The authors of this study claim that, in the aging brain, reduction in the pulsation of cerebral vasculature and fluid circulation causes impairment in the fluid exchange between different compartments and lays a foundation for the neuroinflammation that results in Alzheimer disease (AD). The knowledge that lymphatic vessels in the central nervous system play a role in the clearance of brain-derived metabolic waste products opens an unprecedented capability to increase the clearance of macromolecules such as amyloid β proteins. However, currently, there is no pharmacologic mechanism available to increase fluid circulation in the aging brain.
Based on these considerations, the authors conducted a study to demonstrate the influence of an osteopathic cranial manipulative medicine (OCMM) technique, specifically, compression of the fourth ventricle, on spatial memory and changes in substrates associated with mechanisms of metabolic waste clearance in the central nervous system using the naturally aged rat model of AD.
The rats in the OCMM group received the CV4 technique every day for 7 days for 4 to 7 minutes at each session. Rats were anesthetized with 1.5% to 3% isoflurane throughout the procedure. Rats in the UT group were also anesthetized to nullify any influence of isoflurane in spatial learning. During the CV4 procedure, the operator applied mechanical pressure over the rat’s occiput, medial to the junction of the occiput and temporal bone and inferior to the lambdoid suture to place tension on the dural membrane around the fourth ventricle. This gentle pressure was applied to resist cranial flexion with the aim of improving symmetry in the cranial rhythmic impulse (CRI), initiating a rhythmic fluctuation of the CSF, and improving mobility of the cranial bones and dural membranes. This rhythmic fluctuation is thought to be primarily due to flexion and extension that takes place at the synchondrosis between the sphenoid and basiocciput. The treatment end point was achieved when the operator identified that the tissues relaxed, a still point was reached, and improved symmetry or fullness of the CRI was felt. Currently, there is no quantitative measure for the pressure used in this treatment.
The results showed a significant improvement in spatial memory in 6 rats after 7 days of OCMM sessions. Live animal positron emission tomographic imaging and immunoassays revealed that OCMM reduced amyloid β levels, activated astrocytes, and improved neurotransmission in the aged rat brains.
The authors concluded that these findings demonstrate the molecular mechanism of OCMM in aged rats. This study and further investigations will help physicians promote OCMM as an evidence-based adjunctive treatment for patients with AD.
If there ever was an adventurous, over-optimistic extrapolation, this must be it!
Even assuming that all of the findings can be confirmed and replicated, they would be a very far shot from rendering OCMM an evidence-based treatment for AD:
- Rats are not humans.
- Aged rats do not have AD.
- OCMM is not a plausible treatment.
- An animal study is not a clinical trial.
I am at a complete loss to see how the findings of this bizarre animal experiment might help physicians promote OCMM as an evidence-based adjunctive treatment for patients with AD.
Rats are not human and are not a reliable comparison compared to humans who have been tested for increased blood supply to their brains when their cervical spine sagittal lordosis has been temporarily restored. Seven patients tested had notable improvement to their brain blood supply when their cervical lordosis was induced using a structural rehabilitation traction device developed by an Australian chiropractor, the owner of Dennerwald Industries. The discussion section mentions the possible relationship to poor supply and dementia. A conversation that should be robustly debated.https://www.braincirculation.org/article.asp?issn=2394-8108%3Byear%3D2019%3Bvolume%3D5%3Bissue%3D1%3Bspage%3D19%3Bepage%3D26%3Baulast%3DKatz
are you serious?
retrospective consecutive case series of patients in a private practice
“A conversation that should be robustly debated”
or are you still in April fools mood?
Yes, I’m very serious!
The MRA’s were not performed in a chiropractic private practice and as you know very well that imaging has the highest level of strength of diagnostic evidence compared to any other clinical evaluation. In addition, the journal Brain Circulation is not some low-level journal to be published in.
I was afraid so.
As an oncologist with 30 years’ experience practising in the NHS it has not been my experience that that is true at all.
Dr Joe Gleeson, the Dean of my alter mater Westminster Medical School, himself a radiologist, was very fond of saying (in his gentle Irish brogue):
“You see what you look for. You look for what you know. And you know f**k-all.”
Nothing I have seen or learnt subsequently has given me any reason to disagree with him.
a clever man, your dean!
From my understanding, Professor Nikolai Bogduk would disagree that diagnostic imaging is weak in its strength of evidence compared to other tests like laboratory evidence, innervation tests or pathology tests. The MRA research I commented on regarding change in blood supply when cervical lordosis is induced is notable as this method of investigation is novel.
@ MICHAEL EPSTEIN
You would appear to have a remarkable lack of insight as to the limitations of any diagnostic imaging however “novel” it may be – or perhaps even “because it IS novel.
In addition there is always a distinction to be made between between precision and accuracy and then to determine the actual “significance” of what it is that you think you are measuring.
In addition the authors seem to think that having consecutive patients is a substitute for matched randomized controlled subjects – it is not.
And you can perform all the statistical wizardry you want on a sample of 7 subjects – but the results will always be pretty meaningless and it will remain a case series and nothing more.
I am curious as to why you are so determined to defend this particular mode of imaging as being so “perfect” and beyond criticism when we know that nothing else is? Counting pixels or seeing pixels where formerly there were none sounds like a prime candidate for suspicion and just as fallible as any other method of investigation.
“Pixel intensity analyses were done by the same PhD researcher” – perhaps, but are you seriously asserting that this is a foolproof method? Not prone to human error at all? They are assessing “pixel intensity” – which sounds very much like a quality assessment exceptionally prone to variability to me. Yet you remain certain that this is absolutely impervious to error!
As JM-K’s story tells us, diagnostic imaging is only as good as the brain that interprets the images. A fool with a tool is still a fool.
Applying statistical tools to a tiny collection of highly dubious measurements (neither standardised nor validated?) on cerebral angiograms and cervical radiograms of only seven subjects should be criminal. The data look random in the flyspeck diagram. Applying Student’s t-test and presenting a regression analysis to this minute data set, ought to draw a stroke of a cat o’ nine tails for every sentence in the statistics section.
The word “further” is kind of important.
thin gruel indeed. a lot more evidence than what they have is required before this is remotely convincing.