ideal for electrode configurations found in Cranial EEG caps. This EEG impedance meter has a 25 pin connector for Electro-Cap\r\n                19 channel cap connection. <a href=\"https://bio-medical.com/catalogsearch/result/?q=checktrode\" target=\"new\">Learn More.</a></td>\r\n        </tr>\r\n        <tr>\r\n            <td align=\"center\"><a href=\"http://www.neurofield.org/qcheck/\" target=\"new\"><img src=\"@@PLUGINFILE@@/Qcheck%20impedance%20meter.jpg\" alt=\"QCheck Impedance meter\" width=\"400\" height=\"269\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></a></td>\r\n            <td>QCheck (Electrode Impedance Meter)\r\n                <br> The QCheck is a fully software integrated electrode impedance meter, metering 20 channels on your lexicor pinout EEG cap in real time. With a new interface in NeuroField64, the QCheck makes impedance checking simple and quick.</td>\r\n        </tr>\r\n    </tbody>\r\n</table>',1),(422,112,421,0,20,0,1,1,1564079632,1614234307,'Script to Read to Patients','<br><h3>Listen to this script!&nbsp;</h3><p><audio controls=\"true\"><source src=\"@@PLUGINFILE@@/8496094039108007-audio.ogg\">@@PLUGINFILE@@/8496094039108007-audio.ogg</audio><br></p>\n<p>Now you are ready to record. You want to minimize the amount of movement in your client’s EEG record, which requires these spoken instructions:</p>\n<ul>\n        <li>Relax your forehead.</li>\n        <li>Soften then muscles around your eyes.</li>\n        <li>Relax your jaw.</li>\n        <li>Let your tongue fall away from the roof of your mouth.</li>\n        <li>Let your teeth slightly part.</li>\n				<li><i>Hint—if the client shows frontal eye field when closing their eyes, ask that they lightly place their peace fingers over their eyelids. (Some clinicians opt to use an eye mask when people flutter their eyes.)</i></li>\n</ul><p>You will adopt a script that works well for you. Commit it to memory and repeat every time you gather EEG data. With eyes closed, the same script applies with one main difference: <u>Wait 30 seconds before you ask the patient to close their eyes.</u>&nbsp;This allows you to then see the state change from eyes open to eyes closed, clocking the amount of time it takes for alpha to appear (or not appear!)</p>\n<br>\n<p>It is a standard in the USA that 10 minutes of eyes open and 10 minutes of eyes closed data are collected, this is the minimum length an EEG record must be in order to be held as credible in a court of law.</p><p><br></p><p><br></p>',1),(425,113,0,426,20,0,1,1,1564131050,1564605255,'What Are Artifacts?','An artifact is an alteration of EEG data that is from an extra-cerebral source. The artifacts this section will cover includes: <br><br><ol><li>Electromyographic (EMG) Artifact, AKA Muscle Artifact</li><li>Eye Blink Artifact&nbsp;</li><li>Eye Movement Artifact&nbsp;</li><li>Drowsiness Artifact&nbsp;</li><li>Sweat Artifact&nbsp;</li><li>Pulse and Cardio Ballistic Artifact&nbsp;</li><li>Salt Bridge&nbsp;</li><li>Electrode and Equipment Artifacts</li><li>Environmental Noise Artifact</li><li>Medication “Artifact”</li></ol>',1),(426,113,425,427,20,0,1,1,1564131057,1654212677,'Determining Real EEG vs. Not Real EEG','<p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">Real EEG data will have what we call “field” and “phase.” What that means is that any activity we see in the raw EEG data—if it is real brainwave activity—will have a surround. For example, if you are questioning activity coming from T3, you must check to see: Does the activity you see emanating from T3 have a surrounding similar wave pattern\r\nat the neighboring elecetrodes of T5, C3, and F7? If the activity is similar, then you have real brain activity. If it is not, then you have fake activity (called \"artifact\"). Muscle contamination will not share the same phase and field between two or more electrodes. Muscle contamination is one type of artifact in the EEG.</span></p><br>\r\n<div>Often it is necessary to validate data at O1 and O2, as the occipitalis muscle is sometimes the culprit of high amplitude beta activity and sometimes O1 and O2 beta activity is real brainwave activity.&nbsp;</div><div><br></div><div>Listen to this intro for the EEG video!