Postherpetic neuralgia is associated with scarring of the dorsal root ganglion and atrophy of the dorsal horn on the affected side as a result of the extensive inflammation due to herpes zoster infection (1). Abnormalities of the peripheral and central nervous system produce the pain and other unpleasant symptoms of PHN which include allodynia and hyperalgesia.

The pathology of herpes zoster infection is characterized by acute inflammation, necrosis, and hemorrhage in the dorsal root ganglia (DRG) with a mononeuritis extending out peripherally (2). There is also both myelin and axonal degeneration. Watson et al (3) reported their findings on a postmortem study of a patient with V1 PHN and indicated that the pathology is primarily peripheral. There is no evidence yet to support a pathological pattern specific to PHN.

The pathophysiology of PHN is poorly understood and both central and peripheral mechanisms have been proposed as factors that contribute to pain. Ischemia and ultimately loss of large nerve fibers have been reported after HZ infection.

What causes the pain in postherpetic neuralgia?

The pain associated with acute zoster and post herpetic neuralgia is neuropathic and results from injury of the peripheral nerves and altered central nervous system signal processing. After the injury, peripheral neurons discharge spontaneously, have lower activation thresholds, and display exaggerated response to stimuli. Axonal regrowth after the injury produce nerve sprouts that are also prone to unprovoked discharge. The excessive peripheral activity is thought to lead to hyperexcitability of the dorsal horn, resulting in exaggerated central nervous system to all inputs. Finally, pain could result from abnormal response of residual uninjured fibers.

Based on the clinical and pathological findings three subtypes of PHN have been described (4) and are attributed to:

1. Irritable nociceptor- minimal deafferentation and allodynia

2. Deafferented non-allodynic type- marked sensory loss, no allodynia

3. Deafferented allodynic subtype- sensory loss, allodynia due to central reorganization.

It is possible that each of these subtypes could present individually or coexist in a single patient. The possibility also exists for change of one type to another. This has implications for treatment. The possibility of multiple mechanisms coexisting in one patient may explain the failure of a single therapeutic intervention and may explain the need for a multi-pronged approach.