Postherpetic Neuralgia

Clinical Presentation

Postherpetic neuralgia (PHN) is the most common complication of the varicella zoster virus (VZV) infection, also known as herpes varicella zoster (HVZ). PHN is a long-term, debilitating complication that occurs due to reactivation of VZV. The clinical terminology of herpes zoster is the reactivation of VZV from a dormant state. PHN is classically a burning pain that persists long after the herpes zoster rash resolves. The main clinical presentation of PHN is neuropathic pain. It is said that the pain is a result of severe damage to the sensory nerve ganglia that were infected by the VZV. Usually, patients with history of the herpes zoster virus rash will present to the clinic with a complaint of a burning-type sensation that has persisted for 3 months or longer. The rash itself may or may not have resolved by the time of the initial physical exam. The pain is usually intermittent and may not associated with any type of external stimuli, or it may be triggered by even the lightest touch. Patients have described the pain as burning, deep/aching, or sharp/jabbing.

The pain is located at or follows the distribution of the nerve that was affected by the VSV. Clinicians can visualize the site of pain in the distribution of the VZV rash, and the scarring enables confirmation of the diagnosis. Other associated signs and symptoms that may persist are allodynia, paresthesia, pruritus, hyperalgesia, or dysesthesias. Allodynia describes a situation where the threshold of pain is lowered, and a light brush, a normally nonpainful stimulus that would usually cause light sensation, causes severe pain. Patients may also complain of increased or decreased sensation to light touch or vibration in the involved area. Hypoesthesia is classically considered to be a poorer prognostic sign, as it indicates greater ganglionic injury. It is quite common to see decreased sleep or major depression in patients with PHN. Patients may also have decreased any type of recreational activity due to pain. Symptoms such as constipation, urinary frequency or dysuria, and indigestion may occur, depending on the visceral nerve that is affected. Autonomic dysfunction, such as increased perspiration, may be present at the site of the rash.

Anatomy/Pathophysiology

The anatomy of PHN usually follows the anatomy affected by HVZ. In the beginning of the course of infection during HVZ, the patient experiences painful neuropathy caused by early nerve damage. During an HVZ infection, the virus that was dormant becomes active in the dorsal root ganglion of a single unilateral dermatome that is affected. The most commonly effected dermatomes are T5 to T10. It is said that the virus “favors” infecting the spinal and cranial sensory ganglia. For these reasons, both chest wall and trigeminal PHN are the most common presentations. It can also affect the leptomeninges, the anterior horn cells, and the autonomic neurons. Histological exam of the central and peripheral nervous tissues that were affected by PHN found that these tissues had severe atrophy of the dorsal horn, as well as axon and myelin deficiency. The exact cause of PHN is unknown, but it is thought that the anatomical aberration of these cells plays a huge part in the development of this complication.