</div><div><br></div><div><audio controls=\"true\"><source src=\"@@PLUGINFILE@@/9213022558190946-audio.ogg\">@@PLUGINFILE@@/9213022558190946-audio.ogg</audio><br></div>\r\n<div><br></div>\r\n<center>&nbsp;<iframe src=\"https://player.vimeo.com/video/358114442\" width=\"640\" height=\"373\" frameborder=\"0\" allow=\"autoplay; fullscreen\" allowfullscreen=\"\"></iframe>&nbsp;<br></center><br>Another way to check for field and phase in your data is to switch to a\r\nmontage that places channels in a sequential order, so that the channels are next to their proximal neighbors. In neuroguide, for example, the deymed montage places channels next to their neighboring electrode sites:<br><br>\r\n<div style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/electrode-pair.png?time=1564134176374\" alt=\"\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\" width=\"760\" height=\"703\"><br></div><br>\r\n<div style=\"text-align: center;\"><i>Figure 1e: A deymed montage in Neuroguide software will place electrodes sequentially, which will allow the reader to check for field and phase in the EEG between neighboring electrode pairs.</i> <br></div>',1),(427,113,426,428,20,0,1,1,1564135308,1602694306,'Ten Types of Artifacts — Type 1: Electromyographic (EMG) Artifact, AKA Muscle Artifact','<br>\n<ul>\n    <li>The higher the amplitude, with increasing frequency, the greater the chances that its muscle imitating beta.</li>\n    <li>Muscle artifact will often occur in one or two channels </li>\n    <li>Frontalis muscle artifact arrives at Fp1 &amp; Fp2</li>\n    <li>Temporalis and massater muscle artifact arrives at T3/T4, F7 and F8</li>\n    <li>Occipitalis muscle artifact arrives at O1 and O2</li>\n</ul>\n<br>\n<div><img src=\"@@PLUGINFILE@@/emg.png?time=1564591360275\" alt=\"Figure 1f: A stray line of high amplitude in the beta frequencies in a spectrum denotes deviant amplitude and is often an indicator that one electrode is picking up EMG.\" class=\"img-responsive atto_image_button_text-bottom\" width=\"453\" height=\"411\"></div>\n<p><i>Figure 1f: A stray line of high amplitude in the beta frequencies in a spectrum denotes deviant amplitude and is often an indicator that one electrode is picking up EMG.</i></p>\n<br>\n<h5><b>Massater Muscle (Chewing) Artifact (50–60 Hz)<br></b></h5>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/massater.png?time=1564140872778\" alt=\"Figure 1g: The massater muscle is responsible for mastication of food and can create high amplitude beta artifact in EEG data.\" width=\"400\" height=\"396\" class=\"img-responsive atto_image_button_middle\"></div>\n<p><i>Figure 1g: The massater muscle is responsible for mastication of food and can create high amplitude beta artifact in EEG data.</i></p>\n<br>\n<p>See a video of massater muscle artifact here (maximize the screen).&nbsp;&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\"><source src=\"@@PLUGINFILE@@/Massater%20Chewing%20Video.mp4\">@@PLUGINFILE@@/Massater%20Chewing%20Video.mp4</video>&nbsp;&nbsp;</p><br>\n<h5><b>Occipital Muscle Artifact (Posterior EMG) (20–300 Hz)</b></h5>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/artifact-muscle.gif\" alt=\"Figure 1h: The occipitalis muscles are two rectangular-shaped muscles on the back of the skull, which can give pronounced EMG artifact at the O1 and O2 electrode sites.\" width=\"400\" height=\"400\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p><i>Figure 1h: The occipitalis muscles are two rectangular-shaped muscles on the back of the skull, which can give pronounced EMG artifact at the O1 and O2 electrode sites.</i></p>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/emg-artifact.png?time=1564141541047\" alt=\"Figure 1i: Summary page of a Quantitative EEG showing occipitalis EMG artifact. Image generated from Neuroguide version 3.0.6.\" width=\"600\" height=\"797\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p style=\"text-align: center; \"><i>Figure 1i: Summary page of a Quantitative EEG showing occipitalis EMG artifact. Image generated from Neuroguide version 3.0.6.</i></p>\n<p style=\"text-align: center;\"><br></p>\n<p style=\"text-align: center; \">See a video of occipitalis muscle artifact here.