Is it possible that the incidence of herpes zoster ("shingles") is on the rise? An interesting case of post-herpetic neuralgia in my office has had me pondering this question.
I had heard the suspicion expressed that varicella (chicken pox) vaccination programs of children were having the unintended consequences of increasing the incidence of herpes zoster in adults. The reasoning is this: The wild virus that causes varicella in children, is thought to also boost immunity to the (dormant) varicella virus in adults. With the institution of widespread varicella immunization in the last 20 years, the incidence of varicella has clearly declined. Has herpes zoster increased in response?
This is a difficult subject to research. The quality of epidemiological data is spotty, especially that collected retrospectively from before the vaccine era. The incidence of herpes zoster is age‐dependent, is affected by climate and seasons, and is much higher in immune‐compromised individuals, so comparison of before‐ and after‐ vaccine data is hard.
Some of the most interesting data come from comparative studies of HZ incidence in those who have more or less exposure to varicella, e.g. paediatricians vs dermatologists and psychiatrists or adults living with young children vs those who are not. These small studies show a clear protective effect of wild varicella exposure. Now that widespread vaccination has been instituted (in the US and Canada) more data of its effect on herpes zoster incidence is available. Goldman and King's review is highly critical of the whole varicella vaccination program and its effect on HZ rates. Another review by Leung et al found increasing incidence of herpes zoster but no evidence that varicella vaccination was a contributing factor.
An excellent overview of this whole subject can be found in chapter 40 of: Human Herpes Viruses: Biology, therapy and immunoprophylaxis.
In recent years, the emphasis in research is to demonstrate the efficacy of vaccines in treating both chicken pox and herpes zoster. Unfortunately the vast majority of these "peer‐reviewed" studies have been funded by the vaccine manufacturers.
So now about my patient: This 65 year‐old woman did not actually have active herpes zoster when I first saw her, but rather post-herpetic neuralgia. The herpes lesions had manifested above her right hip about a year before with the typical burning "shingles" pain, but the pain (not the lesions) continued down her leg over the anterior thigh to the medial side of her knee.
Post herpetic neuralgia (or herpes zoster) usually responds to quaddles of dilute procaine injected into the area of skin lesions and/or pain. I have found through autonomic response testing that there is usually an interference field in the skin not far from the nerve's exit from the spine. Treatment of this spot is usually effective, rendering unnecessary treating the whole painful area.
However in this patient, no interference field could be detected near the spine, nor along the course of the pain distribution until the knee, where an interference field could be detected along the whole joint line. The joint was treated with the Tenscam device and the patient had after the first day a day of relief, then some return of pain, but less intense. An interference field could again be detected on the joint line, but only medially and extending a few inches proximally.
Similar response and findings were obtained on two more occasions and then the quality of the pain changed to a muscle spasm, proximally in the mid anterior thigh. Interference fields were found in ensuing appointments in the pelvic diaphragm, the right L3 sympathetic ganglion and the lateral half of a cholecystectomy scar. Overall improvement continued with treatment but some persisting pain and muscle tightness suggested possibly magnesium deficiency. This was confirmed with autonomic response testing; the patient was prescribed magnesium glycinate in increasing doses to bowel tolerance. On the subsequent visit the patient was pain-free, autonomic regulation was "open" and no interference field could be found.
This patient's post‐herpetic neuralgia was unusual in a number of respects. Firstly herpes zoster is uncommon in an extremity; usually it presents in the trunk or the head. Secondly, the first detectable interference field was far from a spinal root, where it is usually found. Thirdly, other interference fields, distinct from the herpetic process were involved. And lastly, the pain was not completely resolved until a nutritional deficiency was corrected.
My patient's course also demonstrated once again the principle of neurological summation: the summation of more than one neurological input to the central nervous system resulting in a signal that reaches threshold, ‐ and then the possibility of affecting the threshold itself by correcting a nutritional (or toxic) factor that alters the nervous system's excitability.
Robert F. Kidd, MD, CM