26 June 2020. This post was rather too long, and overinclusive of some tangentially relevant ideas. I will tidy it up in due course- but have deleted the content for now.
26 June 2020. This post was rather too long, and overinclusive of some tangentially relevant ideas. I will tidy it up in due course- but have deleted the content for now.
Posture, alignment and attention.
Symmetry of afferent impulses
We must all remember being told to sit up and pay attention.
Equally, many of us remember hearing stories of the “olden days”, when doctors used to harangue their patients about straight posture.
I recall being continually harangued by my teachers to keep my hands out of my pockets and hold straighter posture. At the time, it irritated me no end. It was perfectly obvious that the direction to stand up straight had a half life of 15 seconds. I just kept forgetting. It puzzled me enormously. I did not understand then the complexity of the neural systems that control posture.
Regardless of that, when I was diagnosed ADHD, the idea of standing/ sitting up straight to pay attention came back to me when I asked myself what attention was, and who were the best examplars of it.
What I found was that our medical community is so obsessed with medications and neurotransmitter systems that the question of posture, which directly affects the afferent stimuli which drive healthy brain function, is not well covered. Consequently I will need to draw on a number of sources to support this argument. However, one aspect of posture that I did not, at the time, see as being hugely important, was symmetry. We will return to that.
When I looked at the “attention phenomenon”more closely it seemed there was more to it:
Meditation has been round over 2500 years, and the instructions for effective meditation invariably point to upright posture with no asymmetry. The same can be said for martial arts, and specifically, in our day and age, within the military. I do not approve of violence but I am well aware that the army is highly pragmatic– and if they want their sentries guarding a post, they do want them staying awake. So if they want their soldiers standing at attention, it is probably for a good reason, and not just from tradition.
My diagnosis with ADHD was a puzzle to me. I certainly fitted the diagnostic criteria, and had done so for most of my life- but I was always very successful academically – spectacularly so in year 12.
At that stage I was doing a good deal of exercise, and in fact had a very upright, straight posture.
PICTURE orf me.
In retrospect I find that very significant, as one of the strongest marks of successful stimulant treatment in my experience is a shift from a slumped, asymmetrical, fidgety, sweaty presentation to coming in to my rooms on the first presentation following medication initiation upright and straight, not fidgeting. (As an a side some of the patients with worse neck alignment issues could not tolerate the shift in posture and might develop marked chewing type tics or neck spasm.)
I have noted many times the effect of a stimulant in straightening my posture and relieving back pain, and also in improving visual function.
So there is something about the stimulants that facilitates that upright midline motor activation- and in doing so it actually mimics the postural changes that are sought in authentic Buddhist meditation. Interesting. What is more interesting is that the fMRI changes seen with stimulants are broadly similar to those seen in experienced meditators (I wish I had kept that reference!).
This was driven home to me when I had the Atlas Profilax treatment which so radically improved my alertness and attention that I was moved to start this blog. The aims of this blog have always been to synthesise the various streams of evidence for atlas subluxation as a major mechanism driving much pathology ( both physical pathology and psychopathology), and also to help publicise the condition as it affects so many of us as allopathic doctors are aware of it.
The attainment of upright posture (think” Meerkat on sentry duty”) is achieved by the activation of the “midline motor system”’, from the feet through the pelvis, up through the spine, to the tongue.
When that upright posture is fully attained, the three lines of the vertebral bodies and the left and right facet joints aligned and sitting tall- with minimal pressure on any one of the facets. Of course in this posture there is no possibility of asymmetry.The upright and square posture will ensure that all the suboccipital muscles (more later when we cover symmetry) are stretched to the same extent.
So, at this point I want to state some basic principals.
I will flesh them out after defining the thesis.
1) Symmetrical brain stimulation is very important to achieving maximum brain function and longevity. This can be demonstrated both at the level of internal damage to the brain (strokes, TBI) and dysafferentation. (The published evidence here is strongest in the case of dental loss but is also applicable in the case of mechanoreception and the upper neck).
2) Upright posture clearly improves the symmetry of afferent input into the neuraxis, and thus should improve neural function.
3) Upright posture may have other positive effects on brain function.
At this point I suggest at least 2 effects:
3 a)Firstly- an individual with a slumped, asymmetrical posture will have to deal with a collection of variably tight muscles in the upper back and neck. The muscle tension varies as posture varies, and is accompanied by nociception (which further blunts proprioception) and leaves the brain overtaxed when it comes to planning movements. Note that it is easily arguable that most of cognition involves planning movements (even if the movement is just that of speaking- it is still a movement- or a sequence of movements).
Thinking, walking, Talking: Integratory Motor and Cognitive Brain Function
Gerry Leisman1, Ahmed Moustafa3and Tal Shafir
Frontiers in Public Health:
published: 25 May 2016 doi: 10.3389/fpubh.2016.00094
“Postural muscles, ( ie midline musculature) we claim, were the main conduit for this motor and cognitive binding to evolve and continue to exist for a more comprehensive review of the nature of evolutionary brain development, posture, brain size, and the implications for limitations of the pelvis as well as the genetic implications, the reader is referred to Ref. (2, 3 as well as Ref. (4)]. Reduced postural activity in childhood harms natural exploration of the surrounding, thereby reducing the ability to learn from experiences, and leading to developmental delays.
Carruthers (13) argue that working memory has developed to serve motor control in animals.
Numerous authors conceptualized and provided evidence to support the notion that oscillatory patterns propagate and coordinate cross-neuronal interactions
The effect of Movement on cognitive Performance
Raed Mualem1,2,3, Gerry Leisman3,4*, Yusra Zbedat1, Sherif Ganem5, Ola Mualem3, Monjed Amaria1, Aiman Kozle1, Safa Khayat-Moughrabi3 and Alon Ornai2
Frontiers in Public Health 20 April 2018
Postural muscles, we have claimed elsewhere (21), were the chief channels for the evolution of motor and cognitive binding.
Dysfunction associated with developmental delays all involve conditions of reduced optimization of brain integration that in turn disrupt executive function, frontal lobe-based behaviors, and articulation with motor components of the nervous system (22, 28, 31).
Not uncommonly seen in children with developmental delays, is motor incoordination or “clumsiness,” relating to posture and gait that supports the concept of “weak central coherence” that in turn relates to a processing bias for local and featural information and difficulty in extracting the essence of meaning, detecting missing or hidden figures or “seeing the big picture” in daily life experiences
So the issues around KIDD syndrome (one description of our predicament) boil down to this- if we have one of these subluxations, every move we make has to be calculated and planned on the basis of a kaleidoscope of shifting dysfunctional muscle tension patterns. These patterns naturally corrupt the information upon which all our movements are predicated- so we are usually clumsy and socially unpopular.
Our emotional system is strongly linked to movement and posture. It is possible to mimic an emotion by adopting a body posture. ( Actors know this very well, but of course us Medical Practitioners need an authority to prove what is in front of our noses) However, if we care to look in our own backyard, in Murtagh’s “General Practice”, that strategy ( of postural and facial mirroring) is recommended as a way of understanding the patient’s emotional state and showing them that youempathise.
Murtaghs General Practice 6th Edition 2015
P 26 Other rapport-building techniques
A person can develop a rapport with another by mimicking his or her body language, speech, posture, pace and other characteristics. Such techniques can be used to help the doctor communicate better with a patient and also to improve the patient’s attitude by changing the patient’s body language position.
