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Articles    H4'ed 11/10/09

Anxiety, Anger, Depression, TBI and HEG-

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Hershel Toomim & Robert Joneson

This study revealed two candidate pathways from cortical receipt of a stimulus to activity of the amygdala. An excitatory pathway was found through the orbito-frontal cortex. Another emotional regulator pathway was found via the right inferior lateral prefrontal cortex.

The relative speeds and strengths of these pathways were expected to determine the anxiety and overly emotional responsiveness of anxiety, PTSD, depressive, and anger prone individuals.-

It was hypothesized that HEG exercise of the regulatory and inhibitory pathways would strengthen them and bring overly emotional sufferers to remission.-

One of two TBI Cases is reported here. Four examples of nine resolved anxiety cases with before and after QEEG or Loreta studies show EEG effects of HEG frontal cortex training-
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Introduction:

Anxiety, resulting from amygdala activation, has evolutionary advantages in rapidly preparing the individual for flight or fight in threatening situations. A brain exceptionally fast excitatory pathway has been found from the striatum that reaches the amygdala via the special branch of Broca. Another inhibitory pathway traverses the cortex before reaching the amygdala and is slower. This second pathway is inhibitory. A third regulator pathway in the right lateral inferior prefrontal cortex has been shown to regulate activation of the anterior cingulate cortex, a common route for pain and emotional activation. (Eisenberger N. et al. 2003). These pathways are illustrated in Fig 1.-

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Fig 1 Adapted from Baxter, L., et al, Lichter and Cummings (eds.)

Frontal-Subcortical Circuits in Psychiatric and Neurological Disorders

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The normal expectation is that cortical negation activity can subdue anxiety, fear, or negative emotional response. This experimental study exercises the inhibitory pathway. testing whether strengthening the cognitive response with HEG exercise can make it fast and strong enough to limit the norepinephrine release that activates direct uncontrolled amigdalar response.-

Eisenberger et al. (Ibid), report brain areas that activate feelings of hurt and fear the anterior cingulate (ACC) and another near AF8 that inhibits this response. These areas, ACC and the right ventro-lateral prefrontal cortex, are shown to be in a relative strength relationship as diagrammed below in control

of negative emotions such as anxiety and fear. Discovery of several such relationships (Davidson et al. 2000) raises the questions of where and how many agonist/antagonist pathways can be found in the brain and can their relative strengths be modified by suitable brain exercise.-
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Fig 2 Striatum from Brain Coloring Book Diamond M. and Scheibel A.-

Some individuals are more prone to anxiety attacks than the average.- Zubieta et al. (2003) studied disparity in pain tolerance. They found a gene, ComptVAL158met, that regulates pain sensitivity. The gene has two alleles, methionine (met) and valine (val). Each allele is a dominant gene with equal opportunity for inheritance. One inherits a copy from each parent. Thus there are four genotypes: met-met (1), met-val (2a), val-met (2b), and val-val (3). The 2a and 2b genes have identical behavioral effects. There are thus three separable genotypes or grades of pain sensitivity 1,2, and 3. Type 1 and 3 each account for 25% of the population. Genotypes 2a and 2b account for 50% of the

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Lifetime in innovative research resulting in many honors, patents, and pioneering development of biofeedback computer based instrumentation including Biocomp 2010 followed by invention of hemoencephalography (HEG)
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