What’s In A Name? Pt 2. ADHD as a model of the flaws in DSM and in psychiatric thought processes.

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.

Dream on.

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.


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What’s In A Name? Pt 1.

Each profession tends to see the material before them in terms of their own cognitive framework, and, conversely, is blinded to anything lying outside that framework.

“To the man with a hammer, the whole world is a nail”

For many years the chiropractors have been attempting to draw our attention to the issue of upper cervical subluxation (aka, in their language, atlas subluxations) and their wider significance. Generally their comments have been ignored or dismissed out of hand, as no doctor could believe how such a tiny abnormality could cause such severe symptoms. However, in the world of medicine, attention to detail (even tiny details)  is the necessary distinction between success and failure.

We had a hint that things were changing when Dr Michael Flanagan brought out his book “The Downside of Upright Posture”, and more recently we have seen significant work done by chiropractors, radiographers and neurosurgeons.

Now the following comments are referenced to links previously provided here:

In particular the work done by Scott Rosa DC and colleagues has established a link between whiplash injury and craniocervical instability, that link having been confirmed by the neurosurgeon Dr Joel Franck MD, who employs his own technique of “minimally invasive C1-C2 fixation”.

There has also been significant overlap with the work done over the past 30 years by Dr Fraser Henderson MD (Neurosurgeon) who has been involved in the management of Chiari malformations, notably in Ehlers Danlos Syndrome. (See the previous post on this blog:
He describes some of the symptoms associated with these problems as cervicomedullary syndrome- highlighting the issue of impingement on the medulla (lower brainstem) as a generator of symptoms.

I further suggest (and will discuss in a subsequent post) that the majority of symptoms in many psychiatrically defined syndromes can be subsumed under the headline of “cervico-medullary syndrome”.

Cervico-medullary syndrome:

(Bear in mind that these symptoms are described in a quite coarse, broad-brush manner, and a detailed history would find them being described in a much more complex individualised way, generating a good number of sub-symptoms).


Double vision

Memory Loss

Cognitive Changes





Difficulty swallowing

Sleep apnoea

Respiratory abnormalities

Blue hands in the cold weather

Sensory loss


Unsteady walking

Clumsiness/ incoordination

Urinary dysfunction

Irritable bowel syndrome

Gastro oesophageal reflux

Speech difficulties

In fact this list includes most,  if not all of the visceral symptoms (heart, lung, gut, skin, unsteadiness) associated with most psychiatric symptoms.

It seems to me that the reason we have such desperately poor results in managing psychiatric conditions is that we do not understand why or how symptoms are generated, and we foolishly attribute the genesis of all psychiatric symptoms to cognition.

This is a serious defect in thinking and I will cover its ramifications in greater detail later. The more serious point here is that we have to start looking at the idea that there is enormous overlap between these conditions, and that the underlying assumptions which direct us to choosing a particular cluster of signs and symptoms to define a syndrome may be flawed.

To the man with a hammer etc….

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Craniocervical Instability: significant evidence supporting brainstem compromise, and impairment of blood and CSF flow.


In the last few months I have finally come across reliable evidence supporting the association between atlas subluxation (also being called craniocervical instability), and compromise to the cerebrospinal fluid drainage from the brain, jugular venous drainage from the brain, vertebral artery compromise, and finally stretch and compression injuries to the brainstem.

I am presenting some links to that evidence in this post.

Please note that while in some cases the material is more targeted at Ehler’s Danlos syndrome and Chiari malfomation,  both of which are more complex problems that usually involve at least some cervicocranial instability the same considerations apply to simple craniocervical instability/ atlas malalignment and it appears that the upper cervical issues are in play in both those syndromes.

One of the most important issues that I have noted is that it is likely that the instability at the top of the neck is the problem, rather than a static subluxation. That is valuable knowledge that explains why many people do not do well with a single treatment.

These anatomical issues are related to 2 neuropsychological symptom clusters:

Cervico-medullary Syndrome.

and Cerebellar Cognitive Affective Syndrome.
Both of these are relatively newly described and the exact boundaries of them are yet to be established. It is likely  that there are many individuals around with more mild versions of these problems which are difficult to diagnose as we have been unfamiliar with these patterns

The specific mechanisms being proposed are:

Impaired cerebrospinal fluid flow.