So, this is actually conventional medicine and has been for decades.. Equally, our mirror neurone system (feeding into the insula) is so strong that it can mirror the emotional state of the person we are mixing with.
Simply, what I am saying here is that as well as bottom up regulation of emotions by the brainstem there is top down regulation of emotions through cognition and consciousness. That top down control can be mimicked or initiated merely by adopting the upright posture of an awake, calm and confident person, much of that physiology can be generated. No doubt that will be executed by top down control of the key brainstem centres.
However, I do not have published science to support these observations (yet) so for the time being I
In short, stable, clear attention is at least partially dependent on upright symmetrical posture, and fully upright posture will straighten out most kinks in posture.
In Germany this line of enquiry has been pursued more closely by group of specialists centred round Heiner Beidermann MD and a diverse group of specialists from many other countries.
Heiner Biedermann, in his book “Manual Therapy in Children”. describes 2 main syndromes “KISS= Kinematic Instability with Suboccipital Strain, and KIDD- being Dyspraxia and Dysgnosia secondary to KISS. He then goes on to present evidence related to the reduction of ADHD symptoms following manual therapy to the neck and thoracic spine in these children.
One of Biedermann’s biggest points is the outcome of children with these patterns related especially to thoracic postural deformities (secondary to suboccipital strain) and associated autonomic dysfunction. We will return to this theme later as I believe it is a major driver of symptoms in ADHD.
(Manual Therapy in Children: Biederman et al 1991)
“Asymmetry, caused by KISS 1, is often the cause of asymmetrical breathing patterns (and may lead to osteoarthritis of the first rib in 20 year olds).
As the child grows, both the insufficient posture, and the complaints arising from the Autonomic Nervous System increase, with headache and fatigue being the most marked.”
( I will argue elsewhere that autonomic dysfunction is one of the major drivers of dysfunction in ADHD).
The problem unfolds thus:
“So a left overactive ATNR (Asymmetric Tonic Neck Reflex) will result in a left convex C scoliosis extension of the left leg will be stronger, the left leg will become the privileged weight bearing leg and this will cause the sacrum to tilt.
The pathology dictates an asymmetrical reaction.”
So, though triggered by the asymmetric ATNR (asymmetric tonic neck reflex); the problem becomes fixed in place by these thoracic spine asymmetries which are very hard to resolve because the complex, and multiple joints in the thoracic spine.
There is still ongoing discussion as to the nature of the autonomic dysfunction, but a pattern of sympthetic overactivity on one side, firing through the cervical sympathetic chain and causing constriction of blood flow in the middle cerebral artery in the most affected side ( the side on which the shoulder is low and forwards) seems most likely in my experience.
It has been known for some time that ADHD is associated with a transient left visual field neglect which emerges when the subject is fatigued.
We can start with a few more research observations and this is is a good starting point for those interested.
Now the next area to be considered is that of asymmetrical afferent input into the brainstem and pons.
I suspect this is highly important in generating psychiatric symptomatology, as well as ocular dyscoordination, and that one of the major drivers of pathology is whiplash -disrupting the small ligaments around the odontoid process of C2. And leading to an ill fit between the atlas and axis (C 1 and 2)
I propose that the answer is very simple.
The concept that the brain resents asymmetrical afferent information is well understood in neurology.
We understand that some patients who have a stroke causing one sided dysfunction can be improved by surgical intervention that damages the normal side.
We also understand that noradrenergic neurones virtually only originate in the locus coeruleus, and that noradrenaline is one of the key neurotransmitters affected by the stimulants we use for ADHD.
The key outputs of the LC are increased metabolic rate (hence faster thinking and running) increased sympathetic output (hence unstable attention) and increaed vigilance and upright posture.
Hence it is plausible that effects oin the LC may be directly related to both ADHD and bipolar.
The key points are all derived from this paper- but I have referrecd back to the relevan t original papers where practicable.
Trigeminal, Visceral and Vestibular Inputs May Improve Cognitive Functions by Acting through the Locus Coeruleus and the Ascending Reticular Activating System: A New Hypothesis
De Cicco et al
Frontiers in Neuroanatomy 8 January 2018
It is known that sensory signals sustain the background discharge of the ascending reticular activating system (ARAS) which includes the noradrenergic locus coeruleus (LC) neurons and controls the level of attention and alertness. Moreover, LC neurons influence brain metabolic activity, gene expression and brain inflammatory processes. As a consequence of the sensory control of ARAS/LC, stimulation of a sensory channel may potential influence neuronal activity and trophic state all over the brain, supporting cognitive functions and exerting a neuroprotective action. On the other hand, an imbalance of the same input on the two sides may lead to an asymmetric hemispheric excitability, leading to an impairment in cognitive functions. Among the inputs that may drive LC neurons and ARAS, those arising from the trigeminal region, from visceral organs and, possibly, from the vestibular system seem to be particularly relevant in regulating their activity. The trigeminal, visceral and vestibular control of ARAS/LC activity may explain why these input signals: (1) affect sensorimotor and cognitive functions which are not directly related to their specific informational content; and (2) are effective in relieving the symptoms of some brain pathologies, thus prompting peripheral activation of these input systems as a complementary approach for the treatment of cognitive impairments and neurodegenerative disorders.
For the uninitiated, the locus coeruleus is involved in alertness and vigilance. Critical functions in ADHD, and as we have seen, fatigue and loss of vigilance can drive spatial neglect in ADHD individuals.
Previous studies report that chewing improves cognitive processing speed (Hirano et al., 2013), alertness (Allen and Smith, 2012; Johnson et al., 2012), attention (Tucha et al., 2004) and intelligence (Smith, 2009).
Hirano, Y., Obata, T., Takahashi, H., Tachibana, A., Kuroiwa, D., Takahashi, T., et al. (2013). Effects of chewing on cognitive processing speed. Brain Cogn. 81, 376–381. doi: 10.1016/j.bandc.2012.12.002
Allen, A. P., and Smith, A. P. (2012). Effects of chewing gum and time-on-task on alertness and attention. Nutr. Neurosci. 15, 176–185. doi: 10.1179/1476830512y. 0000000009
Johnson, A. J., Miles, C., Haddrell, B., Harrison, E., Osborne, L., Wilson, N., et al. (2012). The effects of chewing gum on physiological and self-related measures of alertness and daytime sleepiness. Physiol. Behav. 105, 815–820. doi: 10.1016/j.physbeh.2011.10.020
Tucha, O., Mecklinger, L., Maier, K., Hammerl, M., and Lange, K. W. (2004). Chewing gum differentially affects aspects of attention in healthy subjects. Appetite 42, 327–329. doi: 10.1016/j.appet.2004.01.003
Smith, A. (2009). Effects of chewing gum on mood, learning, memory and performance of an intelligence test. Nutr. Neurosci. 12, 81–88. doi: 10.1179/147683009X423247
Kohler, M., Pavy, A., and van den Heuvel, C. J. (2006). The effects of chewing versus caffeine on alertness, cognitive performance and cardiac autonomic activity during sleep deprivation. J. Sleep Res. 15, 358–368. doi: 10.1111/j.1365- 2869.2006.00547.x
However, the positive effects of chewing on cognitive performance are not observed following sleep deprivation, although, in this condition, chewing may again improve alertness and mood (Kohler et al., 2006).
The paper then goes on to propose:
Afferent discharge may regulate the excitability of brain networks involved in cognitive functions, which are not directly related to their specific sensory informational content, thus modulating cognition.