&nbsp;&nbsp;&nbsp;&nbsp;</p><p style=\"text-align: center; \"><video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Occipitalis%20Artifact.mp4\">@@PLUGINFILE@@/Occipitalis%20Artifact.mp4</video>&nbsp;&nbsp;&nbsp;</p>\n<br>\n<h5><b>Temporalis Muscle Artifact (40–80Hz)</b></h5>\n<p>The temporalis muscle elevates, retracts, and moves the jaw from side to side.</p>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/temporalis.png?time=1564141213287\" alt=\"Figure 1j: The temporalis muscle is a large fan-shaped muscle that covers the sides of the skull.\" width=\"600\" height=\"711\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p style=\"text-align: center; \"><i>Figure 1j: The temporalis muscle is a large fan-shaped muscle that covers the sides of the skull.</i></p><p style=\"text-align: center; \">The temporalis muscle is responsible for the most common type of artifact, EMG at T3 and T4.</p><p style=\"text-align: center; \">&nbsp;&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/temporalis%202.mp4\">@@PLUGINFILE@@/temporalis%202.mp4</video>&nbsp;<span style=\"font-size: 1rem;\">&nbsp;</span><span style=\"font-size: 1rem;\">&nbsp;</span></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">Temporalis artifact at T3 and T4 will create a map that looks like this:&nbsp;</span></p><p style=\"text-align: center;\"><img src=\"@@PLUGINFILE@@/Temporalis%20Map.jpg\" alt=\"Temporalis Map\" width=\"600\" height=\"492\" style=\"font-size: 1rem;\" class=\"img-responsive atto_image_button_middle\"></p><p style=\"text-align: center; \"><i>Figure 1k: The temporalis muscle can generate artifact in the left or right temporal electrodes, as we see here, with a high amplitude beta artifact arising from T4. Image generated from Neuroguide version 3.0.6.</i></p><p style=\"text-align: center;\"><br></p><br><h5><b>Frontalis (wrinkling forehead) 30–40Hz</b></h5><br><div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/frontalis.png?time=1564141288057\" alt=\"Figure 1k: The frontalis muscle is responsible for much of our expression, wrinkling the forehead and furrowing the brow. Muscle artifact from the frontalis muscle will affect Fp1, Fp2, and Fz electrodes, but may also affect F7, F8 and Fz electrodes.\" width=\"300\" height=\"358\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div><p style=\"text-align: center; \"><i>Figure 1l: The frontalis muscle is responsible for much of our expression, wrinkling the forehead and furrowing the brow. Muscle artifact from the frontalis muscle will affect Fp1, Fp2, and Fz electrodes, but may also affect F7, F8 and Fz electrodes.</i></p><p style=\"text-align: left;\"><span style=\"font-size: 1rem;\">Frontalis muscle artifact is caused by the muscles in the forehead. To check if frontal EEG is real or fake, you will want to</span></p><ul><li>Drop the low pass band filter</li><li>Check for field and phase</li></ul><p>This video is one where we are examining EEG activity in the frontal electrodes to determine if it is real or fake. We examine the waveform and then switch to a deymed montage (in neuroguide software) which shows us the electrodes in sequential order. In this video, the neighboring electrodes have similar field and phase, which means the EEG activity is real! This person has high amplitude frontal beta.&nbsp;</p><p style=\"text-align: center; \">&nbsp;&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Frontalis%20Video.mp4\">@@PLUGINFILE@@/Frontalis%20Video.mp4</video>&nbsp;&nbsp;<br></p>This is the QEEG Map we would see with this type of high amplitude frontal activity.<br><div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears.png?time=1564141620674\" alt=\"Figure 1l: Summary page of a Quantitative EEG showing frontalis EMG artifact. Image generated from Neuroguide version 3.0.6.\" role=\"presentation\" width=\"712\" height=\"956\"></div><p style=\"text-align: center; \"><i>Figure 1m: Summary page of a Quantitative EEG showing high amplitude frontal beta. Image generated from Neuroguide version 3.0.6.</i></p><p style=\"text-align: center;\"><br></p><div></div><br><p><br>\n\n</p><br>Sometimes the temporalis muscle affects the electrodes F7 and F8, as we see in this image<br><div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-2.png?time=1564141695313\" alt=\"Figure 1m: The temporalis muscle can generate artifact in the temporal electrodes (T3, T4, T5, or T6, as well as the left or right frontal electrodes, as we see here, with a high amplitude beta artifact arising from F8. Image generated from Neuroguide version 3.0.6.