Impaired jugular venous drainage from the skull.

Vertebral artery compression causing intermittent brain stem dysfunction. ( I am suspecting a muted lateral medullary syndrome)

Impingement on the brain stem/spinal cord base caused by the inflammatory pannus that develops over the odontoid peg of C2 in cases of cervicocranial instability.

Tension stretching the brainstem and spinal cord both longitudinally and laterally through the dentate ligaments. This can cause direct neural dysfunction (like the odd sensations you get in your hand when you hit your funny bone) and it ca also cause in the longer term degeneration in the stretched neurones. It also appears to interfere with the venous drainage of the cord around those dentate ligaments.

Pressure on the upper cervical spinal cord on extension of the neck, caused by a failure of an atrophied rectus capitis superior minor to pull the dura out of the way during neck extension.

The rest of this page will be devoted to covering the evidence for all these assertions.

Dr Scott Rosa

CV from the CSVVI alliance:


“Dr. Scott Rosa is doing the most compelling upper cervical chiropractic research in the world today. He has spent the last 15 years working developmentally with the inventor of the MRI (Dr. Raymond Damadian) and FONAR Corporation – maker of the UPRIGHT Multi-positional MRI, in developing his advanced dynamic imaging procedure. He has worked with FONAR Corporation in developing cine cerebrospinal fluid (CSF) flow software as well as cine motion MRI and vertebral artery flow studies which have been instrumental in providing advanced images validating upper cervical adjusting pre and post C-1 correction, as well as patho-physiological changes at the cranio-cervical junction.

Dr. Rosa’s latest research is in the area of neuro-degenerative brain disease, cerebellar tonsillar ectopia (CTE), altered CSF and arterial/venous flow dynamics and their correlation to the cranio-cervical junction (gateway between the brain and spinal column), and atlas misalignment. Cerebrospinal fluid is no longer thought of as JUST a cushion for the brain. Recent studies have shown the importance of CSF to clear toxins of the brain through the glymphatic system; also, the draining of CSF from the central nervous system into the deep cervical lymph nodes by the newly found meningeal lymphatic vessels. It is highly important that the CSF is unencumbered in order for these systems to work effectively.”

How Craniocervical Misalignment Effects Fluid Flow


Observations at the craniocervical junction, CTE and observations of CSF.

The second talk- is centred around this paper:

The Craniocervical Junction: Observations regarding the Relationship between Misalignment, Obstruction of Cerebrospinal Fluid Flow, Cerebellar Tonsillar Ectopia, and Image-Guided Correction
Rosa S.a · Baird J.W.b Smith FW, Dworkin JS (eds): The Craniocervical Syndrome and MRI. Basel, Karger, 2015, pp 48-66


Key points and time within the talk
3:42 These Chiari Syndromes are not the same as the congenital ones in which the base of the skull is flatter than normal.
4:53 Research study of 43 MVA patients, but 4 had MS and 2 had Parkinsons
Imaging- all the neuro-degenerative patients had a misalignment of C1 C2 at the skull base, all had low lying cerebellar tonsils, all had obstructed spinal fluid flow

Introduced flow studies- started to find  CSF turbulence and backjetting- into lesioned areas.

18:20 Mechanical issues with upper cervical malalignment
Cord can be tethered by the dentate ligaments- this will pull on the cord, esp spino thalamic (touch, pain and temperature) and spinocerebellar tract

Note that often brain fog diminishes with in hours to days of atlas treatment.

Transverse process of C1 can impinge on vessels like the jugular veins
correction of misalignment can improve vascular supply to the brain stem

Cranio-Cervical Syndrome The vulnerability of the neck and its impact on fluid flow. (CCS) Symposium – April 6, 2013, Scott Rosa, DC, BCAO


Key Points:

5:42 3,000,000 car accidents per year in USA ; 35-50% will never recover, 40% of those will be disabled for the rest of their lives
10 mile an hour collision is the equivalent of catching a 200 pound bag of cement dropped from one story.
Patients usually don’t hurt when they are lying down

The correct imaging post trauma often not done
Upper Cx spine the most complex part of the spine sacrifices strength for mobility Strong simultaneous shear and extension forces at 50-120 mSec
S curve- retraction of chin into neck
muscle guarding does not start until 200 mSec
8.6 mile an hour accident– head acceleration is 15 G

Cranio-Cervical Syndrome (CCS) Symposium – April 6, 2013, Raymond V. Damadian, MD.