In the same way, vestibular and neck signals acting on spinal projecting neurons belonging to the RF (Pompeiano et al., 1984) and to the LC (Manzoni et al., 1989) modulate the discharge of motor networks controlling the postural tone.
Pompeiano, O., Horn, E., and d’Ascanio, P. (1991). Locus coeruleus and dorsal pontine reticular influences on the gain of vestibulospinal reflexes. Prog. Brain Res. 88, 435–462. doi: 10.1016/s0079-6123(08)63827-3
Manzoni, D., Pompeiano, O., Barnes, C. D., Stampacchia, G., and d’Ascanio, P. (1989). Convergence and interaction of neck and macular vestibular inputs on locus coeruleus and subcoeruleus neurons. Pflugers Arch. 413, 580–598. doi: 10.1007/bf00581807
So, based on this assumption, it could be expected that sensory afferent stimulation may boost cognitive performance by increasing the ARAS/LC discharge.
An asymmetry in the level of specific tonic sensory signals may lead to an asymmetric ARAS activity and, in turn, to an imbalance in hemispheric excitability. There is indeed evidence that a lesion-induced hemispheric imbalance may lead to specific cognitive deficits which are abolished by a second symmetric lesion (Lomber and Payne, 1996).
Lomber, S. G., and Payne, B. R. (1996). Removal of two halves restores the whole: reversal of visual hemineglect during bilateral cortical or collicular inactivation in the cat. Vis. Neurosci. 13, 1143–1156. doi: 10.1017/s09525238000 07781
So, asymmetries in the level of sensory afferent inputs may potentially induce cognitive dysfunctions, which could be prevented by counteracting the afferent asymmetry. Alternatively, an asymmetric stimulation of specific sensory afferents may compensate for hemispheric imbalance (Rubens, 1985; Bottini et al., 1995; Schiff and Pulver, 1999).
Similar relevant papers
De Cicco, V., Cataldo, E., Barresi, M., Parisi, V., and Manzoni, D. (2014). Sensorimotor trigeminal unbalance modulates pupil size. Arch. Ital. Biol. 152, 1–12. doi: 10.4449/aib.v152i1.1567
De Cicco, V., Cataldo, E., Barresi, M., Parisi, V., and Manzoni, D. (2014). Sensorimotor trigeminal unbalance modulates pupil size. Arch. Ital. Biol. 152, 1–12. doi: 10.4449/aib.v152i1.1567
Finally, malocclusion leads to increase of apoptosis markers in the hippocampus and to accumulation of β-amyloid (Ekuni et al., 2011), which is one of the clinical findings associated with AD (Sisodia et al., 1990).
Sisodia, S. S., Koo, E. H., Beyreuther, K., Unterbeck, A., and Price, D. L. (1990). Evidence that β-amyloid protein in Alzheimer’s disease is not derived by normal processing. Science 248, 492–495. doi: 10.1126/science.1691865
When considering this question of asymmetry we have to ask ourselves what are the inputs that can be asymmetrical.
One of the biggest is mechanoreceptor/ proprioceptive input from the suboccipital muscles (which have very high innervation with mechanoreceptors- more than any other muscles).
Secondary thoracic outputs may skew the system into sustained asymmetry.
Sensation from the face, and chewing ( all covered b y the trigeminal nerve) can be highly relevant in worsening asymmetry.
Internal lesions like a stroke can drive asymmetric inputs and throughputs in the brain.
If we return to the pattern described by Biedermann we can see that he is talking about children who, due to birth injury have been left with asymmetries of posture in the suboccipital region and the thoracic spine.
We all know perfectly well that a child who is interested and engaged will sit up straighter (with full engagement of that midline motor system) and that an ADHD child when dispirited and fatigued will slump into an asymmetrical posture.
What has not been understood is that that asymmetrical posture is largely dependent on previous injury AND will drive asymmetry of afferent inputs setting the child up for exactly the sort of dysfunction that is described in the above paper. It will also be likely to set the scene for a transient unilateral visual neglect:
At this point I believe we have established the association between functional or structural brain symmetry and function, and the effect of posture on asymmetry.
More will be coming and this post will at some point be split in two.
ADHD and oculomotor control.
Attention Deficit Disorder is a controversial subject for a number of reasons. Many are uncomfortable with the idea of medicating children over a long period. Many believe that because the definition and the key symptoms have been modified (I would say refined, in light of experience) that that means it can’t be true. The idea of having something wrong with your attention is troubling to others – as it hints at a gross incompetence at the spiritual level.
One of the more endearingly inattentive views on ADHD was a book called “ADHD Does Not Exist” by Robert Saul MD. Saul, a Pediatrician in Behavioural Neurology wrote a useful book listing many of the physical issues that can cause ADHD symptoms, and then declared ADHD non existent, because it had been reclassified into different categories.
This valiant effort did list one important item contributing to ADHD (vision problems)., but it failed because it did not pay close attention to the DSM classification. Saul also claims that mood disorders could be causes of ADHD. Mood disorders present very differently to ADHD, and secondly, they are actually specifically excluded from the ADHD definition if the attention symptom occurs solely during the active phase of the mood disorder.. I guess attention deficit strikes again!
The DSM listing for ADHD consists of a list of behavioural symptoms, some restrictions regarding age of onset and situationality, impairment caused by symptoms, and exclusions.
What DSM does not do is provide any data about physical signs or speculate on cause .
ADHD is now widely understood as a neurobehavioural disorder but DSM does not give any information about neurological signs. This, in itself seems a remarkable lapse of attention.
The DSM classification of ADHD separates it from various learning disorders:
Dyspraxia (Developmental Coordination Disorder- in at least 50% of ADHD children)
Sensory processing issues,
Then mood disorders, anxiety and oppositionality
What is at issue here, apart from the absence of physical examination to guide our treatment, is tht the decision to separate these disorders is arbritrary.
Current understanding in neurology are putting more emphasis on the primary role of the subcortical structures in normal function and dysfunction.
A new diagnostic category “Cerebellar Cognitive Affective Syndrome” has been proposed and it covers all these disorders.
Additionally in Sweden, doctors there have been doing neurological examinations and finding enough positives to create a new category “D.A.M.P. – Deficits of Attention, Motor Control and Perception”
This regrouping has several advantages- these disorders share common neurological features, the features are germane to the manifestation of attentive behaviour, using th broader classification ensures that this neurological assessment is done routinely. The structuring of DSM almost makes this assessment seem redundant. Certainly many patients are surprised when they are asked about them, instead of questions more focussed on the DSM list.
However, should the clinician choose to do even abasic screening questionnaire some things come up again and again:
Poor sense of direction, often getting lost.
Ive often seen ADHD patients take a series of photos on their phone camera to ensure they don’t get lost.)
Fear of heights (sometimes extreme- and sometimes covered by elaborate avoidance strategies).
Intermittent issues with mild agoraphobic or claustrophobic symptoms
Difficulty formatting writing on a blank page writing all crowded into one corner the page)
Difficulty with reading and focussing.
These symptoms (sometimes described called convergence insufficiency, or binocular vision disorder) are remarkably similar to the core ADHD symptoms, but we will return to that.
Often these patients are so good at avoiding these disabilities that they have even forgotten that they have them, and they are one found by close verbal questioning.
Other significant items in the history include symptoms of dysautonomia, and also very widespread and strong stress response. These contribute strongly to many ADHD traits.