\" width=\"600\" height=\"796\" role=\"presentation\" class=\"img-responsive atto_image_button_middle\"></div><p><i>Figure 1n: The temporalis muscle can generate artifact in the temporal electrodes (T3, T4, T5, or T6, as well as the left or right frontal electrodes, as we see here, with a high amplitude beta artifact arising from F8. Image generated from Neuroguide version 3.0.6.</i></p><p><br></p>',1),(428,113,427,436,20,0,1,1,1564605136,1597381497,'Ten Types of Artifacts — Type 2: Eye Blink Artifact','<br>\n<p>Eye movement artifact are some of the easiest to spot with the naked eye. Eye blinks are commonly found at Fp1, Fp2, Fz, F7, and F8 locations, respectively. The reason we see artifacts with eye blinks is because eyeballs are dipoles, with a positive polarity up front and a negative polarity in the back.</p><p style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/Eyes%20are%20dipoles.jpg\" alt=\"Eyes as dipoles\" width=\"700\" height=\"423\" class=\"img-responsive atto_image_button_middle\"><br></p><p style=\"text-align: center; \"><i>Image 1o: The eyes are dipoles, with a positive polarity at the cornea and a negative polarity at the retina.</i></p><p style=\"text-align: center; \"><i><br></i></p><p>Here is a video of eye blinks, watch the channel locations that are affected so you can later\n    spot eye blinks yourself.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/eye%20blinks.mp4\">@@PLUGINFILE@@/eye%20blinks.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<p>Sometimes a client will blink quite a lot, so much that there isn’t a moment in the record where their data is not affected by eye movements. When recording the data from these types of clients, ask that they try to NOT blink for 5 seconds after each\n    blink. When artifacting data that is contaminated by eye blinks, you want to make sure that you are not collecting data that has the delta-like swing that follows each blink. We call this the “whiplash.” The following video shows how to avoid the\n    whiplash in your editing process.</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><span style=\"font-size: 1rem;\">&nbsp;&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/whiplash%20%282%29.mp4\">@@PLUGINFILE@@/whiplash%20%282%29.mp4</video>&nbsp;</span></p>\n<p><br></p>',1),(429,113,434,430,20,0,1,1,1564596020,1596578387,'Ten Types of Artifacts — Type 7: Salt Bridge Artifact','<br>\n<p>A salt bridge is caused when there is too much electrogel in a cap, causing two electrodes to conjoin and destroying the signal. Salt bridge artifact will show up in low amplitude channel (often Fz). Typically Fz and the ground create a salt bridge, since\n    they are so close together. Very often the artifact will show up in maps as asymmetry stemming at Fz or a 28Hz artifact (sometimes 16Hz) at Fz, which are subharmonics of an electrical artifact.</p>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-4.png?time=1564142753887\" alt=\"Image 1p: In this summary map, the salt bridge disrupted the Fz electrode, causing a focal high amplitude artifact, as well as questionable asymmetry and hypocoherence. Image generated from Neuroguide version 3.0.6.\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\" width=\"716\" height=\"921\"></div>\n<p style=\"text-align: center; \"><i>Image 1s: In this summary map, the salt bridge disrupted the Fz electrode, causing a focal high amplitude artifact, as well as questionable asymmetry and hypocoherence. Image generated from Neuroguide version 3.0.6.</i></p>\n<p style=\"text-align: center;\"><br></p>\n<div><img src=\"@@PLUGINFILE@@/fz-electrode.png?time=1564142814872\" alt=\"Image 1q: In this raw recording, the salt bridge disrupted the Fz electrode, causing a low amplitude signal to arrive at the Fz channel, the active electrode in the pain of bridged electrocdes.\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\" width=\"1917\" height=\"1100\"></div>\n<p><i>Image 1t: In this raw recording, the salt bridge disrupted the Fz electrode, causing a low amplitude signal to arrive at the Fz channel, the active electrode in the pain of bridged electrocdes.