This month I would like to present a case of “abdominal migraine” in a young woman. I enclose “abdominal migraine” within quotation marks because it, like “migraine” is a syndrome, – a shorthand description of a clinical picture, but indicating nothing about its cause or treatment. Syndromes, especially of pain, should always alert the physician to the possibility of an interference field.
Abdominal migraine is rare in adults, and affects perhaps 1 to 4% of children. The picture is episodic mid-abdominal pain, sometimes associated with nausea and vomiting. As with cephalic migraine, these symptoms may by associated with tiredness, anorexia and sometimes headache. The attack may last from hours up to three days. Diagnosis is made by exclusion of organic pathology. Usually a family history of migraine can be found.
My patient was an 18 year-old young woman who presented with a 10-year history of episodic epigastric pain. The attacks were becoming more frequent (every 4 to 6 months), more intense (requiring emergency room visits) and were lasting up to 5 days. They were preceded by a feeling of weakness and hunger. There was no nausea or vomiting or disturbance of bowel function. Eating had no effect on the pain; nor did taking a deep breath.
Multiple investigations including gastroscopy revealed no pathology. A trial of lansoprazole for four months had no effect.
In addition, the patient’s energy level had declined over the last two years. She was sleeping 8 hours a night during the week and 12 hours a night on the weekends.
Her past medical and surgical history included tympanostomy and ear tubes as a child, recent wisdom teeth extraction, and pneumonia at age 12.
Physical examination revealed a pale young woman with dark circles around her eyes, slight clubbing of her fingernails, mild dental enamel hypoplasia, and no abdominal tenderness, organomegaly or masses. (The clubbing and the dental enamel hypoplasia suggested gluten sensitivity.) Autonomic response testing indicated an interference field in her large intestine. Additional autonomic response testing indicated deficiencies in iron, zinc, vitamin A, D, B-Complex, and magnesium. The interference field was treated with a Tenscam device and normal autonomic regulation was restored.
Because of the fatigue, blood testing was performed which confirmed multiple nutritional deficiencies: (vitamin D=50, vitamin A=1.17, ferritin=42). Stool testing for antigliadin IgA was positive, indicating gluten sensitivity – the most likely underlying cause of the nutritional deficiencies resulting from malabsorption. The patient was advised to start a gluten-free diet.
Four months later the patient (who lives in another country) reported a “radical change in (her) strength and energy levels”. She had had no further attacks of pain or the symptoms that lead to attacks.
There were a number of unusual aspects to this case. The first was the increasing severity and duration of the attacks with age. “Abdominal migraine” typically subsides with maturity, although it often transforms into the more typical cephalic migraine. The second unusual feature was the fatigue that had developed over the preceding two years. And another was the interference field found in the large bowel, a location inconsistent with any current or previous history of problems.
I suspect in this case that the good response was as much due to the elimination of gluten from the diet as due to neural therapy of the large intestine. Although the best- known area of the gut to be affected by gluten sensitivity is the small intestine, gluten sensitivity can affect any part of the GI tract from the mouth to the anus. The most symptomatic manifestation in the large bowel is ulcerative colitis, but microscopic colitis, polyps and cancer may also be present. The fact that this patient had no large bowel symptoms does not mean something was not occurring there.
As Speransky pointed out years before neural therapy was even discovered, any irritation of the nervous system can cause symptoms anywhere in the body. The irritation can range from the electrical instability of a scar to an immune or inflammatory irritation anywhere in the body. The manifestation of the process is not dependent on where the irritation occurs, but rather on pre-existing conditions, e.g. genetics, “tissue memory”, or biochemical milieu.