Examination will reveal a range of signs consistent with at least some of these symptoms in virtually all ADHD adults (and presumable children, but I was seeing adults).
Impaired balance and coordination
Mild cerebellar signs
Poor tone in the midline muscles, such that they are often hunched
Usually some issues with neck pain, with associated head tilt, and on occasions some issues referable to TMJ (Stimulant side effects are common in this group until the jaw issue is settled0
Rapid fidgetting tapping their feet. This could represent a response to orthostatic intolerance or it may e an escape phenomenon involving basal ganglia.
Eye signs: usually at least saccadic intrusions to pursuits, difficulty with saccade and antisaccades (a failure of inhibition)and sometimes more complex signs such as a unilateral mydriasis (dilated pupil). More severely affected individuals may sow signs of discomfort such as blepharospasm when the eye tests are done.
So it should be clear that all these issues will be impairing function many ways.
In fact our attention is executde through eye movements, speech and motor activity, all of which are listed here.
It is also possible to find good neurological rehabilitation to attend to many of these issues.
However, of all these functions, eye control (oculomotor) is the stand out issue.
Learning to read ( and continuing ) is a demanding task requiring expenditure of executive effort. The task continues to get more difficult with the introduction of more difficult words and phrases and finer print.. Thus we combine a task which is demanding in terms of oculomotor control with conceptual difficulty.
$ years ago I found a questionnaire on convergence insufficiency from a local optometry school, and I was surprised at the similarity of the questions to ADHD questions:
There are a number of other resources available on the internet:. This one is
Screening is easy:
The situation is that there is very marked cross over between ADHD and Binocular Vision Disorder (BVD), to the extent that it is probable they are in many cases, the same thing.
These conditions can present simply as ADHD, or as more complex syndromes with neck pain and head tilt, or with very few symptoms, so there is not a full, one to one overlap between them. The incidence
Ophthalmologists classically highlight traumatic brain injury as a cause, and highlight vertical eye misalignment (vertical heterophoria) as the most troublesome variant.
At this point it is worth highlighting some of the main features:
If we are to see the world properly we need to have both eyes looking at exactly the same point. The structure of the retina is in layers, deep to the rods and cones there is a layer of ganglion cells. All rods and cones feed I to only one ganglion cell, so the ganglion cell is the measure of visual field. Each one covers an area about 40 seconds of arc wide. ( A very small distance).
If the images are not matched, the brain will receive 2 images one into each eye.
The neurological response is to suppress one image, and use the other one for sight, but the second image is used for the balance system- which is now receiving asymmetrical information.
The outcomes here are a stress response- all the time (hence much weight gain, irritability, impulsivity) and a failure of muscle tone. If the brain has an orientation issue like this it has difficulty in maintaining upright posture and good muscle tone. Very frequently the patient will develop a persistent head tilt, and hence an upper cervical subluxation, and now we finally see why this is relevant to “Atlas Subluxation and ADHD” In fact these three systems (proprioception, vestibular, and oculomotor) are interlinked and a perturbation in one will disrupt normal function in the others. It is likely then that a wide range of initial insults could initiate this pattern.
We will return to this systems theme and deal with upright posture and attention in a later piece, but for now we will focus on more detail relating to vision..
Working memory is a term often discussed in ADHD. The traditional view has been that we do not have enough of it. I always felt that was wrong. The alternative hypothesis is that we have some “resource hog” wasting all our working memory.
Saccadic eye movement and working memory deficits following damage to human prefrontal cortex
In short, saccading as we move along the line reading is a process that demands working memory. The system has to be able to hold in working memory the initial position of the eyeball, and the target position of the eye ball. This is all very well if your system is working efficiently but many ADHD individuals have enormously dysfunctional reading patterns maybe needing 5 times as many eye movements to read the same passage. That consumes a lot more working memory.
The other item consumed is neurotransmitters:
Effects of Dopamine and Norepinephrine on Exercise-induced Oculomotor
Article in Medicine & Science in Sports & Exercise · April 2017
This experiment looked at oculomotor fatigue as an item compromising athletes in demanding events. It demonstrated that acute dopamine reuptake inhibitor (Ritalin) and Noradrenaline reuptake inhibitor (reboxitine) prevented fatigue-related impairments in oculomotor control.
This gives us a clear relationship between the current use of stimulants in ADHD, oculomotor fatigue (overdrawn working memory) and dysfunctional oculomotor control, as seen in binocular vision disorder.
Binocular vision disorder is common (about 10% of the population), but its presentation is heterogenous, and many will not present with attention issues. However the idea that it may be a major final common mechanism for ADHD symptoms is strong and well supported.
Finally, the main emphasis in ADHD research has been the fronto- striatal loops in the brain, which are typically underachieve, and the relevant areas of the brain marginally smaller.
It is important to understand that that information about the fronto striatal loops is not at all inconsistent, with this understanding of subcortical contribution to ADHD symptomatology.
the likes explanation is that due to these issues with eyes balance and coordination is perfectly consistent with the information about the fronto striatal region. The basic idea here is that, as a result of the unstable autonomic nervous system (read by our brains as a sign of danger, plus the added burden created by these balance, coordination and eye coordination issues) more decision making becomes automatic/ reflexive and bypasses the fronto striatal process. The fronto striatal system, like all brain parts, requires the stimulus of repeated and diverse activity to grow fully. In this context ADD can be seen not as a “dopamine deficiency disorder” , not as a striata- frontal problem, but more as a particular whole brain issue. However, the old assumptions about behaviour and the coaching and counselling issues become less relevant. A neurologically informed approach to ADHD emotion and behaviour counselling is arguably better directed towards dealing with the underlying neurological issues, but understanding that most of the trouble is driven by stress responses of which we have become unaware. IE If we proceed with a psycho-education approached buffered with at least some basic body mindfulness (I suggest the term diagnostic body scanning- like going to the mechanic), and an understanding that our brittle systems create a situation in which we are more likely to hit overload and “tilt”. To me, it seems that we need to focus on stress response prevention, coupled with as much awareness as possible, and the understanding that if we pull back when we are fatiguing (but others are not) we are acting with compassion towards ourselves, and everyone else.
While I have had several improvements in the past, they, for one reason have not been as long lived as I hoped. It turns out that the factors maintaining this problem and causing relapses are more complex that I had at first imagined.
Still, experience is one way to learn, I guess, I was aware that my neck pain was still only partially controlled, and there were odd little side issues like a persistently dilated right pupil, coupled with a tendency to sweating on my right forehead (yep, it looks pretty silly), which both suggested an overactive sympathetic nervous system on the right side of my body.
This blog has been an invaluable learning experience and it generates a good deal of correspondents. One of them, a highly acute young woman, suggested to me that I review another You Tube talk on the subject:
Thankfully that clarified something I had only half understood for the last few hours- namely the role of the upper cervical muscles as a source of sensory input into the brain.
These small muscles contain a very high number of mechanoreceptors, which unlike many other sensory inputs to the brain are always active and keep our brain cells ticking over rather than dying for lack of stimulation. (Lack of stimulation is as harmful for brain cells as overstimulation).
If there is a lack of stimulation there are “downstream ” problems. The stimulus should go through the vestibular system and cerebellum, right up to the cerebral cortex, and then provide a descending stimulus through the reticular formation and into a column of cells devoted to the function of the sympathetic nervous system (the IML, or intermediolateral column).