</i></p>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-5.png?time=1564142905223\" alt=\"\" width=\"700\" height=\"441\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p><i>Image 1u: Often with a salt bridge, a high amplitude spot at the site of the bridge (commonly Fz) will show up at 28Hz. Image generated from Neuroguide version 3.0.6.</i></p><p>A rare salt bridge artifact will look like what we see in the below recording, high amplitude 16hz activity, stemming from the ground electrode. This is a difficult artifact to spot with the naked eye because it looks real.&nbsp;</p><p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Salt%20Bridge%202.mp4\">@@PLUGINFILE@@/Salt%20Bridge%202.mp4</video>&nbsp;&nbsp;<br></p>',1),(430,113,429,432,20,0,1,1,1564599968,1597383126,'Ten Types of Artifacts — Type 8: Electrode and Equipment Artifact','<br>\n<p>Electrode artifacts are brief transients typically at one channel at a time.</p>\n<br>\n<h5><b>Electrode Pop</b></h5>\n<p>A spontaneous discharge of electric potential (because the skin or electrode can act a capacitors and hold electrical charge across the paste).</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Electrode%20Pops.mp4\">@@PLUGINFILE@@/Electrode%20Pops.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<h5><b>Loose Electrode</b></h5>\n<p>Poor contact with varying and disorganized morphology (sharp and slow, high amplitude, etc.).</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Loose%20Electrode.mp4\">@@PLUGINFILE@@/Loose%20Electrode.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<h5><b>Bad Ear Lead</b></h5>\n<p>A bad ear lead will typically distort all of the data—it will appear that all of the data is moving together in synchrony—everything going electro negative and electro positive together. What this will typically produce is a map that shows hypercoherence\n    across all channels. Generally a record with a bad ear electrode is immediately suspicious to the eye, even if novice.</p>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-6.png?time=1564143146857\" alt=\"\" width=\"700\" height=\"934\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p style=\"text-align: center; \"><i>Image 1v: Coherences such as these, with every frequency showing hypercoherence in every channel, should be questioned as it is always a product of a defective ear electrode. Image generated from Neuroguide version 3.0.6.</i></p>\n<p style=\"text-align: center;\">&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Bad%20Ear%20Lead.mp4?time=1597383119548\">@@PLUGINFILE@@/Bad%20Ear%20Lead.mp4?time=1597383119548</video>&nbsp;<br></p>\n<p></p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><span style=\"font-size: 1rem;\">&nbsp;&nbsp;</span></p>\n<hr>\n<br>',1),(431,113,432,0,20,0,1,1,1564604875,1592831170,'Ten Types of Artifacts — Type 10: Medication \"Artifact\"','<br>\n<h5><b>Gabaergic Drugs (i.e. Benzodiazepines)</b></h5>\n<p>This video and imagery is of benzodiazepine toxicity. In this case, the individual is taking Xanax on an “as needed” basis for pain, which is enough to alter the EEG. When taking a benzodiazepine we see an increase in the amount of GABA, an inhibitory neurotransmitter, which creates a global beta spindling, as we see in this video. This is an EEG finding that we see with GABAergic drugs.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Benzos.mp4\">@@PLUGINFILE@@/Benzos.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<p>Benzodiazepine toxicity will lead to a quantitative EEG that has a copious amount of high amplitude beta. Since this is a medication side-effect, neurofeedback and neuromodulation will not help to reduce the amount of high amplitude beta we see in the record.</p>\n<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-8.png?time=1564142985979\" alt=\"\" width=\"700\" height=\"938\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p style=\"text-align: center; \"><i>Image 1w: The EEG of someone taking a benzodiazepine will often show a high amplitude beta marker focused centrally. Image generated from Neuroguide version 3.0.6.