I am sure that this post will be seen to be controversial by anyone coming from a conventional medical background who comes across this and reads it.
However iI have been on a mission of sorts to understand why my initial Atlas Profilax treatment improved my ADHD symptoms as much as it did back in 2009, why it did not improve all symptoms, and why it was so hard to get those improvements to stick properly. I will address the third question in a second post.
The trouble is that the research that is done into the subject of ADHD (and probably any highly speculative area) is heavily biassed by previous precedent. Anyone who does any work in this area will be struck by the way in which most papers simply repeat “what we already know” even though those primary assumptions about what we already know are just that, assumptions. However these assumptions get repeated in book after book, paper after paper, internet discussion after internet discussion, until “everybody knows” that ADHD is a primarily genetic condition involving the frontal lobes, the reward centre and dopaminergic transmission.
That has never been established.
I’m convinced now that the majority of ADHD actually relates to1) Distorted and variable afferent proprioceptive input into the vestibulocerebellar system, leading to clumsiness and dysregulation of ocular coordination.
2) Compromise to the vertebrobasilar circulation secondary to high cervical malalignments- leading to hypoxia to the parts of the brainstem responsible for regulating blood flow to the rest of the body. The downstream consequence here is orthostatic intolerance and episodic cerebral hypoxia (inattention) and sympathetic overarousal– (hyperactivity and impulsivity).
3)Compromise to middle cerebral artery blood flow as a downstream consequence of rigid segments (“subluxations” ) in the upper thoracic area leading to overactivity in the sympathetic chain feeding up to the superior cervical sympathetic ganglion and through to the sympathetic innervation of the Middle Cerebral Artery.
I would suggest that the working memory deficits that have been observed in ADHD can be explained by
a) the greater burden on working memory caused by the poor co-ordination. Coordination problems will increase the amount of work required to execute even the most simple questionnaire.
b) An added burden on working memory caused by the need to restrain a hypervigilant, hypersympathetic attention and keep it on track.
c) Relative hypoxia will impair neural function and if the area involves working memory then that will be compromised. Remember here that relative blood flow impairment in the middle cerebral artery territory
We have made a number of systematic thinking errors in dealing with this problem
Just because a drug which has dopaminergic and noreadrenergic effects helps the problem does not mean that ADHD is some sort of dopamine deficiency disorder. it doesn’t even mean that the problem is primarily a neurotransmitter one at all.Interestingly here, one of the reliable effects that dexamphetamine has had on me is to shift me from a rather slouched and tired posture to a much more upright one- which is associated with midline cerebellar activation. The posture is also widely associated with alertness- especially in the context of possible threat, but also in the posture of meditation and martial art instructions.
I would speculate that the probable neurotransmitter and pathway involved here is through the locus coeruleus noradrenergic outputs- but will need to dig a little more for that. However the interesting thing is that this more upright posture will help improve neck alignment and will at least temporarily improve most of the cerebellar symptoms by normalizing and stabilizing afferent proprioceptive input.
However there is now more than enough reason to propose a completely different pathway for the causation of this problem, and also to insist that the primary modes of management should include manual therapies and neurorehabilitation.