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I found that upon careful questioning of sALS patients and their families, most recalled a cervical injury that they had dismissed or forgotten. Occasionally the patient and family could not remember a specific trauma incident, but the patient still had palpable tenderness over the posterior cervical spine overlying the neuroforaminal stenoses, as seen on their CT scan. Infrequently the patients were diagnosed as having a radiculopathy, yet little or no neuroforaminal stenoses will be seen on the CT image. These patients invariably have (a) palpable tender spot(s) over the perispinal process at the location where the nerve is being compressed. These tender areas are believed to be areas of nerve root avulsion or constriction, for some other reason than the bony neuroforaminal stenosis, as is seen in most other patients.
While this posited correlation of spinal column injury (and often reinjury of the same area) with sALS onset lies at the heart of my hypothesis and is testable, scientists and physicians who work with ALS will naturally ponder how such bone pathology could trigger this insidious disease process.
What I suspect is that spinal column injury and reinjury creates a "breach" in the blood–spinal fluid barrier that becomes inflamed and admits neurotoxic misfolded proteins, pro-inflammatory cytokines, activated monocytes, and so on, into the central nervous system. It is anticipated that this process is responsible for the CSF aggregates linked to motor neuron destruction, and that this process may stimulate execution of necroptosis in astrocytes, which is selectively destructive to motor neurons.
Interestingly, the descriptions of the neurovascular components of ALS described by Garbuzova-Davis and Sanberg in 2014 are in my opinion consistent with the spinal motor nerves being recently reinjured and developing a blood-CSF barrier breach or breaches.15
One way in which blood–CSF barrier breaches might be readily (and noninvasively) revealed is by having Fonar Upright MRI scans done of sALS patients. This sophisticated scanner was used in one seminal study which linked craniocervical trauma and resulting pathology in multiple sclerosis patients to dynamically visualized abnormalities in CSF hydrodynamics, which is hypothesized by the authors of the study as to play an "important etiologic role in the genesis of Multiple Sclerosis."16
If the correlation of spinal column osseous pathology caused by injury (and reinjury) to the onset of sALS is upheld in subsequent research, it follows that earlier diagnosis and treatment of the disease swifter and more certain. Accordingly, it is my sincere hope that researchers and clinicians reading this article will question their patients with respect to a history of both remote and recent neck injuries, then study their patients' cervical spine CT images and palpate to identify areas of inflammation (especially those that point to the presence of a blood-CSF barrier breach). In those patients presenting with evidence of injury or recent reinjury, I would urge these professionals to examine them for neuroforaminal stenoses and spinal motor axonal constriction, then to tabulate, analyze, and publish findings that substantiate the hypothesis I have posited herein, bring it into question, or overturn it entirely.
Disclosure of Interests
Other than seeing and treating sALS patients as a licensed physician, I have no other conflicting interests.
Thanks to Donna Hanna, ND, for input on data analyses and graphing, and to Anthony G. Payne, NMD, PhD, and Ryan Wallace for writing, formatting and editorial input.
Dr. David A. Steenblock earned his BS degree from Iowa State University, then an MS in biochemistry and doctor of osteopathy (DO) degree from the College of Osteopathic Medicine and Surgery in Des Moines, Iowa. His postdoctoral training included three years at Case Western Reserve University, one year at the Oregon Health & Sciences University, and a clinical rotating internship at Providence Hospital in Seattle, Washington.
During the late 1970s he founded the first integrative medicine clinic west of the Mississippi River. In the years since, he has done pioneering clinical work including the use of hyperbaric oxygen therapy to treat stroke (starting in 1989), live cell therapy 1991–2001 (Mexico), umbilical cord stem cell therapy (Mexico from 2001) and, since 2005, stem cell rich bone marrow aspirate concentrate (BMAC) therapy for a variety of conditions.
In October 2015 he was awarded the Academy of Comprehensive Integrative Medicine's (ACIM) "Lifetime Achievement Award" at its NeuroRegeneration Conference (Orlando, Florida) in recognition of his many years of contributions "to the betterment of mankind and the advancement of integrative medicine."
In 1978 Dr. Steenblock saw his first ALS patient, who had severe degenerative spine disease but did not have cord compression and was told by specialists that the osteoarthritis and perispinal calcification had nothing to do with the disease process. This observation led to a lifetime of observing ALS patients in regard to their having chronic degenerative joint disease and trying to determine how this relates to the underlying disease processes. Dr. Steenblock's clinic is devoted to understanding and treating this disorder with a state-of-the-art approach. To this end he has a microbiology lab to study the patient's biofilms and how to treat this effectively and also a state-of-the-art molecular biology lab with a variety of instruments including a flow cytometer, FT-IR spectrophotometer, and HPLC. Currently there are three PhD molecular biologists working with Dr. Steenblock, who is in charge of the research.
Dr. Steenblock's e-mail address is Drsteenblock@yahoo.com. His clinic phone number is 800-300-1063 and his websites include www.strokedoctor.com, www.stemcellmd.org, and www.stemcelltherapies.org.
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