This month I would like to present an unusual case of post‐concussional syndrome. Last month I wrote about intracranial interference fields; this month I want to demonstrate that extra-cranial structures can contribute to post‐concussional symptoms too.
A 48‐year old carpenter presented with headaches, memory loss, neck pain, insomnia, impulsivity, photophobia, tinnitus and fatigue since a motor vehicle accident 1 ½ years before. In the accident he had sustained a blow to his right cheek, causing loss of memory for a few minutes. The next day he experienced dizziness, fatigue, confusion and an upset stomach.
His past history included a cerebral concussion in his teens with ten minutes loss of memory. A head‐on motor vehicle collision in his twenties resulted in a fractured arm, a "whip‐lash" syndrome and resultant chronic low‐grade neck pain.
Numerous investigations followed with little in the way of abnormal findings except for a "low DHEA". He rated his energy level at 5 on a scale of 10. His symptoms persisted and the diagnosis of "post‐concussional syndrome" was made. He had attempted to return to work (unsuccessfully) as both he and his co‐workers noticed that he was making mistakes.
On examination, neck rotation was restricted toward the right; atlanto‐axial rotation was restricted toward the left and cranio‐sacral motion was restricted throughout the cranium and in the sacrum. "Arcing" (a 60 cycle/minute pulsation emanating from a specific locus, usually indicating trauma) could be felt from the maxilla and extending into the cranial base. This was treated using an osteopathic unwinding technique; cranio-sacral motion was greatly improved and atlanto‐axial motion was restored to normal.
Autonomic response testing produced a "therapy localization sign" (page 51 of my neural therapy book) corresponding to an interference field in tooth 1.6 (#2 in the American system) that had undergone a root canal procedure 5 years before. The tooth was asymptomatic but tested as if a chronic infection were present. Neural therapy using a dental homeopathic was instituted and open regulation resulted.
Six weeks later the patient reported that he "felt better than (he) had in years". And his serum DHEA increased to normal range.
Post-concussional syndrome has attracted considerable attention among researchers in recent years. This is being driven partly by the need for information for advising athletes about when (or whether) they can return to play. The other patient group being studied are soldiers who have sustained concussions from direct head trauma or "blast injuries" (from explosives). Because many of these injuries have occurred in combat, the clinical picture is complicated by the prevalence of concurrent PTSD (post-traumatic stress disorder).
Most of the research has concentrated on measuring psychological and neurological deficits, but blood tests have been discovered that are bearing fruit in research and may soon have application clinically. Plasma biomarkers including S‐110B and SDE have been shown to correlate with brain and spinal cord pathologies including strokes, brain injury during cardiac arrest, vertebral fracture, brain inflammation, etc. They appear to be sensitive enough to be useful in studying and prognosticating relatively minor cerebral concussions as well. This tool has also helped uncover a genetic factor in how the brain copes with trauma. One intriguing paper has shown that the brain does not do well when the APOE4 gene is present. This is the gene that is a major risk factor for Alzheimer's Disease.
As exciting as this research is, I get the feeling that clinicians are well ahead of the scientists in understanding (and treating) post‐concussional syndrome. Cranial osteopathy has been a safe and effective treatment for many years. Neural therapy can also be helpful, through the "crown of thorns" or by treating cranial and/or cervical autonomic ganglion. In short, we know that the autonomic nervous system has a lot to do with post-concussional syndrome.
In the case presented above, part of the irritation of the nervous system was an infected root canal, possibly activated by direct trauma to the jaw. It is difficult to say how much of his symptoms could be attributed to the cranial somatic dysfunction, and how much to the tooth. (I often find that classical interference fields and somatic dysfunction are intertwined ‐ treatment of one correcting the other.)
The "take‐home" is how the brain reacts to trauma is not entirely determined by intra‐cranial pathology. Much of the response is decided by the autonomic nervous system and extra‐cranial factors are important in that process.
Robert F. Kidd, MD, CM