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EEG Assessment and Neurotransmitters

Publication date: 24 December 2011

Let's summarise the drift of my last few posts.

  1. I find EEG assessment to be useful and percipient in clinical practice.
  2. I think it has more potential yet. The system I use derives from neurotherapy where it is used for selecting neurofeedback protocols, but I think it's use can go beyond that. My ambition is to use it to inform my decisions in nutritional therapy.
  3. A lot is known about how neurotransmitter brain chemistry relates to symptomatology in mental, emotional and neurological disorders. Mainstream medicine's approach targets brain chemistry adjustment – even though for the most part no attempt is made to objectively assess patients' neurochemistry.
  4. There are EEG patterns that correlate to symptom patterns, albeit loosely rather than definitively. So it might be possible to use EEG patterns to predict which nutritional interventions are more likely to be successful.

So the final step is to relate EEG patterns to neurochemistry. This is what this post is about. I must say it is speculative – I'm not really aware of any research that directly addresses this question – but I would love to see that research happen some day. I also stress that neurotransmitter balance is not the whole story of brain function, so not every EEG pattern is interpretable in terms of neurotransmitters, and none is wholly explained by neurotransmitter balance. And just to complicate matters further, there's no reason why the classifications I'm making should be mutually exclusive.

I'll organise this post by work through the main neurotransmitters and linking them to EEG findings. I'll also suggest some subjective (symptom related) differences between categories.

  1. Dopamine deficit
  2. Dopamine stimulates the frontal part of the brain only, so a deficit would be expected to leave the frontal areas under-active. In EEG terms, this manifests as the ratio of theta to beta being high over the frontal areas. (Remember that in general for the EEG, beta represents activity or engagement whereas the lower frequencies, delta theta and alpha, in some way represent disengagement or inactivity.)

    ADHD is an example of a disorder associated with dopamine problems. Indeed you do tend to see high theta to beta in ADHD – at least in the most common varieties, but not all (which just goes to show that ADHD like most mental / emotional disorders, is not one thing).

    Sometimes the high theta to beta extends as far back as the crown of the head, and interestingly this tends to go with the hyperactive form of ADHD. I don't know the significance of this in terms of neurochemistry – if there is a significance.

    Some types of depression involve dopamine imbalances, and you can also see the high theta to beta pattern in depression. The symptoms tend to be low drive and motivation, and emotional flatness rather than mood problems. Sleep tends to be excessive and unrefreshing rather than actual insomnia.

  3. Serotonin deficit
  4. Serotonin imbalance is most commonly associated with depression – the variety involving low mood and sleep disturbance.

    What EEG pattern is seen here? The short answer is I don't know. However there is a commonly seen left-right imbalance seen in the EEG, that is known to be associated with depression: some depressed patients show more left frontal alpha and/or less left frontal beta, when compared to the right. In the absence of any firm information my guess would be to go for serotonin boosting therapy.

    Another EEG pattern is seen only at the brain's midline (dividing the left and right hemispheres). At certain points the EEG originates from a brain region called the anterior cingulate cortex (ACC). The ACC may be over-active or under-active. Dr Dan Amen, who I mentioned in previous posts, associates ACC problems with what he calls over-focused anxiety / depression / ADHD. A classic example would be OCD. Many cases of OCD are helped by sertonin targeting meditations (SSRIs), and in nutritional therapy, William Walsh of the Pfeiffer Treatment Centre has reported success with OCD patients by targeting increased methylation (which will boost serotonin levels).

  5. GABA and Glutamate
  6. These two neurotransmitters tend to have opposite effects, as I explained in my last post, so a deficit of GABA can look like an excess of glutamate and vice versa.

    GABA deficiency is associated with anxiety. In terms of the EEG, there are a number of correlates of anxiety, but perhaps the most common is a low theta to beta ratio seen at the very back of the head. More generally this marker goes with an over-active or racing mind, or an inability to quieten down the mind. Where I see this pattern the most obvious nutrients to try are ones that boost GABA, such as the herb valerian or the amino acid L-theanine (though the latter has quite complex effects on the brain).

    Another of Dr Amen's classifications is temporal lobe based anxiety-depression. In the EEG another common anxiety pattern is seen in the temporal lobe areas, as either excess activity (high beta) or as asymmetry between the two temporal lobes.

    There is a link between temporal lobe issues and explosive symptoms such as sudden rages or panic attacks or other abrupt emotional swings; also migraines and seizures. These symptoms also connect with glutamate excess. So, again very speculatively, if I saw both this symptom pattern and this EEG pattern I would go for glutamate countering agents such as magnesium, vitamin D etc.

  7. Acetylcholine deficit
  8. Acetylcholine loss is seen in dementia cases. A common EEG marker for dementia is a slowing of the alpha speed – and indeed there is some evidence that speeding up the alpha rhythm using neurofeedback or neurotherapy can reverse to some extent the symptoms of memory loss seen in dementia cases.

    If I saw alpha slowing in the EEG in conjunction with problems with memory and cognitive fogginess, I would lean towards acetylcholine boosting agents such as phospholipids.

In this posting I've by no means covered every significant EEG pattern, nor every type of neurochemical imbalance, but hopefully I've given you some sense that EEG assessment can give some very useful information. The low cost and time efficient system that I use doesn't give a complete picture of brain function of course, but when you think that in so many cases there is no objective assessment of brain function at all, it's got to be a step forward.

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