</i></p>',1),(432,113,430,431,20,0,1,1,1564596675,1597383226,'Ten Types of Artifacts — Type 9: Environmental Noise Artifact','<br>\n<p>Environmental noise should always strike the electroencephalograher as strange, due to its fast, rhythmic appearance. When an electrical system is not grounded, when there is poor connectivity between devices, when there is “electro-smog” in the environment,\n    as we sometimes see in large cities, these are all situations where environmental noise such as this appears. Its best to check a building for environmental noise before moving in, as sometimes the solution is difficult to arrive at.</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;&nbsp;&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Environmental%20Noise.mp4?time=1597383179926\">@@PLUGINFILE@@/Environmental%20Noise.mp4?time=1597383179926</video>&nbsp;</span></p>This next EEG is one where the electrical noise is not easy to spot with the naked eye, that is, not until we remove the low pass filter, allowing all frequency activity to enter the recording. Once we remove the filter, we can see that there is environmental noise that contaminates the entire EEG, making it a bad recording--not impossible to interpret, but certainly dirty.<br><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><span style=\"font-size: 1rem;\">&nbsp;&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Electricity.mp4?time=1597383222174\">@@PLUGINFILE@@/Electricity.mp4?time=1597383222174</video>&nbsp;</span></p>&nbsp;<br>',1),(433,113,435,434,20,0,1,1,1564604729,1592830567,'Ten Types of Artifacts — Type 5: Sweat Artifact','<br>\n<p>Sweat artifact arises when the sodium and water in sweat interacts with the salt-impregnated past of the EEG cap. What you see are high amplitude slow waves, that look like giant delta waves, sometimes slower than 1Hz.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/Sweaty.mp4\">@@PLUGINFILE@@/Sweaty.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<p>Some analysis programs filter out frequencies less than 1Hz or less than 2Hz, causing the sweat artifact to disappear in the filtered image. It is important to catch sweat artifact when it is happening and try to cool down your client and the room to avoid a poor recording.</p>\n<p>In the following video, we can see how checking the filters can prevent slow artifacts, such as sweat, from being noticed by the electroencephalographer. We are removing the low pass filter to see how the data looks with and without automatic filtering.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\"><source src=\"@@PLUGINFILE@@/check%20the%20filtering.mp4\">@@PLUGINFILE@@/check%20the%20filtering.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<hr>\n<br>',1),(434,113,433,429,20,0,1,1,1564594925,1597382415,'Ten Types of Artifacts — Type 6: Pulse and Cardio Balistic Artifact (EKG)','The below image is of a cardiac artifact (heartbeat) affecting the EEG. You can tells its heartbeat because it happens approximately once per second (the average heartbeat is 72 beats per minute) and it is rhythmic.&nbsp;<br>\n<div><img src=\"@@PLUGINFILE@@/cardiac-artifact.png\" alt=\"Figure 1n: A pulse artifact coming from an ear electrode, which contaminates the ear electrode reference and places the cardiac artifact in every channel.\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\" width=\"1784\" height=\"1076\"></div>\n<p><i>Figure 1r: A pulse artifact coming from an ear electrode, which contaminates the ear electrode reference and places the cardiac artifact in every channel.</i></p>\n<br>\n<p>Watch the video here for the case example with the cardiac artifact stemming from an ear electrode.</p><p style=\"text-align: center;\"><span style=\"font-size: 1rem;\">&nbsp;</span><span style=\"font-size: 1rem;\">&nbsp;&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/Cardiac%20Artifact.mp4\">@@PLUGINFILE@@/Cardiac%20Artifact.mp4</video>&nbsp;</span></p>\n<p>Often when a global pulse artifact (like this) contaminates the data, the anatomy of the individual is part to play. Often, folks who are stocky, with short large necks, produce artifacts such as this. One possible way to mitigate this artifact is to\n    place cottonballs behind the ears. That said, this preventative measure doesn’t work a majority of the time.</p>\n<p>Here is another video of a cardiac artifact, only this time it is showing up in only one electrode location.