<p></p>
<h5>Jay Gunkelman has done a service to the field in his explanation of the 11 phenotypes in EEG.&nbsp;</h5>
<p>Here is a short video of Jay explaining the Phenotype model:&nbsp;</p>
<div style="padding:56.25% 0 0 0;position:relative;"><iframe src="https://player.vimeo.com/video/429426691?h=875f70a63c&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479" frameborder="0" allow="autoplay; fullscreen; picture-in-picture" allowfullscreen="" style="position:absolute;top:0;left:0;width:100%;height:100%;" title="JAY - PHENOTYPES"></iframe></div><script src="https://player.vimeo.com/api/player.js"></script>
<p>And here is a long video (2 hours) of Jay discussing phenotypes:</p>
<div style="padding:56.25% 0 0 0;position:relative;"><iframe src="https://player.vimeo.com/video/589486357?h=cb70efe2cb&amp;badge=0&amp;autopause=0&amp;player_id=0&amp;app_id=58479" frameborder="0" allow="autoplay; fullscreen; picture-in-picture" allowfullscreen="" style="position:absolute;top:0;left:0;width:100%;height:100%;" title="Phenotypes Tools for Advanced Neurotherapy"></iframe></div><script src="https://player.vimeo.com/api/player.js"></script>
<p><br></p>
<p></p>
<h3>Electroencephalography (EEG)/Quantitative EEG Phenotypes</h3>
<p><br></p>
<table border="0" cellspacing="0" cellpadding="7" width="100%">
    <tbody>
        <tr>
            <td valign="top"><b>Candidate Phenotype</b></td>
            <td valign="top"><b>EEG Findings</b></td>
            <td valign="top"><b>Associated Neurofeedback Approach<br><br></b></td>
        </tr>
        <tr>
            <td valign="top">Low-voltage fast</td>
            <td valign="top">Low-voltage EEG overall</td>
            <td valign="top">Reward alpha activity posteriorly<br><br></td>
        </tr>
        <tr>
            <td valign="top">Epileptiform</td>
            <td valign="top">Transient spike/wave, sharp waves, paroxysmal EEG</td>
            <td valign="top">Inhibit low and high frequencies; sensorimotor rhythm training; also consider slow cortical potential control<br><br></td>
        </tr>
        <tr>
            <td valign="top">Diffuse slow activity (with or without lower alpha)</td>
            <td valign="top">Increased delta and theta (1-7 Hz) with or without slower posterior alpha</td>
            <td valign="top">Inhibit midline fronto-central activity slower than 10 Hz, add reward for anterior beta for increased stimulating effect</td>
        </tr>
        <tr>
            <td valign="top">Focal abnormalities (not epileptiform)</td>
            <td valign="top">Focal slow activity or focal lack of activity</td>
            <td valign="top">Inhibit slower activity and reward higher frequencies (consider medical referral)<br><br></td>
        </tr>
        <tr>
            <td valign="top">Mixed fast and slow</td>
            <td valign="top">Increased slower activity, lack of organized alpha, increased beta</td>
            <td valign="top">Inhibit slow frequencies, reward alpha and SMR, inhibit faster beta<br><br></td>
        </tr>
        <tr>
            <td valign="top">Frontal lobe hypoperfusion disturbances</td>
            <td valign="top">Frontally dominant excess theta or alpha frequency activity</td>
            <td valign="top">Inhibit midline fronto-central activity below 10Hz, reward anterior beta for increased effect</td>
        </tr>
        <tr>
            <td valign="top">Frontal asymmetries</td>
            <td valign="top">Frontal asymmetry primarily measured at F3, F4<br><br></td>
            <td valign="top">Adjust frontal symmetry with alpha, theta, and beta</td>
        </tr>
        <tr>
            <td valign="top">Excess temporal lobe alpha</td>
            <td valign="top">Increased alpha activity generated in temporal lobe</td>
            <td valign="top">Inhibit alpha over affected temporal region(s),and inhibit frontal slow activity<br><br></td>
        </tr>
        <tr>
            <td valign="top">Faster alpha variants, not low voltage</td>
            <td valign="top">Alpha peak frequency greater than 12 Hz over posterior and parietal cortex<br><br></td>
            <td valign="top">Reward 8-10 Hz alpha at Pz, shift alpha frequency slower with alpha/theta protocol</td>
        </tr>
        <tr>
            <td valign="top">Spindling excessive beta</td>
            <td valign="top">Rhythmic beta with a spindle morphology, often with an anterior prominence<br><br></td>
            <td valign="top">Inhibit beta’s spindle frequencies, wide band inhibit; alpha-theta training may help</td>
        </tr>
        <tr>
            <td valign="top">Persistent eyes-open alpha</td>
            <td valign="top">Alpha doesn’t attenuate by at least 50% with eyes open; it is generally slower alpha</td>
            <td valign="top">Reward beta frequencies, inhibit alpha; reward higher frequency alpha</td>
        </tr>
    </tbody>
</table><br>
<p></p>
<p>His research on Phenotypes can be seen in the article in the Articles section of this chapter.</p>
<p>Johnstone, Gunkelman, and Lunt (2005), Clinical database development: Characterization of EEG phenotypes. Clinical EEG and Neuroscience, 2, 99-107, and is used with the permission of Clinical EEG and Neuroscience.</p>
<h2><a name="_Toc29328831" style="color: rgb(55, 71, 79); font-size: 2.143rem; background-color: rgb(255, 255, 255);">Low
Voltage Fast EEG</a><br></h2>