Dr Damadian is the inventer of  MRI and has been closely involved with Dr Rosa’s work.

Key points:
craniocervical syndromes- and the possibility that they will turn into neurodegenerative diseases 5:12

resolution of low back pain with severe arthritic changes post upper cervical treatment

9:45 CSF cine pictures of CSF flow vs obstruction

Myles Koby, MD: Imaging Cervical and Cranio-Cervical Instability in Connective Tissue Disorders


See imaging at 2:32 ff
5:31 odontoid process of C2  pushing on brainstem- screenshot 6:40 slide of skull on neck
8:36 3D CT of neck C1-2 instability

9:13 MRI disc prolapse Cx spine- problem is not just the movement but stretching and pulling of the spinal cord/brainstem.
Forward and back sliding implies ligamentous failure and excess stretching of the spinal cord (NOT desirable).

Craniocervical Instability (Dr Henderson the 2012 EDNF Conference)
(Fraser C Henderson MD Neurosurgeon Chevy Chase Maryland)


2:00 flexion stretches the glossopharyngeal nerve, and the back of the brainstem (dissection) Stretching underlies symptoms
2:42 deformative stress brain stem- on flexion- total bending should be worst on the dorsal side

3:34 out of plane loading (intrusive pressure) on the spinal cord and brainstem leads to local histopathological changes AND increased tensile stretch

4:29 Histological evidence/ electron microscopy

6:20 epigenetic effects leading to preprogrammed apoptosis (upregulation of NMDA receptors leading to increased reactive oxygen species, mitochondrial dysfunction and

7:00 snoring and sleep apnoea- remove ventral brainstem compression and sleep apnoea goes away Respiratory abnormalities due to craniovertebral junction compression in rheumatoid disease 1994

7:36 Deformative stresses occur in Chiari
Cranio- cervical instability atlanto-axial subluxation

Cervical hyper -angulation

Tarlov cyst
Tethered cord syndrome

11:44 Basilar impression due to softening of bone. (causes)
11:50 Cranio- cervical instability (loss of ability under physiological loads to maintain the relationship of the vertebra and occiput in such a way that there is no irritation of the spinal cord, nerve roots and there is no development of incapacity, deformity or pain due to structural changes.

Cranio-Cervical Syndrome (CCS) Symposium – April 6, 2013, Francis W. Smith, MD.


Cranio-Cervical Syndrome (CCS) Symposium – April 6, 2013, Joel Franck, MD.


Some direct evidence of restoration of CSF flow following upper cervical treatment:



What is pleasing about the above is that we have clear cooperation occurring between chiropractors, neurosurgeons and radiologists, (including Dr Demadian, the inventer of MRI) clarifying an area that has been the source of much doubt for many decades.

The following link comes from the FONAR (upright MRI) site and is well worthwhile reviewing for the cluster of symptoms being discussed. Those symptoms resemble closely a cluster of symptoms being called cervicomedullary syndrome by some neurosurgeons.

Cranio-Cervical Syndrome (CCS) Symptomatology and Its Origin in Prior Trauma to the Neck


This one is a very detailed discussion with a long symptom list. It largely mirrors other material here- but is worth reading.

Another talk by a radiologist:
Cranio-Cervical Syndrome (CCS) Symposium – April 6, 2013, Francis W. Smith, MD.



This one is pretty technical and probably only of interest to those with a professional interest.

