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
- sympathetic activation from spinal pain acting to stimulate the cervical ganglia, thus producing the perfusion defect.
- 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.