Perhaps I am not alone in finding myself forced to come to grips with that all-too-common condition known as "irritable bowel syndrome" i.e. abdominal pain and bowel dysfunction of unknown cause. Gastroenterology has never been my favourite subject and for many years my central focus in medicine was the musculoskeletal system. This led me to study orthopaedic medicine, osteopathy, neural therapy, and other methods of direct treatment. However the deeper I dug, the more I found myself confronting gastrointestinal dysfunction and related nutritional, immune and endocrine deficiencies. Patients just didn't seem to get better without healing the gut.
So what does this have to do with neural therapy? Readers of this newsletter and my book will know the emphasis I put on optimizing general health in order to achieve success in neural therapy. But the other side of the coin is: the role of neural therapy in correcting gastrointestinal dysfunction.
Before writing case histories I usually turn to PubMed for a literature review. Using "irritable‐bowel‐syndrome" as search words, I came up with 11,104 items, over 200 published (so far) in 2016 alone ‐ a formidable task to review! The majority of these papers had to do with gut micro biota, use of probiotics, visceral hypersensitivity, immune function, non‐celiac gluten sensitivity, etc. ‐ little on the role of the nervous system. However a subset of these papers explored psychological and neurological factors (including the brain) in IBS. A truly excellent (and readable) review entitled Irritable bowel syndrome: Is it "irritable brain" or "irritable bowel"? discusses this interplay. And in a thoughtful recent editorial in the Journal of Neurogastroenteroligical Motility, the whole concept of "functional disorder" in relation to IBS is pondered.
In the research literature, lip service is sometimes given to the role of the autonomic nervous system, but usually in the context of cortical (prefrontal and cingulate gyrus) signals transmitted through the descending tracts. Without downplaying these central influences, almost nothing is said about reflex modulation of visceral function through local somato‐visceral and viscero‐visceral reflexes. And needless to say, the idea that a scar or tooth could affect autonomic nervous system function is nowhere to be found. As neural therapists, these are the phenomena that we are interested in.
One exception I stumbled across was an interesting paper from the urological literature that opened my eyes to research on "cross‐talk" between pelvic and other viscera, e.g. higher incidence of bladder irritability in patients with IBS. It even showed changes in bladder function with dilation of the oesophagus.
Neural therapists should not be surprised by this and should perhaps be reminded in cases of IBS to search for interference fields in other organs, not just scars, teeth and the lower gastrointestinal tract. Speransky's experiments in the 1930s explored the autonomic innervation of the whole gastrointestinal tract and helped explain why (for example) an interference field in the anus could possibly cause gastric reflux.
Now about my case report:
A 20‐year old male heavy equipment operator presented with six years of irritable bowel syndrome beginning with surgery for a ruptured appendix. In addition to bowel complaints he also had stomach bloating and gas, increased urinary frequency and incomplete emptying of his bladder. He also had become tired, lacked stamina and rated his energy level at 5/10.
His general examination was unremarkable except for dark circles around his eyes and tight hamstring muscles. Autonomic response testing provoked no response in the abdominal scars, the ileo‐coecal region or other abdominal viscera. However an interference field was detected in the coeliac plexus and was treated energetically using a Tenscam device. (The classical neural therapy injection of procaine is an easy and safe alternative; ‐ see page 187 of my book).
Six weeks later he reported more energy and improved bowel movements for a week following treatment; then a relapse as before. By this time his laboratory investigations were available and showed multiple nutritional deficiencies, gluten sensitivity, and probable intestinal candidiasis.
Treatment was directed primarily at eliminating dietary gluten and other food irritants, nutritional support, adrenal support and treatment of intestinal dysbiosis. Neural therapy was used at times, but in most cases was an adjunct to other therapies. Over the ensuing year, there was an overall improvement, with many ups and downs. Interference fields were found at various times in his adrenal glands, abdominal scars, coeliac plexus, T10 sympathetic ganglia and anus. A year later his energy was much improved and he was having periods of normal bowel function lasting weeks.
I consider this case to be one in which the interference field was both a cause and a result of the associated dysfunctions. Most likely not only the surgery, but also the antibiotic exposure and other stresses, triggered gluten sensitivity and a cascade of gastrointestinal and nutritional problems. Because so many therapies were introduced concurrently, it was difficult to evaluate the role of neural therapy. At times improvement coincided clearly with neural therapy treatments, but in my opinion the chief value of neural therapy in these complicated conditions is to provide (with autonomic response testing) a diagnostic framework within which to create a systematic treatment strategy.
Robert F. Kidd, MD, CM