6:10 venous drainage upright and horizontal
6:45 advances in anatomy
8:00 anatomy MRI can demonstrate even small ligaments (such as the alar ligaments that hold C1 in place on C2

13:20 – normal Cx MRI sagittal

14:20 posterior longitudinal ligament injury

15:50 Sagittal MRI clinically unstable Cx spine – acute- inc haemorrhage

17:40 atlanto occipital dislocation

18:30 tectorial and posterior atlanto- occipital membranes

20:30 Cervico myodural bridge- also vis on MRI

24:30 Cerebellar tonsils – nb fluidity of these tissues- as opposed to cadavers

26:19 50 yo female neck pain yrs C5-6 disc bulge, transient loss muscle tone in legs transient paresthesiae, drop attacks upright MRI = Chiari I- position dependent

Chiari II is congenital- medulla also displaced


A further issue of significance is that injuries of the upper neck often cause atrophy of one particular neck muscle (rectus capitis posterior minor).
This muscle runs from the spinous process of C2 (the second cervical vertebra) up to the base of the skull, but one small slip of it actually tethers to the dura (the membranes around the spinal cord) and appears to act to pull that soft tissue out of the way when extending the neck. Without its action the risk is that these membranes will bunch up and compromise the vertebral artery as it enters the skull. This can be a cause of a cluster of symptoms called cervicomedullary syndrome.

This posterior view of the skull and back of neck shows the position of the relevant muscles:

Rectus capitis posterior minor.jpg

 This question is well covered at this link, which actually shows cine MRI of the upper neck showing the dural membranes around the upper spinal cord kinking upon extension of the neck:


Further detail is also available here:

https://www.ncbi.nlm.nih.gov/pubmed/27116115   ( Spine 2017 Jan 1;42(1):49-54.)

A Systematic Review of the Soft-Tissue Connections Between Neck Muscles and Dura Mater: The Myodural Bridge.

Finally, on the question of cerebellar cognitive affective syndrome ( a cluster of symptoms associated with cerebellar dysfunction) this talk with its 2 2 case histories of severe psych disorder being resolved through surgery is of great interest.

“Cerebellar Cognitive Affective Syndrome: Anatomy & Implications” – Jeremy D. Schmahmann, MD




2:10 The doctors don’t listen because there is no fertile ground (the symptoms don’t fit their recognised pattern sets and they don’t know what to do with the symptom complex presented)

This is very true, but I don’t think I have ever hears anyone, express the problem so succinctly. That was very well put.

5:54 First case- symptoms include mania

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Upper Cervical Malalignment and the Brain (gross anatomical effects).

It has long been held that malalignments in the upper cervical spine compromise blood and cerebrospinal fluid (CSF) flow to the brain and also cause mechanical traction and localised blood flow compromise to the brain stem, which can lead to both dysfunction and long term neuronal damage.

This concept has been vigorously resisted by many, but more recent evidence gained from use of upright MRI by a number of practitioners is convincing. I will attempt to withhold the evidence until the end

The major findings are

1) In a malalignment CSF flow to and from the spinal cord is obstructed is obstructed, and that abnormal pressure jets of CSF directly impact the brain in areas like the Substantia Nigra, a key site of degeneration in Parkinson’s Disease. The jets have been shown to be forceful enough to damage brain tissue.

2) There is now documented evidence of jugular venous obstruction by the anteriorly rotated atlas transverse process, and of an overall holdup in venous drainage from the skull.
Both of these will contribute to impaired removal of toxins and metabolic by products from the brain. That cannot be good for brain health, and it may explain some of the immediate improvements in conscious state that people feel following an atlas correction.

3) There is also evidence that the vertebral arteries can become relatively compressed as a result of these obstructions, and that this can have a direct effect on brainstem function
Which is likely to cause a host of effects on autonomic function (see symptom list for atlas subluxation) and also on mood and other symptoms like anxiety.

4) The existence of a myodural bridge between the skull and C1 has been demonstrated.
The rectus capitis posteriori minor muscle is actually meant to help pull the dura out of the way when the neck extends, so that it does not kink and compromise vertebral artery flow.  However this muscle is highly prone to atrophy after injury to the upper neck.
(For images of a dysfunctional myodural bridge)

This data is extremely significant in understanding the role of craniosacral therapy.