<p>The low voltage fast EEG phenotype is driven by over arousal. This profile shows a genetic alteration of gene number 4, the gene that controls GABA A receptors, and if you make more receptors than you can saturate, you are over aroused. This is a prominent
    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.</p>

The low voltage fast EEG phenotype is driven by over arousal. This profile shows a genetic alteration of gene number 4, the gene that controls GABA A receptors, and if you make more receptors than you can saturate, you are over aroused. This is a prominent
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&nbsp;variant
that is present in about 10% of the population. Typically, their alpha is fast and desynchronized.
<br>
<p></p>
<p></p>
<h4>Low Voltage Fast EEG</h4>
<p style="text-align: center;"><span style="font-size: 1rem;">&nbsp;</span><img src="@@PLUGINFILE@@/Low%20VOltage%20Fast.png" alt="Low Voltage Fast" width="723" height="942" class="img-responsive atto_image_button_middle" style="font-size: 1rem; text-align: center;"></p>
<p style="text-align: center;"><span style="color: rgb(55, 71, 79); font-family: &quot;Open Sans&quot;; font-size: 1.715rem; text-align: left;"><br></span></p>
<h4 style="text-align: left;">Low Voltage Individual Hertz Bins</h4>
<p style="text-align: center; ">&nbsp;<img src="@@PLUGINFILE@@/Low%20Voltage%20Individual%20Hz%20Bins.png" alt="individual hz bins low voltage" width="717" height="462" style="text-align: center;" class="img-responsive atto_image_button_middle"></p>
<p style="text-align: center;"><br></p>
    <p></p>
    <h2 style="text-align: left;"><a name="_Toc29328832">Trauma</a></h2>

    <p style="text-align: left;">According to Porges: there is no way to understand trauma without understanding the biology of trauma: first hyperarousal, crying then screaming, the best clinical term that describes the state of the infant at the level of abuse is panic. In panic
        there is a dysregulation of the body—the sense of self collapses or explodes in a reenactment of the abandonment.</p>

    <p style="text-align: left;">Sympathetic excitation is now in the body, as well as in the organs, but its being shut down by a parasympathetic inhibition that tries to regulate this via disassociation—this is considered a moment of psychic death. Dissociation by means of parasympathetic
        inhibition is the role of the unmyelinated subdiaphrammatic vagus nerve, which is reptilian in its evolutionary origin. It is this dissociative mechanism that creates the feigning of death.</p>
    <p style="text-align: left;">Dissociation is a right brain survival defense against overwhelming, unbearable, painful emotional experiences. This can manifest, symptomatically, in a number of ways. Dissociation can arrive in the presence of mu rhythm (covered earlier in this
        chapter), dissociation can occur in the presence of Temporal lobe Alpha. </p>

