Herpes Zoster

Herpes zoster complicates 10% of lymphomas, particularly Hodgkin disease. One in 25 active shingles patients harbor undetected carcinomas, lymphomas, or other diminished T-cell immunity pathophysiology, particularly immunosuppression with corticosteroid or medication for transplants or human immunodeficiency virus (HIV) infection.

Postherpetic neuralgia (PHN), characterized by severe and relentless pain highly refractory to treatment, is an important HZ complication. PHN risk factors include age older than 50 years, female gender, severe disseminated rash, initially severe pain, and polymerase chain reaction (PCR)-detectable viremia. VZV is associated with other neurologic complications, including cerebral arteriopathies, particularly with ophthalmic trigeminal zoster. Other potential issues include cranial nerve palsies, myelitis, segmental motor weakness, and herpetic neuralgia without the zoster rash (zoster sine herpete)—a difficult diagnosis.

PATHOLOGY

The dorsal root ganglion (DRG) is the primary infectious site. VZV, a DNA-type virus similar to herpes simplex virus, also causes childhood chickenpox. Subsequently, the VZV probably migrates up the peripheral/sensory nerve to the DRG, remaining dormant for years until immunocompromise potentiates reactivation. Here an acute inflammatory reaction leads to DRG destruction. Concomitantly, the VZV spreads peripherally to the skin, producing the rash. The neuropathic pain component of zoster, independent of pain associated with the actual lesions, occurs with intraneuronal virus replication, leading to neuronal lytic damage, inflammation, and hemorrhage with virus eruption from the neurons.

CLINICAL MANIFESTATION

The rash, reminiscent of chickenpox is confined to a radicular or cranial nerve distribution. Its onset is often heralded by a few days of either severe localized pain or nonspecific discomfort in the affected area. The vesicles appear 72 to 96 hours later. They have an erythematous base with a tight, clear bubble that eventually becomes opaque and dries and crusts over after 5 to 10 days; scarring and hypopigmentation may occur. Typically, the pain ceases in 1 to 4 weeks.

More than half of patients are affected in the thoracic region as with varicella. Ophthalmic trigeminal herpes zoster is fairly common and carries the risk of corneal anesthesia and consequent scarring, along with conjunctivitis, keratitis, and iridocyclitis. This also has the uncommon potential for middle cerebral artery infarction from viral arterial wall invasion. Common motor deficits result from infections of the facial nerve when the geniculate ganglion is affected. This infection, also referred to as Ramsay Hunt syndrome, is usually associated with vesicles in the external ear and sometimes leads to tinnitus, vertigo, and deafness.

A serious primary complication of acute herpes zoster (AHZ) is postherpetic neuralgia (PHN), or chronic neuropathic pain in the affected nerve territory that persists after the skin eruptions and acute inflammatory response have subsided. Although PHN may improve over time, the incidence and severity of symptoms directly correlate with advanced age at rash onset and the degree of rash severity. Once the initial lesions of HZ have healed, the scarred regions have decreased sensation and numbness, although the surrounding skin is marked by allodynia, hyperalgesia, and hyperesthesia. The pain may either be characterized as persistent burning or lancinating pain precipitated by friction of the skin, intense itching and formication can be present as well.

TREATMENT

A live attenuated vaccine (Zostavax; Merck, Whitehouse Station, NJ) is approved by the U.S. Food and Drug Administration (FDA) for the HZ prevention in patients older than 50 years. Protection against HZ begins around 4 to 6 weeks postvaccination. This is not for treatment of herpes zoster or PHN per se. Antiviral agents, including acyclovir, valacyclovir, and famciclovir reduce the acute and symptomatic period if administered within 3 days of rash appearance. The latter two drugs also decrease the incidence and severity of PHN, although not preventing its occurrence.

For treatment of PHN per se, oxycodone has demonstrated analgesic benefit in the acute and subacute phase after acute herpes zoster reactivation. Tricyclic antidepressants, adjuvants such as gabapentin and pregabalin, topical lidocaine (5%), topical high-dose (8%) capsaicin, and opioid medications are all efficacious for PHN pain relief.

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