There is evidence to support the role of both traction on the brainstem via dentate ligaments, and undue compression on  the brainstem due to an inadequate clivoaxial angle. At this stage I am not sure just how far outside the world of Ehler’s Danlos and Chiari malformations this latter finding remains relevant.


The Craniocervical Junction: Observations regarding the Relationship between Misalignment, Obstruction of Cerebrospinal Fluid Flow, Cerebellar Tonsillar Ectopia, and Image-Guided Correction

Rosa S.a · Baird J.W.b Smith FW, Dworkin JS (eds): The Craniocervical Syndrome and MRI. Basel, Karger, 2015, pp 48-66


Misalignments of C₀-C1, C1-C2 brought on by head or neck trauma can manifest in different outcomes. Some of those outcomes can affect or cause neural compromise, and/or some may contribute to cerebrospinal fluid (CSF) flow obstruction as well as arteriovenous compromise. C1 misalignment may also contribute to distention of the cerebellar tonsils (cerebellar tonsillar ectopia), i.e. down through the foramen magnum due to caudal tension by way of dentate ligament pathological stress on the spinal cord leading to obstruction of the normal flow of CSF.

Mechanical compression of the jugular vein by the transverse process of C1 has been found to lead to obstruction of outgoing venous blood flow. Such obstruction has been found in chronic cerebral spinal venous insufficiency which has been observed in neurodegenerative brain diseases such as multiple sclerosis.

Image-Guided Atlas TreatmentTM (IGATTM) has been shown to be a method of gentle correction of misalignment of C₀-C1, C1-C2, resulting in improved CSF flow as well as venous outflow. Image-guided atlas treatment utilizes advanced dynamic upright MRI as the means of evaluating misalignments at the craniocervical junction, and the images obtained are used to calculate the appropriate alignment vectors to correct the misalignment. Post-correction advanced upright MRI images are then used to validate the appropriate realignment of C₀-C1, C1-C2 to establish improvement in proper CSF as well as arteriovenous flow”


The authors (neurosurgeons) conclude that it is reasonably established from the literature (both neurobiological evidence and mathematical modelling) that mechanical deformation of the brainstem may cause neurological deficit and that decreased clivoaxial angle is one mechanism vulnerable to surgical intervention.

Also of significance is the number of alternative descriptions of the altas subluxation problem- notably cranio-cervical syndrome, and cervico medullary syndrome.







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Uniting Atlas Subluxation and ADHD

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 to

) Distorted and variable afferent proprioceptive input into the vestibulocerebellar system, leading to clumsiness and dysregulation of ocular coordination, and also impairing autonomic regulation of blood pressure and flow.

2) Compromise to the brainstem via traction and compression and compromise to the vertebrobasilar circulation, both secondary to high cervical malalignments. Symptoms are probably driven by hypoxia to the parts of the brainstem responsible for regulating blood flow to the rest of the body. The downstream consequences here likely to cause ADHD symptomatoogy are orthostatic intolerance and episodic cerebral hypoxia (inattention) and sympathetic overarousal– (hyperactivity and impulsivity).

3) Compromise to middle cerebral artery blood flow associated with, and plausibly 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.



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Neck Pain and Cerebral Perfusion

I recently became aware of the following paper – which casts some light on issues like brain fog in people with neck conditions, and also further light as to why these conditions persist.

I emphasise though that the observations here relating to this paper are probably only one mechanism causing difficulty with impaired cerebral blood flow.
I have gone into some detail here as the findings are strongly supporting some of the key tenets of chiropractic. There has been a good deal of skepticism about this from anti chiropractic lobby groups who like to pretend they are the gatekeepers of “evidence based medicine” so I am sacrificing brevity for detail.


Cerebral perfusion in patients with chronic neck and upper back pain: preliminary observations

Maxim A Bakhtadze, Howard Vernon, Anatoliy V Karalkin, Sergey P Pasha, Igor O Tomashevskiy, David Soave

Journal of Manipulative and Physiological Therapeutics 2012, 35 (2): 76-85

The study examined 45 patients with varying degrees of neck and back pain, looking at the following parameters:
1) Neck Disability Index (a self rated score of the limitation in daily life caused by the neck pain)
2) Number of “blocked segments” in the cervical spine, the thoracic spine and upper thoracic costovertebral joints, as assessed by one examiner
3) The pain score (measuring tenderness as experienced during physical examination)
4) Cerebral perfusion as measured on SPECT scan.