    <h2 style="text-align: left;"><a name="_Hlk530979595"></a><a name="_Toc29328833">Temporal Lobe Alpha</a></h2>

    <p style="text-align: left;">With eyes open, in Temporal Lobe alpha, we see the appearance of alpha gating at T6, which has been found to be a common finding in soldiers who have even been in active combat. This appearance suggests an affective perceptual problem, a prosodic
        comprehension difficulty, and even a deficit in spatial reasoning. “Excess Temporal Lobe Alpha” (TLA) classification is used when evidence exists that the temporal lobe generates abnormal amounts of alpha. TLA suggests frontal lobe disengagement
        which results in temporal lobe idling. This excessive gating is often seen in individuals dealing with trauma or anxiety.</p>
    <h2 style="text-align: left;"><a name="_Toc29328834">PTSD</a></h2>

    <p style="text-align: left;">Sometimes an individual dealing with post-traumatic stress disorder will create alpha blocking or a rise in the amplitude of beta with eyes closed. For most individuals, when we close our eyes we are able to relax. The brain signals to the body that
        we are safe and able to rest or fall asleep. The parasympathetic nervous system kicks in, assuring the body (and the brain) that it is safe to rest, digest and recuperate from the activities of the day. </p>

    <p style="text-align: left;">In the case of PTSD, the opposite happens. When the eyes are closed again, vigilance appears (which can be seen in the rise of amplitude in beta brainwaves). &nbsp;Beta and high beta are the frequencies in which we process cognitive data. These are
        the brainwaves in which we think. Typically, the waveforms of alpha and ultimately theta and delta rise when we close our eyes. Additionally, we may see a drop in delta and theta when eyes are closed, signifying a further inability to relax.</p>
    <p style="text-align: left;">What can be expected from an EEG response such as this is difficulty falling asleep and staying asleep, nightmares&nbsp; (due to an overly active brain at rest), and the results from poor or compromised sleep (fatigue, grumpiness, feelings of heaviness,
        poor attention, inability to stay on task, difficulty sequencing thoughts, et cetera.).</p>

        <h3 style="text-align: left;"><a name="_Toc29328835">OCD and Mood Disorders</a></h3>

        <p style="text-align: left;">Very often obsessive compulsive disorder will live at the anterior cingulate cortex and will have the presence of alpha and other frequencies. This appears as a malfunction in a network node in the error detection and processing network. Usually
            if you are getting a lot of error codes (“that’s wrong,” “did you forget to lock the door,” “your hands are not yet clean,” etc.) this maker could signify an obsessive compulsive or oppositional defiant marker. </p>

        <p style="text-align: left;">The anterior midline holds a model of what is going on in the world at the subgenual anterior Cingulate location. When that spot is not working properly, you end up having error codes. In addition, Mood Disorders are often seen stemming from a
            dysregulation in this area and can manifest as depression, amotivational, and angry behaviors.</p>
        <h2 style="text-align: left;"><a name="_Toc29328836">Reactive Attachment Disorder and Trauma</a></h2>

        <p style="text-align: left;">There are different attachment styles: (1) secure attachment, (2) insecure attachment with anxious/avoidant and anxious/resistant subtypes, and (3) disorganized attachment (Ainsworth, Blehar, Waters &amp; Wall, 1978; Bowlby, 1988; Main &amp; Solomon,
            1986).&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; The child needn’t be abused to be in trouble, he merely needs to experience himself as abandoned by his mother. Reactive Attachment Disorder describes the effects of pathogenic care on
            the child’s ability to bond appropriately. These children are either hypervigilant, aggressive, and averse to comfort, or in fewer cases, inhibited, ambivalently needy, and withdrawn. They are suspicious of caretakers, a suspiciousness that,
            sadly, they come by honestly. They are prone to dissociative states and in the fugue of mother loss, they do not readily perceive their primary caretaker (Fisher, 2014, p. 4).</p>

