Is Bipolar driven by a brainstem mechanism?

 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: 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.

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Towards a mechanism for some ADHD symptoms relating especially to alertness.

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.

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Breakthrough, at last.

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.

It worked.
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.

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.

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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:   ( 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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