Now that stimulus (as is true of about 90% of the stimulus from the cortex) should play a role in inhibiting the role of the spinal cord.
So in this case a right handed subluxation with associated muscle tension in the rectus capitis muscles will result in a lack of inhibitory control of the sympathetic nervous system on the same side.
That sympathetic overactivity tends to generalise to both sides.
The muscle tension will also give false positional information into one side of the system, causing what I have described as sensory mismatch in previous posts.
I am assuming that the confusion caused to the proprioceptive system will make it much harder for the system to find its way back to the correct position.
Im not recommending this, but once I had read all this i thought to myself “I think if I target that muscle and stretch it repeatedly by turning my head in the right direction while applying gentle pressure then that might correct the problem- at least mostly.”
So that was the way it worked out- thumb pressure (not too hard) over the right rectus capitis muscles while I repeatedly pressed down while turning my head down and to the left.
I think the biggest reason I am cautious about suggesting we all do this willy nilly is that i have been working on this problem for years with apps etc that give me very good detailed anatomical information.
Now the end result of this was an immediate decrease in my neck pain, followed abut 10 minutes later by warming of the fingers as the sympathetic nervous system self corrected. I was able to feel my posture (flexed above T6 extended below T6- with a spinal rotation (all described as part of this syndrome) self correct, but it took about 2 days for my body to stop aching from the change in posture.
As of a week later I have lost almost all the tremor I had, my typing has become remarkably fast, and there has been no sign of return of the sympathetic nervous system issues- including the fact that I am sleeping much better and am handling interpersonal interactions better because I give less sign of being wound up.
The sleeping is a particular positive, because it had been taking me about 8 hours to go to sleep due to this chronic stress response. Eight— extremely boring hours.
So, as I said, there are a number of feedback loops maintaining these problems, and I believe we should all be aware that despite the difficulties we experience, we should all expect complete recovery, and be satisfied with nothing less.
I have an advantage- a Medical Education,and it was still damn difficult.
I remain horrified at the commentaries of professional medical skeptics who try to block our access to these remedies based in chiropractic. To me this smacks of nothing less than an attempt to gain a monopoly in the health market. Science based medicine? Bollocks. Greed based medicine more like.
This comes from a discussion I was having on an ADHD users forum.
It is clear to me that the oculomotor problems contribute to many of the specific ADHD symptoms, especially in academic and workplace environments, and they effectively suck up a lot of working memory.
So I was asked whether I thought the eye problems caused ADHD or the ADHD caused the eye problems.
Another very powerful brain based model is called cerebellar cognitive affective syndrome- and that provides the clue to some of the linkages between these conditions.
There is a little said here but the article is well out of date:
The list of associated disorders is interesting: depression, bipolar, ADHD, autism, dyslexia, schizophrenia.
So here comes the association with these neck subluxations. As of 5 years ago we now have hard proof of exactly the kinds of impairments to the craniocervical junction that these chiropractic ‘subluxations” can cause.
This is due to pioneering work by Dr Ralph Demadian (inventer of the MRI and the upright MRI) and several other neurosurgeons, radiologists and chirpractors.
I have put a list of the readily available evidence (from things like talks given to the Cranio Cervical Syndrome Symposium) on my blog. These talks are not papers but they are based on peer reviewed papers. This page is a bit of a mess, because there is just so much of it. Im grabbing as many papers as I can get without having to pay for them and will put it all up very soon.
Now so far as the cerebellum is concerned I would say that the now proven intermittent interference in vertebral artery blood flow in subluxations will directly compromise cerebellar blood flow via the Posterior inferior Cerebellar Artery – depending on your personal anatomy and your personal spine issues.
|“The posterior inferior cerebellar artery (PICA) is the vessel that perfuses the lateral medulla, and is usually occluded due to thrombosis or embolism in its parent vessel, the vertebral artery.”|
However its anatomy is highly variable- and many people will have a better functioning circle of Willis that will compensate better for compression of the Vertebral artery. Those sorts of anatomical variants are heritable traits– another possible target for genetic investigations.
So what is showing up is that these subluxations cause amongst other things a reversible, highly individual cluster of symptoms- for which the name “Cervical Medullary Syndrome is proposed.
This syndrome is interesting as it includes most of the symptoms of most psychiatric disorders and is highly associated with neuropsychiatric as well as “soft” neurological signs.
Looking at the cluster of symptoms I note that virtually anything in the “Affective Spectrum Syndrome” (a familial clustering of disorders that includes fibromyalgia, bipolar and ADHD) could be fully explained by this “Cervical Medullary syndrome”
Affective Spectrum Disorder:
Family Study of Affective Spectrum Disorder
James I. Hudson, MD, ScD; Barbara Mangweth, PhD; Harrison G. Pope, Jr, MD, MPH; Christine De Col, MD; Armand Hausmann, MD; Sarah Gutweniger, MA; Nan M. Laird, PhD; Wilfried Biebl, MD; Ming T. Tsuang, MD, PhD, DSc
(REPRINTED) ARCH GEN PSYCHIATRY/VOL 60, FEB 2003
|Affective spectrum disorder (ASD) represents a group of psychiatric and medical conditions, each known to respond to several chemical families of antidepressant medications and hence possibly linked by common heritable abnormalities. Forms of ASD include major depressive disorder (MDD), attention-deficit/ hyperactivity disorder, bulimia nervosa, cataplexy, dysthymic disorder, fibromyalgia, generalized anxiety disorder, irritable bowel syndrome, migraine, obsessive- compulsive disorder, panic disorder, posttraumatic stress disorder, premenstrual dysphoric disorder, and social phobia. Two predictions of the ASD hypothesis were tested: that ASD, taken as a single entity, would aggregate in families and that MDD would coaggregate with other forms of ASD in families.
Now what I am proposing is that affective spectrum disorder is one of the presentations of cervicomedullary syndrome, and ADHD is a subset of both affective spectrum disorder and cervicomedullary syndrome- one which has more cerebellar effects than some other variants.
I believe that the saccading issue is one of the major generators of symptoms in the classroom, because if you have got it and nobody notices you experience reading in the classroom as “boring” and wont do it.
So the oculomotor problem generates many of the symptoms that are characteristically ADHD.
Other symptom clusters are generated by sympathetic dominance, a degree of learned helplessness, and direct brain fog so characteristic of ADHD PI and also fibromyalgia and depression, and CFS) probably represents a direct energy supply issue to the brainstem.
These issues are less severe if your posture is more upright- and that is a real benefit of exercise and meditation.
The last issue to bae addressed is “dopamine” and this popular idea that ADHD is a dopamine deficiency disorder, or an issue with the transporters or something like that.
I suspect the dopamine issue in ADHD is that the need to constantly adjust and adapt to an unstable body means that multiple fast re-fixations of attention are needed- and those neurones just get a bit fatigued. Stimulants do help, a lot, but lets face it- retrofitting an explanation on to a serendipitous discovery that stimulants worked, especially at a time when we had such little knowledge of neurology, might be superficially attractive but it is not intellectually justifiable.
This post is somewhat speculative, but it is very clear to me that the nomenclature of psychiatric conditions is in an awful mess. Some conditions include physical symptoms, some do not, some like ADHD, are alleged to be neurobehavioural conditions but their descriptions include no information about neurological examination or neurological signs. (These can actually be found). They also include many symptoms without making reference to the neurological paths that could generate them. The nomenclature is so bad that there is inadequate distinction between syndrome, symptoms, and actual discrete medical conditions.