The following correlations were found
1) A highly significant negative correlation between the Neck Disability Index and Cerebral Perfusion- ie the more strongly positive the NDI was the the more the cerebral perfusion was impaired.

2) A slightly less significant (but still highly significant) negative correlation was found between the examiner’s findings and the cerebral perfusion.

3) The association between pain scores on the VAS  (when the back was examined)and cerebral perfusion is was significant.

4) In patients with higher NDI, the cerebral perfusion deficit occurred in frontal and parietal regions- in Middle Cerebral Artery (which receives its sympathetic innervation from the Superior Cervical Ganglion).

The paper reviewed the various theories around the interaction between pain and the ANS:


1)- central sensitisation- altered somatoautonomic reflexes

  1. sympathetic activation from spinal pain acting to stimulate the cervical ganglia, thus producing the perfusion defect.
  2. Role and response of sympathetic ganglia to somatic afferent nociceptive stimulation

93. McLachlan EM, Davies PJ, Häbler H-J, Jamieson J. On- going and reflex synaptic events in rat superior ganglion cells. J Physiol 1997;501:165-82.

Littman and Purves patterns of end-organ sympathetic reaction in the territory supplied by the superior cervical sympathetic ganglion in response to stimulation of the thoracic ventral roots (predominantly Th1-Th5). One of their findings was constriction of the arterioles of the eye and ear.

94. Lichtman JW, Purves D, Yip JW. On the purpose of selective innervation of guinea-pig superior ganglion cells. J Physiol 1979;292:69-84.

In 1980, the same investigators studied the territory of the stellate ganglion (SG), which also receives afferents from the Th1 to Th5 spinal segments.

95. Lichtman JW, Purves D, Yip JW. On the innervation of sympathetic neurons in the guinea-pig thoracic chain. J Physiol 1980;298:285-99.

Leading to point 4) That irritation of the spinal segments Th1-Th5 can produce a reflex response through the cervical sympathetic ganglia– that response including MCA constriction.

References 96-104 cover experimental proof of the role of the superior sympathetic ganglion in cerebrovascular regulation.


We report here, for the first time, a correlation in patients with chronic neck pain between scores of self-rated disability (NDI), painful spinal joint dysfunction, and brain hypoperfusion.



One noteworthy aspect of this paper is that it is nociceptive signals that activate the response to pain. Nociceptive signals can be generated below the threshold of conscious awareness of pain. Therefore it might be possible (I think very likely but don’t have enough material to prove that statement yet) that this mecahanism may operate without conscious awareness of pain, and impairing cerebral perfusion even in less severely affected patients.

The most pain sensitive structures in the spine (excluding rupture of a disc with leakage of nucleus pulposus producing an inflammatory reaction) are the facet joints, and the dura.

In any case of chronic severe neck pain, the local muscle spasm will drive tender facets together and increase pain- thus creating another feedback loop.

Also of note is another mechanism that might be driving neck dysfunction- namely orthostatic intolerance (Poor adaptation of blood flow distribution to the upright posture).. This mechanism is found in a wide range of conditions. It is a significant issue in ADHD, for instance. It can result in multiple episodes of decreased cerebral perfusion with loss of muscle tone and slumping into a posture that can drive back pain and displace vertebrae.

There appear to be a number of drivers of this dynamic and I am working on a summary of them.


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Why am I not getting better despite repeated adjustments, and why do my vertebrae keep “slipping out”?

This is a common question raised in the comments section of the blog.

Of course it is unsafe to give out individualised health advice to anyone over a blog, so the best way for me to handle this question is as a generalised post. Im notentirely happy with this post- it wanders a little too much for my liking, but this is a complex question.

I’ve been wondering myself– it has taken me 9 years to get to the point where I am now, and much of the improvement has really only consolidated in the last 2 months.

Firstly an acute injury is very different to one that has been carried since childhood.

I would guess that most acute injuries would settle back easily once corrected.


