Migraine would seem to be a happy hunting ground for neural therapists. After all, among its most distinctive features are the autonomic nervous system disturbances that to go with it. With some categories of migraine, they are the only symptoms.
Migraine comes in many forms. The International Classification of Headache Disorders list 29 subcategories, including many that do not included headache at all. The most common variants are migraine without aura (common migraine) and migraine with aura.Both of these groups have many subcategories.
Migraines are classified entirely by symptoms. Moreover, a defining characteristic of migraine is that there are no symptoms between attacks. Most of the time the symptoms indicate the parts of the brain that are affected, e.g. familial and sporadic hemiplegic migraine, retinal migraine, cluster headache, vestibular migraine etc.
An interesting kind of migraine is abdominal migraine diagnosed mostly in children. Physicians easily miss it, and the onset of attacks can be similar to the onset of acute appendicitis – loss of appetite, central abdominal pain, vomiting, etc. The key to diagnosis is its cyclical pattern with complete normalcy between attacks.
I was referred a case recently to my office, by an astute family physician who made the diagnosis after others had not. Here is the story:
A 12 year- old boy was brought by his mother for consultation because of recurring attacks of abdominal pain – several times a day for the previous three weeks. Each episode lasted a few minutes. There was no radiation of pain or nausea or vomiting, but the pain was severe enough that he had been taken by ambulance to the Emergency Department. Later his family physician diagnosed “abdominal migraine” and prescribed propranolol. This had the effect of the pain moving superiorly to the chest and neck.
He had a “sensitive stomach” since infancy and three years previously had a similar series of attacks, with no diagnosis being made. Four or five bowel movements a day were normal for him.
On examination he was a healthy-looking, although overweight boy in no distress. (He had almost doubled his weight – to 165 pounds – in the previous three years.) His hamstring muscles were tight, suggesting magnesium deficiency and his fingernails displayed leukonychia, indicating zinc deficiency. These findings combined with chronic gastrointestinal sensitivity and a large unexplained weight-gain made a diagnosis of gluten sensitivity highly likely.
Autonomic response testing revealed an interference field in the coeliac plexus. This was treated with a Tenscam device. (A classic neural therapy injection of procaine ½% would have been equally effective. This easy and safe injection is described in my book on page 187.)
Two days later he had a bad headache, and on day 3 a mild attack of abdominal pain. He required no further treatment and had no more attacks in the following five months.He was prescribed a gluten-free diet to prevent recurrence.
In many ways the pathogenesis of migraine continues to be a mystery. Autonomic, sensory, cognitive, emotional and motor function can be affected and many parts of the brain may be involved. Autonomic nervous system function has attracted the most research interest, but few clear-cut answers have emerged An imbalance between sympathetic and parasympathetic tone is frequently observed. All four phases of migraine (premonitory, aura, headache and postdrome) appear to be affected and some studies show autonomic dysfunction even between attacks.
For the most part autonomic dysfunction is assumed on clinical grounds with the presence of nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion, and/or ptosis. Cranial parasympathetic symptoms are common, but overall sympathetic impairment is dominant and can be detected even during the interictal period.
We know there are many potential triggers of migraine, including certain foods, weather changes, stress levels, hormonal fluctuations, sensory overstimulation, over-exercise, head trauma etc. The potential for migraine is inherited in an autosomal dominant manner.
So where does neural therapy come in? Migraine is a syndrome, and syndromes can be triggered by what Speransky would call a “second blow”, i.e. an irritation of the nervous system anywhere in the body that re-awakens an existing “tissue memory”. Experienced neural therapists look for scars, dental problems and other nervous system irritations that may have initiated or maintained a propensity for migraine headaches. Osteopaths look for somatic dysfunction anywhere in the body. In my experience somatic dysfunction is probably a more common irritation than scars or troublesome teeth, especially somatic dysfunction of the cranium.
In my young patient’s case, the irritant was the coeliac plexus. Interference fields in the celiac plexus usually develop from chronic or intense irritation of both the upper and lower gut – “both” being the operative word. In his case it was probably a relatively silent reaction to dietary gluten – an allergen that can affect any part or all of the gut.
Letter to the editor:
Dear Dr Kidd:
With regard to objective methods to find/document ‘interference fields’, do you know if anyone has investigated thermography? Despite the shortcomings of thermographic analysis, thermography shows physiologic alterations, especially those of microcirculation. It would be fascinating to have a thermographic image of a interference field producing scar before and after neural therapy (it could potentially also document effectiveness of TENSCAM as well). I have a simple thermographic camera, and will do some basic studies, and will let you know if I find anything worth pursuing.
Theodore Jordan, DO