More recently there has been a push to make more brain based definitions. One of those is cerebellar cognitive affective syndrome 9which overlaps many psych conditions) and it appears to me that so is “Cervicomedullary syndrome”, being proposed by some neurosurgeons.
So lets go through the symptoms again- and I will make some comments beside them.
Cognitive Changes—- this could include brain fog, or many of the inattentive symptoms of ADHD
note here that these states are being described as smptoms. Much of the drug research around them is predicated on the idea that they are distinct illnesses. In fact they are syndromes- that are symptoms of another bigger syndrome. No wonder people get muddled.
POTS I would add any dysautonomia/ orthostatic intolerance , consistent with current thinking that sees them as part of the same problem.
Sleep apnoea———– I suggest also snoring without apnoea, and probably UARS.
Blue hands in the cold weather
Irritable bowel syndrome
Gastro oesophageal reflux
So it is clear that Cervicomedullary syndrome (which is predicated on the idea of a local energy supply impairment to the brainstem) can cover an awful lot of ground.
So here are some questions that I am mulling over with my friends. I don’t know the answers to all of them, but I do think they are good questions:
1) Cervicomedullary syndrome actually contains most of the physical symptoms of many emotional states, and psych and functional neurological illnesses – hence the idea of reframing mental illness with a view to that being a foundational element. The simple concept here is this: if your system is constantly skewing your emotional perceptions and responses (including subliminal facial expressions), then how can you function? You may feel more threatened than you logically should. Equally due to the tensing up into forward head posture in adverse conditions (or when recalling them) it is likely that that will further compromise the craniocervical junction and cause undue persistence of emotional states ( a big issue in humans).
This observation can be taken further by considering the proposed syndrome Affective Spectrum Disorder- which was based on the observation that many of these conditions are familial (but a family may have multiple members with different conditions on this list:
Family Study of Affective Spectrum Disorder
James I. Hudson, MD, ScD; Barbara Mangweth, PhD; Harrison G. Pope, Jr, MD, MPH; Christine De Col, MD; Armand Hausmann, MD; Sarah Gutweniger, MA; Nan M. Laird, PhD; Wilfried Biebl, MD; Ming T. Tsuang, MD, PhD, DSc
(REPRINTED) ARCH GEN PSYCHIATRY/VOL 60, FEB 2003
|Affective spectrum disorder (ASD) represents a group of psychiatric and medical conditions, each known to respond to several chemical families of antidepressant medications and hence possibly linked by common heritable abnormalities. Forms of ASD include major depressive disorder (MDD), attention-deficit/ hyperactivity disorder, bulimia nervosa, cataplexy, dysthymic disorder, fibromyalgia, generalized anxiety disorder, irritable bowel syndrome, migraine, obsessive- compulsive disorder, panic disorder, posttraumatic stress disorder, premenstrual dysphoric disorder, and social phobia. Two predictions of the ASD hypothesis were tested: that ASD, taken as a single entity, would aggregate in families and that MDD would co-aggregate with other forms of ASD in families.
All the above could be accounted for by the symptomatology of cervicomedullary syndrome with an overlay of adjustment disorder as the unfortunate patient struggles to self regulate an utterly unreliable system.
2) Forward head posture and hunching will worsen it. This may be one reason why some people become symptomatic many years after a whiplash— ie they hit a period of high work demand, or emotional adversity and the descent into poorer posture sets off a self reinforcing loop.
3) Impaired energy status in the brainstem is a critical element of the problem- and it may not just be direct impingement on vessels. My own recent experience with cold laser clearly shows how potent this can be in improving energy status in inflamed tissues. (We already have work that shows this sort of inflammation and damage in tissues of the brainstem).
4) Clumsiness and ataxia are both elements of cervicomedullary syndrome. Both will worsen spinal alignment. (On this note I have been staggered at the improved integration in my movement since I have started the treatment. I’m not usually all that coordinated).
5) Direct sun exposure is important and should be considered an important part of an exercise regime. Same wavelengths as the IR cold laser. Later afternoon sun and early morning sun have a better incident angle for the back of the neck- esp above and below the arch of C1. Midday sun has the same IR, but the UV can be problematic and the angle of incidence is not ideal.
6) – and this is really pushing the envelope of credibility-maybe the old yogic practice of sun eating has direct benefit to structures in the posterior pharyngeal wall- inc vagus and glossopharyngeal nerves.
(However- lets face it- the old guard has been wrong on almost everything else- so why not this one too?)
7) Given the role of the locus coeruleus in maintaining upright posture and alertness- the role of norepinephrine in improving alertness both in ADHD (stimulants) and depression (SNRI effects) may be very important.
8) other concurrent issues like secondary dysbiosis may explain specific characteristics of conditions like depression
9) The debilitating effects of dysautonomia (and other symptoms which accentuate forward head posture) may create another negative feedback loop which causes persistent dysfunction.
10) Manic episodes may be explained by situations which cause a sudden improvement in medullary energy (ie LC activation, or lots of sun) in individuals who have an underlying hemispheric dominance which predisposes to sympathetic nervous system dominance. dominance.
11) Individuals with the above neuropsychiatric conditions are going to have lots of issues as they will think their adversity is caused by other people- thats what we are taught to think. Being able to explicitly demonstrate how their difficult emotions arise and the issues this causes with subverbal empathy may make untangling this end of the problem in therapy much faster and easier. Lastly- schizophrenia- I don’t know to meaningfully speculate.
12) There is more to come here but I am also encountering information that supports the idea that fibromyalgia and chronic fatigue syndrome may often be caused by upper cervical problems.
Sometimes you miss the weirdest things. I have been really noticing just how bloody good I am feeling with all this low level laser treatment. With my history of Biploar I am always somewhat suspicious of feeling good- especially in spring. However this time I
I know why in terms of anatomy and neurophysiology.
I also know that what is going on is remarkably analagous to descriptions of enlightenment ( Roshi Philip Kapleau is one that comes to mind.). Now it is clear that I have gone through all of my life feeling like shit- and much of my restlessness has come from discomfort. The current situation is a huge improvement and the improvement continues to deepen.
Now I think that this is a major key to understanding psychiatric illnesses because all this felt experience does have an impact about what we think about ourselves and others. There are all kind of feedback loops there. The question of mental illness is dogged by linguistic imprecision- and really the Western field of psychiatry does not have a proper definition of mind. As “mental” is “of the mind”– we have a problem here.
So what I missed is 2 comments from the Zen master Dogen (do yourself a favour- look him up). 1) That the Buddhas entire dharma (ie the enlightenment experience can be fully apprehended by sitting in lotus. (Interesting, and neurologically plausible too) 2) just the other day– that enlightenment is an experience of the body. Enlightenment is also sometimes referred to as cessation or extinction- which is intriguing in terms of the cessation of unpleasant feeling I am noting. I’m not making any claims about me here- just looking for ways to understand complex concepts.
One issue which interests me greatly is bipolar- as I have had several episodes (and when this event started with the laser I was very careful to exclude another episode). The first episode was triggered by a serious whiplash (from which I thought I had got off unscathed!!!). However within days the change started- I was more energetic, I was happier, I was really seeing the beauty of nature in an amazing way. I felt good, (like Jame Brown!) whereas I had been feeling physically terrible probably since early adolescence when I first developed dysautonomia.) That good feeling felt right- it felt like our birthright. — and it is.