        <p style="text-align: left;">Often the mother of a baby may be physically present but emotionally absent.&nbsp; Even though mother may change diapers, feed her baby, and pick baby up from the crib, she may have difficulty interacting with the baby—that is, mirroring facial
            expressions, mimicking baby’s coos, etc. The depressed mother who cannot, from her own deadened state, enliven her baby. </p>
        <p style="text-align: left;">This could result in a dissociative EEG presentation, such as <b><u>mu rhythm</u></b>. Attachment research has shown that babies depend on face--, eye-to-eye, voice-to-voice emotional reciprocity (Bowlby, 1988; Ainsworth et al., 1978; Main &amp;
            Solomon, 1986; Tronick, 2007). Alexithymia means inability to describe or articulate feelings, and for some it means trouble recognizing that they even have feelings. (107), this type of symptomology would be present in a child who was not
            mirrored.</p>

        <p style="text-align: left;">Sebern Fisher has seen excess slow wave (as low as 2 Hz) in the temporal lobes of people with developmental trauma. High amplitude, of 50 microvolts, is also seen. This can indicate dissociative processes. If there is excess slow wave—particularly
            delta to slow theta—at a particular site, it is not communicating adequately with the outside world; it is mainly talking to itself.</p>
        <h3 style="text-align: left;">Dementias</h3>
        <p></p>
        <p style="text-align: left;">Parahippocampal slowing and slow alpha will indicate an Alzheimer’s type dementia. If there is a frontal slowing of alpha fronto-temporally, with a steady pace of alpha parietally and occipitally, that indicates vascular dementia, working away
            at the frontal lobes memory content. If there is a generalized slow EEG, there are tropic changes, which can indicate Korsakov’s syndrome (which we see in severe alcoholics). Thalamo-cortical dysrhythmias and subcortical abnormal activity
            indicate Parkinson’s disease (which is seen in the substantia nigra) and Lewy body disease is seen in cortical and subcortical abnormalities. However, Parkinson’s dementia can have a Lewy body mix in it. The anterior temporal pole and insulae
            deteriorate disproportionately in Lewy Body dementia, which can lead to hallucinations, loss of sense of smell (which is the mesial temporal surface, the uncus, degrading). Lewy body is difficult because the individual will drift in and out
            from hallucinatory states to normal states, making the hallucinations seem all that more real. This is the same disorder that Robin Williams had when he died. </p>
        <h3 style="text-align: center; "><br></h3>
        <h3 style="text-align: left;">Diffuse Slowing in the Raw EEG in Lewy Body Dementia</h3>
        <p style="text-align: center; "><img src="@@PLUGINFILE@@/diffuse%20slowing.png" alt="diffuse slowing" width="655" height="976" style="text-align: left;" class="img-responsive atto_image_button_middle"></p>
        <h3 style="text-align: center; "><br></h3>
            <h3 style="text-align: left;">Diffuse Slowing as seen in WinEEG Spectral Analysis</h3>
            <p style="text-align: center; ">&nbsp; &nbsp;&nbsp;<img src="@@PLUGINFILE@@/Diffuse%20Slowing.png" alt="Diffuse Slowing" width="930" height="494" style="text-align: center;" class="img-responsive atto_image_button_middle">&nbsp;</p>
            <p style="text-align: center; "><br></p>
                <h3 style="text-align: center; ">Diffuse Slow Sources at the Anterior Cingulate Cortex and the right insula in a Lewy Body Dementia Case</h3>
                <p style="text-align: center; ">&nbsp;<img src="@@PLUGINFILE@@/ACC%20and%20Insula.png" alt="ACC and insula" width="858" height="548" style="text-align: center; " class="img-responsive atto_image_button_middle"></p>
                <p style="text-align: center;"><br></p>
                    <p></p>
                    <p style="text-align: center; "><br></p>
                    <p></p>
                    <p></p>