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/pulse%20artifact%202.mp4\">@@PLUGINFILE@@/pulse%20artifact%202.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<p><b><i>How do I know that its cardiac artifact and not something else?</i></b></p>\n<p>A regular heartbeat occurs at 72 beats per minute. So, a bump in the raw data that arrives once per second, approximately, will give away that the source of the artifact is the rhythmic beating of the heart.</p>',1),(435,113,436,433,20,0,1,1,1564600493,1597382277,'Ten Types of Artifacts — Type 4: Drowsiness Artifact','<h3><br></h3>\n<p>Drowsiness is difficult to see for the untrained eye and would not classify as artifact, however it is data that must be thrown out, unless the quality of someone’s sleep or how quickly they fall asleep are being monitored. In this video, within one minute of closing his eyes, this patient falls asleep, generating beta spindles, high amplitude alpha, K-complexes down the vertex, and low amplitude beta. These findings are part of falling asleep! We see this type of EEG activity in NREM 2 and NREM3 stages of sleep.</p><p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/drowsiness.mp4\">@@PLUGINFILE@@/drowsiness.mp4</video>&nbsp;&nbsp;<br></p>\nThe EEG architecture of sleep will be covered further in the chapter on neurophysiology. If you happen to edit a drowsy recording, this is the kind of map you will get! This is not good data, because is it not representative of the patient in normal eyes closed conditions. He is asleep and we see high amplitude central theta (because of the vertex sharp waves) as well as high amplitude frontal beta (because of the beta spindles-the stabilizing mechanism of sleep).<br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-7.png?time=1564143083126\" alt=\"\" width=\"600\" height=\"803\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<p style=\"text-align: center; \"><i>Image 1q: The drowsy EEG was showing vertex slow waves and frontal spindling beta (aka sleep spindles), which show up in a fast fourier transform as high amplitude central theta and high amplitude frontal beta. Image generated from Neuroguide version 3.0.6.</i></p>\n<p style=\"text-align: left;\"><br></p><p style=\"text-align: left;\">Sometimes you will catch a patient falling into stage 1 of sleep (aka NREM1). This is the beginning of drowsiness. The video below is what we see when a patient enters stage NREM1, alpha followed by alpha dropout (this coheres to the vigilance stages of A1, A2, A3, and B1). The image below is of the vigilance model and details what we can expect to see as a patient is falling asleep.&nbsp; &nbsp; &nbsp; &nbsp;</p><p style=\"text-align: left;\">&nbsp;&nbsp;<video controls=\"true\"><source src=\"@@PLUGINFILE@@/vigilance%20.mp4\">@@PLUGINFILE@@/vigilance%20.mp4</video>&nbsp;</p><p style=\"text-align: left;\"><div><div><h2>EEG-vigilance algorithm “VIGALL”</h2></div></div><div><div><p>In parallel to the transition from active wakefulness to deep sleep the human brain takes on different global functional states. These functional states are reflected in the spectral composition and topography of the EEG and have been termed vigilance stages. These states correspond to different levels of alertness at the behavioral level. Several stages can be separated during the transition from tense to relaxed wakefulness and further on to drowsiness until sleep onset.</p><p>In 1937, Loomis et al. (1937), later modified by Roth (1961), Bente (1964) and others (e.g. (Klimesch, 1999; Ulrich &amp; Frick, 1986); proposed classifications for vigilance stages occurring during transition from active wakefulness to sleep onset. They are based on the following EEG phenomena during eyes closed, which have been demonstrated in several studies:</p><p><strong>A1)</strong>&nbsp;Posterior alpha mostly seen after eye-closing with a frequency of 8-12 Hz and an occipital focus. This oscillation has been referred to as “idling rhythm” (Niedermeyer, 1997) because it marks a state of relaxed wakefulness, corresponding to vigilance stage A1 according to Bente (1964) and Loomis (Loomis et al., 1937).