However most of us have carried the injury for a long while and there are issues with mild scoliosis, often localised arthritis and muscle spasm, and multilevel subluxations, often with flat feet and pelvic tilt. Any longstanding atlas issue will usually be accompanied by issues at the sacro-iliac joints, the feet , the thoracic spine, and often the jaw joint. The question then becomes one of how many need individual attention? Ive needed work on all but the jaw joint.

The posture chronically adopted will open some facet joints more and predispose them to go out of alignment.

Specific work to loosen up individual muscles is very helpful- and learning to self apply trigger point therapy or acupressure will save a lot of money.

I have used the Trigger Point Therapy Workbook- which is comprehensive and available as a cheap Kindle App and also an anatomy app called 3D 4 medical Muscle System Pro.

I have found that particularly valuable as it helpfully peels away the muscle layers and makes it very clear which level the problem is likely to be at.


One other comment I would make is that many of us, myself included, talk of the vertebrae “slipping out of place again”. To some extent I guess that is true— given the instability in my spine over the past 55 years there has to be some wear and tear predisposing to things slipping out of place. As a rule though I am led to understand that only usually happens when there is either loss of intervertebral disc space, or posture has become so poor that the facet joints are nearly fully open at the best of times. (That is more of an issue in the neck- where the facet joints open wider).

So in most cases the vertebrae are pulled out of place not slipping> The pull can come from tense muscles guarding other areas:A problem in one part of the spine can cause trouble elsewhere– ie for myself- pain in the right mid thoracic will cause tension in the cervicocostalis muscle, and THAT will cause reactivation of some of the subluxations in my neck ( the muscle attaches to the rear of the transverse processes of C3/4/5 and the net pull caused bowstringing of the cervical spine and a tendency to anterior subluxations at C6/7 and C7/T1).

Sometimes the pull can come from impaired orientation reflexes:  The functional neurology work I have done has demonstrated issues such as a tendency to rotate to the left- because my acoustic attention reflexes are neglected on the right. We have corrected that and it is no longer a problem.

Equally I developed a chronic pain syndrome that turned out to be purely a feedback loop within the medial pain pathways in the brain. Until that was identified it caused enormous trouble with chronic muscle spasm making everything worse, but it resolved within a couple of weeks of functional neurology treatment once it was identified 2 months ago.

These are also abnormal brain reflexes related to balance, coordination, orientation reflexes, abnormal brain reflexes related to the autonomic nervous system, often leading to low brain blood flow when upright, or to unpredictable emotional responses.

The autonomic reflexes have been a particularly tricky one to nail- and they apply as much to atlas problems as to ADHD. They cause a difficulty in regulating cerebral blood flow when transitioning from flat to upright. . This often translates to having a lower cerebral blood pressure when sitting and being on the edge of a fight or flight response (orthostatic intolerance). However,the wrong stimulus (ie getting too hot and sweaty on a humid day for instance, can trigger a collapse- where blood pressure drops and in my case, I feel a little sweaty and vague. I usually feel back pain with this-and “coathanger pain in the upper neck or back” is well known as a symptom of orthostatic intolerance.

I had had some inkling that this was going on, but the last time it happened to me (the day before I wrote this post) I happened to be starting with a back that was painfree and in good position.

This time, however, the outcome was obvious, as I had had my back nicely lined up and no pain- then the collapse re-activated all the currently troublesome subluxations and it took me 30 minutes to disentangle them.

So I do not think the vertebrae just randomly drop out of place- there has to be a trigger of some sort- and the action is driven by the muscles- which either pull the spine in the wrong direction, or fail to maintain core tone.

Other triggers that I can think of include being unfit, sitting too much in poor posture, emotional traumas and intestinal dysbiosis. (the latter is common as atlas problems interfere with normal gut contractions).

However, recovery from a significant subluxation problem takes time, patience and careful observation. My clinical training did not prepare me to do what was needed to get on top of my problems, and I have had to educate myself- relying on resources such as the ones I posted and repeatedly asking questions.

I have found functional neurology treatments extremely helpful- and also understanding the complex nature of the feedback loops which maintain the problem.

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