However there was too much to see too much to respond to, and it was difficult to not go with that and get carried away into silliness. Equally the intensity of my experience made it difficult sync well with others in conversation, and caused a good deal of aggravation. I would also say that there was too much sympathetic stimulation (leading to restlessness, whereas now, I am feeling very restful and can drop off in bed in a couple of minutes). All other episodes have been associated with increased sun exposure in spring or summer.
So lets advance a little hypothesis here- the whiplash that started this off actually improved circulation to and neuronal metabolism within the brainstem (which was functioning poorly and causing me to feel poorly (though I thought that was normal) and I suddenly felt amazingly happy and positive. Increased sun exposure in the other episodes was the equivalent of the low level laser and set the process going again- because we did not understand it.
So that glimpse of positivity at the start of of the manic episode is very interesting. Many bipolar people actually grow out of it and mature into serious spiritual practitioners. ( ie the Jungian Therapist and Tibetan Buddhist practitioner Paul Levy: https://www.awakeninthedream.com/ They have all recognised their manic episodes as part of their awakening.
I’m inclined to think that the more positive feeling at the start of a manic episode is actually truly a feeling of better functioning. Its interoceptive signature is actually one of absence of unsatisfactoriness- you feel less of your body unless you choose to observe it.
That is the danger though, a full blown episode is very destructive and we tend to try and deny the whole experience, throwing the baby out with the bathwater.
Since the first low level laser treatment to the brainstem via the back of my neck, five days ago I have been very different. No brain fog, able to see multiple interactions between simultaneous streams of data, elbowing quick choices of the shortest, easiest way through, I’m more concise, far more coordinated, more able to sleep or wake as needed, and getting far more precise instructions from my body about what food it wants, and how much.
A zen master was one asked about the experience of enlightenment, and he said that when enlightened, one eats, when hungry, and sleeps when tired.
Well that’s what is happening and it was brought about by light therapy.
Does that mean that I am “ enlightened” , or “enlasered”, or just that I seen the light? Maybe even just good at bad puns
However, all jokes aside, I realised after I wrote the above last night that I have had this experience once before- in 2008, just after I started dexamphetamine.
The result then was staggering. All of the above, the weight just fell off, my body decided what it wanted to eat. I had always been shy, but now was able to talk fluidly and be sociable.
So- why the similarity?
This is interesting, very interesting.
Now alertness is largely regulated through the locus coeruleus, a pontine brainstem nucleus.
The LC uses norepinephrine as its effector neurotransmitter.
Stimulation of the LC causes an increase in vigilance/ sensory sensitivity, it somewhat increases metabolic rate (good for running away, and also for thinking as low metabolic rate is associated with a functional drop in intelligence). and it also causes some sympathetic activity,
Additionally the LC is involved in posture regulation and higher alertness is associated with more upright posture (think meerkat on guard). As an aside- deliberately shifting to an upright posture will help alertness- hence the meditation instructions we are given if we have a good teacher).
Finally a more upright posture will improve hydrodynamics and neural compression around the craniocervical junction associated with malalignments.
Now we usually think of ADHD as being associated with dopamine, but the stimulants also affect norepinephrine, and improve norepinephrine neurotransmission.
So it is very clear to me that there is at least a norepinephrine driven effect on the locus coeruleus that improves alertness and attention at least by improving neck posture and the function of the craniocervical junction and probably also by more direct neural effects.
Ive had some level of symptoms from what looks like a birth injury to my neck in 1962- mostly along the lines of ADHD, and dyspraxia,low grade dyslexia. That worsened in 1985 with the onset of what was to be 2 years of sever R sciatica
It seems that I was set up for more trouble in 1987 by a whiplash injury, which within a week was followed by the abrupt onset of my first ever manic episode. In due course that was controlled with Lithium, and the problem seemed to be over.
However my work involves much home visiting and much paper work.
From abut 1993 I experienced (as well as the declining episodes of sciatica) gradually increasing neck stiffness- becoming unable to turn around properly, misjudging distances, having minor car accidents (ie reversing into other cars in car parks) becoming intolerably vague ( I will write for you all one day the full list of types of inattentive episodes leading to my diagnosis of ADHD), and also a good number of other odd symptoms- increasing sleep dysregulation, episodes of nausea, episodes of sensory processing disorder. One symptom of the ADHD in particular was losing track- once I was doing something I had to lock on to it to the exclusion of everything else.
“Please don’t interrupt me while I am ignoring you” reads the coffee cup my partner gave me– but it was not in jest.
ADHD diagnosis and stimulant medication was a live saver, and to this day I remain of the opinion that even though they only symptom relievers, stimulants are the most effective medications and predictable I have ever had or prescribed. So much for all the bad publicity they get.
However like virtually everything else in Internal Medicine (barring antibiotics)- symptom relief is all they offer.
The ADHD diagnosis was on 4 October 2008, and by that time the pain was worsening, but it seemed unrelated.
Soon after that I realised that meditation can be regarded as a form of attention training- and started investigating.
By chance, in December 2009, while in dire straits I encountered a brochure for Atlas Profilax, and I had treatment within days. That was puzzling– how could those”quack chiropractors” who treated a non existent subluxation, be right. However they were, and I started seeing many other people with the same problem, particularly chronic orthopedic issues like frozen shoulder. Diagnosing and referring these patients was an imperative, because they were in great trouble. However the attitude of the profession, the health regulation authority and my professional defence organisation was hostile– so this was very stressful. However I did not do this job to curry favour, I did it to help people, and to dishonestly conceal useful information. thatwould have been a breach of mBuddhist vows. So after finding and reading some textbooks I started referring. Yes, it was devastatingly stressful, but I will say no more as there is a good chance i will pursue legal action.
The outcome of Atlas Profilax in terms of mental clarity and reduction of pain was staggering- far stronger than the stimulants, and very fast, within 24 hours. However I still had a very crooked spine and that kept stirring the issue up. You will not keep your neck straight if it is not sitting straight on your body. That’s not rocket science.
I learned mindfulness integrated CBT- (body scanning) to use as a psychotherapy with my patients. It also proved useful for me and helped me be more precise in localsing remaining issues. That + the outcome of the Atlas issue was enough from me to taper from 50g dexamphetamine to zero from 15April to 15 June 2010. (I had to resume a lower dose later- April 2012 to now).
In June 2010 I had a further stroke of luck- a chance meeting with a chiropractic neurologist and we started work on my dysfunctional movement patterns, eye movements etc that were maintaining the pain and postural issues.
That proved very resistant to treatment and despite steady progress there were setbacks related to my marriage breakdown, and a further severe manic episode due to a change of medications. However, by May this year the pain and subluxation feelings were largely gone and the return to work process for me was initiated.
However there were still ongoing issues with irregular sleep pattern (sometimes as much as 5 days straight with no sleep) with bizarre right sided sweats, with mental fog, and terrible issues staying on track in tasks. I would get ice cold fingers, upset gut, postural hypotension, alternating with skyrocketing blood pressure episodes (up to 240/160), frequency of urine all night, strange skin discomfort (dysaesthesiae). I was not having a good time. I was also not my best- though I was actually much better than an entire profession whose prejdices prevented them from seeing what was needed to get me well. Ie I was that sick and STILL a better diagnostician and researcher.