</p><p><strong>A2-A3)</strong>&nbsp;Alpha power anteriorisation occurs increasingly after several minutes of relaxed wakefulness. Alpha peak frequency shows a slight decrease. This phenomenon is reported to occur during transition to drowsiness (Broughton &amp; Hasan, 1995; Connemann et al., 2005; De Gennaro, Ferrara, Curcio &amp; Cristiani, 2001; De Gennaro et al., 2004; De Gennaro et al., 2005; Pivik &amp; Harman, 1995) and corresponds to vigilance stage A2 and A3 (Bente, 1964; Loomis et al., 1937).</p><p><strong>B1)</strong>&nbsp;Low voltage EEG is increasingly observed during lower vigilance stages. The alpha rhythm disappears (alpha drop-out) and beta power increases (De Gennaro et al., 2001; Tanaka, Hayashi &amp; Hori, 1996; Tanaka, Hayashi &amp; Hori, 1997). This EEG pattern corresponds to vigilance stage B1 (Roth, 1961). The EEG in this state is similar to the EEG during intense mental activity and eyes open condition.</p><p><strong>B2-3)</strong>&nbsp;Increased delta and theta activity is observed in parallel with increasing subjective drowsiness (Strijkstra, Beersma, Drayer, Halbesma &amp; Daan, 2003; Tanaka et al., 1996; Tanaka et al., 1997), corresponding to vigilance stages B2 and B3 (Roth, 1961).</p><p><strong>C)</strong>&nbsp;The occurrence of K-complexes and sleep spindles mark the beginning of definite sleep &nbsp;(Cash et al., 2009; De Gennaro &amp; Ferrara, 2003; Tanaka et al., 1997).</p><p>Based on these EEG features a computer-based algorithm has been created for separating different EEG-vigilance stages (also see figure 4) for consecutive EEG segments. The first version of the algorithm “VIGALL” (Vigilance Algorithm Leipzig) was based upon the Fast Fourier-derived power of the four main EEG frequency bands alpha, beta, delta and theta during two-second segments of continuous EEG data at different sites. An improved second version of the algorithm now takes into account the intracortical source power (derived by Low Resolution Tomography-LORETA) of different regions of interest (ROIs).</p><img src=\"@@PLUGINFILE@@/vigilance%202.jpg\" alt=\"Vigilance model\" width=\"667\" height=\"490\" class=\"img-responsive atto_image_button_left\"><br>\n\n</div></div><br></p>\n<p><br></p>\n<br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br><br>\n<hr>\n<br><br><h3></h3><br>',1),(436,113,428,435,20,0,1,1,1564605133,1592830368,'Ten Types of Artifacts — Type 3: Eye Movement Artifact','<br>\n<h5><b>Eyes Closed Eye Artifacts</b></h5>\n<p>Sometimes people have a hard time keeping their closed eyes closed. It seems they have to will their eyes shut. You will sometimes see this in small children or adults—they will have an eye flutter. In these cases, you will want to ask the client to place\n    their middle finger and index finger lightly atop their eyelids to prevent this type of artifact.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/eye%20movements.mp4\">@@PLUGINFILE@@/eye%20movements.mp4</video>&nbsp;&nbsp;<br></p>\n<br>\n<h5><b>Lateral Eye Movement artifacts</b></h5>\n<p>Lateral eye artifacts can be seen in channels F7 and F8, typically, and are large swings that look like they’re in a delta frequency. This is because the eyeballs themselves are dipoles with a positive and a negative polarity. Each time we look left and\n    right, it causes a large swing in the electrodes.</p>\n<br>\n<p style=\"text-align: center; \">&nbsp;&nbsp;<video width=\"600\" height=\"400\" controls=\"true\" class=\"\"><source src=\"@@PLUGINFILE@@/lateral%20eye%20movement.mp4\">@@PLUGINFILE@@/lateral%20eye%20movement.mp4</video>&nbsp;&nbsp;<br></p>\nIf lateral eye movements are included in the EEG data, this is what it looks like in a map: high amplitude delta (of course, its not real!)<br><br>\n<div style=\"text-align: center; \"><img src=\"@@PLUGINFILE@@/linkears-3.png?time=1564142186232\" alt=\"Figure 1o: Lateral eye artifact can appear as high amplitude delta, since the waves are generally under 4Hz. Image generated from Neuroguide version 3.0.6.\" width=\"600\" height=\"798\" role=\"presentation\" class=\"img-responsive atto_image_button_text-bottom\"></div>\n<br>\n<p style=\"text-align: center; \"><i>Figure 1p: Lateral eye artifact can appear as high amplitude delta, since the waves are generally under 4Hz. Image generated from Neuroguide version 3.0.6.</i></p>',1);

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