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11 Articles in Volume 10, Issue #9
Activated Glia: Targets for the Treatment of Neuropathic Pain
Acute Herpes Zoster Neuritis and Postherpetic Neuralgia
Acute Treatment of Cluster Headache
Chronic Overuse Sports Injuries in the Adolescent/Pediatric Population
Clinical Recognition of Central Abnormal Neuroplasticity
H-Wave® Stimulation: A Novel Approach In Electromedicine
Homeopathy Enters Contemporary Pain Practice
Immune-modulating Effects of Therapeutic Laser
Pain and Addiction: Words, Meanings, and Actions in the Age of the DSM-5
Partial Plantar Fasciectomy With Autologous Platelet Concentrate
Tethered Spinal Cord Syndrome: Pathophysiology and Radiologic Diagnosis

Acute Herpes Zoster Neuritis and Postherpetic Neuralgia

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Dr. John Nelson is both a highly respected pain physician as well as a personal friend. We are fortunate to have him write this article on an important and often over-looked treatment for a common pain problem. Shingles/PHN is said to be the second most painful condition known to man (trigeminal neuralgia being the first) and few physicians are aware that there are simple interventions to both treat the pain and prevent occurrence of PHN. Presented here are some of those interventions.

Acute herpes zoster neuritis and postherpetic neuralgia continues to be one of the most painful, acute and chronic conditions to afflict mankind. It will continue to be a major health problem as the baby-boomer generation in the United States ages and is at risk for the reemergence of the varicella zoster virus. The impact of the chickenpox vaccine has yet to be known on the ultimate expression of this disease. As is well known, acute herpes zoster neuritis is the reemergence of the varicella zoster virus, or chickenpox virus, which has been dormant in the sensory dorsal root ganglia of the nervous system since childhood infection. Herpes zoster is a disease of the elderly as an expression of the loss of immune surveillance related to aging. With the decline in cell-mediated immunity, the virus awakens in the dorsal root ganglion and causes an intense inflammatory response with a ganglionitis. The virus eventually reaches the sensory root and travels through the nerve, eventually reaching the skin in one or, occasionally, two dermatomes and with the development of the typical blistering rash and vesicles so that the diagnosis is self-evident.

The disease is certainly more common in patients with immune deficiency such as AIDS, lymphoma, leukemias, high dose corticosteroids, or immunosuppression from cancer therapy. Usually once the virus has reawakened, the immune response contains it to one or two dermatomes and, if there is widespread dissemination, it suggests a significant defect in immune function. Many clinicians feel that the presence of herpes zoster in the younger population warrants an investigation for an occult malignancy or other problems with cell-mediated immunity.


Acute herpes zoster is the most common neurological disorder in the United States, is equally prevalent in both sexes, and probably is more severe in diabetics. The incidence of acute herpes zoster is 125 cases per 100,000 and is more common as the person gets older. The percentage of patients who will have recurrent herpes zoster—with half at the site of their original eruption—is less than 5% to 8% implying that once the immune system responds to the re-exposure to the virus, it is sufficient to last the life of the patient. Less than 11% of patients may have the syndrome with pain but without the rash. The onset of pain may precede the rash by as much as one to two weeks and may pose diagnostic dilemmas in patients. The most common area of involvement is the thoracic region followed by the ophthalmic division and clearly many patients have been evaluated for pleurisy, cholecystitis, acute myocardial infarction, etc. before the diagnosis was self-evident with the appearance of the rash. Rarely, the ganglionitis can involve other parts of the central nervous system including motor fibers such as the Ramsay Hunt’s syndrome with facial weakness due to involvement of the 7th nerve and the geniculate ganglion and there have been rare reports of myelopathy. Other complications include dermatologic dissemination, varicella encephalitis, pneumonitis, blindness due to corneal scarring from ophthalmic zoster and localized or systemic infection at the breakdown of the skin barrier.

Persistent Pain

The most common complication is postherpetic neuralgia, which is persistent neuropathic pain after the eruption is healed and usually occurs in about 3 to 4 weeks. Most clinicians, by definition, label postherpetic neuralgia as persistent pain at six weeks beyond the acute phase of the disease. The percentage of patients who will develop postherpetic neuralgia increases with the age of the patient and one study quoted 50% at age 50, 60% at age 60 and 70% at age 70, etc. The duration of postherpetic neuralgia may be months to years and the pain may be mild to excruciating to the point of placing patients at risk for suicide. Postherpetic neuralgia is the most common cause of suicide in patients with chronic pain over the age of 70 in the United States and Western Europe. As I mentioned, it is most common in the thoracic and ophthalmic distribution but can occur in any dermatome.


The treatments for acute herpes zoster and postherpetic neuralgia have been myriad in the literature and include corticosteroids, opioids, antiviral agents, small pox vaccination, topical local anesthetics and capsaicin and even iontophoresis vincristine. What is clear is that the acute phase of acute herpes zoster neuritis seems to have a significant sympathetically-mediated component and the development of postherpetic neuralgia represents the evolution of this condition to a sympathetically-independent neuropathic condition that can be very resistant to treatment. This resistance to successful management is certainly represented in the high incidence of suicide. There are some early studies suggesting that aggressive treatment of the acute pain with analgesics, including opioids, may decrease the percentage of patients with postherpetic neuralgia. With the development of antiviral medications—such as acyclovir, famiciclovir, etc.—it was hoped that there would be a significant impact on the percentage of patients with postherpetic neuralgia but this has not been shown to be the case.

The drugs, if given during the acute phase, probably decrease the amount of viral shedding and the development of new lesions and the duration of postherpetic neuralgia but do not decrease the frequency or incidence of postherpetic neuralgia. This will be discussed in the next several paragraphs and probably represents the fact that the inflammatory response to the varicella zoster virus is the major factor in the development of post-herpetic neuralgia. This response probably occurs even to viral particles in sera—even when the virus has been killed.


As anesthesiologists, we have long recognized and felt passionately about the role of neural blockade and especially sympathetic blockade in the treatment of acute herpes zoster neuritis. This was first written about in 1938 by Dr. Rosenak, a practicing physician in Budapest, Hungary. Dr. Rosenak was a dermatologists whose next door neighbor was an orthopedic spine surgeon who was seeing a patient for peripheral vascular disease and had performed a diagnostic lumbar sympathetic block to determine if the patient’s pain was amenable to sympathectomy. The patient, coincidentally, had acute herpes zoster lesions on the buttock and, following the sympathetic block, reported to the surgeon that the lesions had crusted over, dried up and his pain was essentially gone. When this was reported to Dr. Rosenak, he subsequently compiled a series of 21 patients with acute herpes zoster whom he treated with sympathetic blockade with local anesthetic. Of these, 19 patients had immediate and permanent relief of their pain with one block and one patient with two blocks. This represented a 95% success rate. Dr. Rosenak published his work in Lancet in 1938.1

Last updated on: April 11, 2012