I found the functional neurology profoundly interested and have studied as much as I could given my illnesses. The quality of the information and its obvious applicability have caught my interest. It is worthy of my attention. The sort of articles we so often see in medical magazines about various tedious demographic studies of the incidence of championship level tiddlywinks playing amongst Aboriginal and Torres Strait islanders are not worth my attention.
The functional neurologists have also been incredibly kind, making time to answer my incessant questions and handle my endless theorising. Several have directly reached out from the far side of the world and guided me in the study that I needed to do to understand my chronic pain. That is generous on a scale usually only seen in bodhisattvas. Thankyou George, and Amy, Brandon, and Lynn, the queen of photobiomodulation.
In the last few months though the information has started flowing in much faster.
I found on You Tube several excellent short presentation on dysautonomia in ADHD (I have been observing this and clinically confirming it for some years)
-then a huge cache of information on the recent discoveries made around the cervicocranial dysfunction following the advent of upright MRI.
Now closer inspection of all that and my new book “The Cervicocranial Syndrome and MRI)
made several things clear. The symptoms troubling me fit neatly in to “cervicomedullary syndrome”. In the context of a neck issue the causative chain is
Whiplash- ruptured alar +/or transverse ligaments between the peg of C2 and C1 and the base of the skull
leading to minor lateral instability of the odontoid peg (C2)— leading to mild inflammation over the odontoid peg, which, on neck flexion compresses the upper spinal cord /lower medulla
That causes a low grade inflammation and localized energy deficiency in the brain stem which can lead to neuronal deaths (apoptosis) but certainly leads to dysfunction.
There are other likely issues such as lateral stretch of the cervical spinal canal irritating the lateral spinothalamic tract. That could have huge ramifications for chronic pain.
The instability in my spine at that level is obvious and I am strangely unenthusiastic about getting parts of my neck bolted together.
I had heard about photobiomodulation- low level laser therapy (frequencies 640, 808 and 904 and thought it worth a try. I had my first dose last Thursday 13th September.
Essentially the target is the front of the spine- going through the gaps between the back of the skull, the back of C1 and the back of C2.
20minutes later ALL symptoms apart from a little local instability are gone.
It actually feels really good to be alive- and not imprisoned in a body that feels like a torture chamber.
Sadly this particular advance did not last long as I was exposed to a stressful event that derailed me for many months after that. See the post”the Functional Neurology of Atlas Subluxation” for that,
This has enormous implications though. The neurosurgeon Joel Franck lists global neuropsychological, multifocal brainstem, spinal pain, and radiculomyelopathic clusters of conditions. That’s all of my problems.
Now I believe there is real work to be done optimising treatment. With the work I have had has straightened my spine up I think that the minor instability I do have at C1/C2 will require not much more than basic fitness and postural care- but for people earlier in that process, that might be harder and they will need to work with their therapists.
On the matter of neuropsychological problems it should not be lost on any psychopharmacologist that the neurones carrying those important neurotransmitters dopamine, norepinephrine, serotonin are all neurones that originate in the brainstem. Given time I hope that we shall see the “neurotransmitter model of psychiatric illness dead and buried. The symptoms of all these conditions can mostly be understood as variants of cervicomedullary syndrome.
Another small point on self care involves walking in the sun before 9 and after 3 and getting it to shine on the back of the neck. That is the same wavelengths. It also occurs to me that the old yogic practice of sun eating would shine sunlight on the rear pharyngeal wall and would also help.
The current situation in medicine has been incredibly wasteful and destructive.
I have had a great deal of psychotherapy over all this time (he is a lovely man and he actually learned quite a lot from me. it was nice having a specialist who did not think you a nut case. However looked at one way– we spent $90,000 trying to talk my alar and transverse ligaments to grow back together!
To me this post seems more brief and to the point than my early efforts– I suppose better energy supply will do that. As always I am happy to clarify any questions. I am learning more every day.
Before I commence this critique, lets be totally clear that I have been diagnosed with ADHD, and am happy with the positive effects of the treatment with stimulants that I have received from my doctors. I am also aware, however, that that treatment has been inadequate, no more than a band aid covering a bigger problem.
Many commentators have drawn attention to their concerns about the DSM (Diagnostic and Statistical Manual of Psychiatry, but it seems to me that none have hit the mark.
ADHD is a particularly apt example of the defects at the core of the DSM system.
ADHD is said to be a “neurodevelopmental condition”, but, remarkably, it is defined entirely by a list of behavioral abnormalities. Despite being conceived as a “neuro-developmental condition” no mention is made in the symptom profile of neurological symptoms, and no mention is made any where of examination findings. That is curious, to say the least. The only significant figure looking at this is Prof Martha Denckla, working with her classification of “Deficits of Attention, Motor Control and Perception”. Her work seems to have disappeared almost without trace into a deep pit of intellectual conformity. It seems to me that only a handful of individuals or groups have chosen to investigate the neurological basis of ADHD ( the one that all the academics and clinicians on the speakers circuit reference), and when they have done so they have been systematically ignored.
ADHD is defined as a neurodevelopmental disorder, but its defining features as listed in DSM are all behavioural. However, everyone acknowledges that it is strongly co-morbid with dyspraxia, dyslexia, ocular convergence issues and sensory processing disorder.
In fact, all of these disorders have demonstrable neurological deficits, even if many of them can only be reliably demonstrated clinically through what are described as “soft signs”. These soft signs can actually be demonstrated in ADHD as well, but few if us ADHD individuals can find practitioners competent to either elicit these signs or understand their relevance.
Now here is the trap- correctly understood, all these conditions are part of the same problem, but due to the thinking deficits underpinning modern medicine conditions like dyspraxia (Developmental Coordination Disorder- present at full syndromal levels in at least 50% of ADHD individuals) are regarded as being co-morbid with ADHD rather than a different manifestation of the same problem.
Furthermore the great consensus of opinion in the world of neurology now is that cognition is an internalisation of movement, and involves planning the next movement. This position has very substantial support through fMRI studies of individuals planning a response to a stimulus. (more on that in later posts).
If we choose to separate out the group that has convergence insufficiency or another related ocular coordination problem, we can immediately note a very large overlap between ADHD symptoms and convergence insufficiency disorders.
While convergence insufficiency is not considered an exclusion for the diagnosis of ADHD, the 2 conditions share 5 overlapping symptoms, and if CI was treated in patients with the 2 conditions co-morbid, it is likely that most patients post treatment would fall below ADHD diagnostic criteria. This is not a causal or careless observation, as most of us who have been treated for ADHD can attest to the fact that the effect of ADHD medications diminishes with time.
Now it does not take a lot of thought to understand that a movement disorder or an issue with filtration of irrelevant sensory stimuli might just reduce the capacity to pay attention, and that reduction of these issues might just significantly and positively affect the performance of the “attention impaired individual”, but for the life of me I can’t understand why most individuals interested in this area cannot immediately grasp that we are actually working with different ways of viewing the same problem.
So, depending on which way you choose to look at it your ADHD individual could fit in to any one of the categories already mentioned. Hence–“To a man with a hammer…..”.
The truth is, that as patients we are entitled to expect a better class of thinking from the professionals charged with our care.
Now this question of the way syndromes arise from our model of thinking. the next post is going to be more challenging, discussing the neurological underpinnings of pathological emotional processes. I suspect that cervico-medullary syndrome underpins the majority of psychiatric presentations, but I want to have my arguments reasonably well buttressed before I go there.