Practice Essentials
Herpes zoster (HZ) is a viral infection that usually presents as a childhood infection of varicella (ie, chicken pox). The pathogen is human herpesvirus-3 (HHV-3), also known as the varicella zoster virus (VZV). Following the acute phase, the virus enters the sensory nervous system, where it is harbored in the geniculate, trigeminal, or dorsal root ganglia and remains dormant for many years. With advancing age or immunocompromised states, the virus reactivates and an eruption (ie, shingles) occurs. Even after the acute rash subsides, pain can persist or recur in shingles-affected areas. This condition is known as postherpetic neuralgia (PHN).
Hypopigmented rash in thoracic dermatome of postherpetic lesion.
Signs and symptoms
A painful vesicular eruption in a dermatomal distribution is typical of herpes zoster (HZ). With resolution of the eruption, pain that continues for 3 months or more is defined as PHN. Pain is intense and may be described as burning, stabbing, or gnawing.
HZ can reactivate subclinically with pain in a dermatomal distribution without rash. [1] This condition is known as zoster sine herpete and may be more complicated, affecting multiple levels of the nervous system and causing multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. [2]
Diagnosis
No laboratory work is usually necessary in cases of PHN.
Results of cerebrospinal fluid (CSF) evaluation are abnormal in 61%.
Managment
The goal of therapy for PHN is to reduce morbidity through the use of tricyclic antidepressants, anticonvulsants, anesthetics, analgesics, corticosteroids, and antiviral agents. An approved vaccine is also effective for preventing HZ outbreaks and PHN
Background
Herpes zoster (HZ) is a viral infection that usually presents as a childhood infection of varicella (ie, chicken pox). The pathogen is human herpesvirus-3 (HHV-3), also known as the varicella zoster virus (VZV). Following the acute phase, the virus enters the sensory nervous system, where it is harbored in the geniculate, trigeminal, or dorsal root ganglia and remains dormant for many years. With advancing age or immunocompromised states, the virus reactivates and an eruption (ie, shingles) occurs. Even after the acute rash subsides, pain can persist or recur in shingles-affected areas. This condition is known as postherpetic neuralgia (PHN).
Hypopigmented rash in thoracic dermatome of postherpetic lesion.
Pathophysiology
Some patients with postherpetic neuralgia (PHN) appear to have abnormal function of unmyelinated nociceptors and sensory loss (usually minimal). Pain and temperature detection systems are hypersensitive to light mechanical stimulation, leading to severe pain (allodynia). Allodynia may be related to formation of new connections involving central pain transmission neurons. Other patients with PHN may have severe, spontaneous pain without allodynia, possibly secondary to increased spontaneous activity in deafferented central neurons or reorganization of central connections. An imbalance involving loss of large inhibitory fibers and an intact or increased number of small excitatory fibers has been suggested. This input on an abnormal dorsal horn containing deafferented hypersensitive neurons supports the clinical observation that both central and peripheral areas are involved in the production of pain.
Epidemiology
Frequency
Frequency 1 month after onset of shingles is 9-14.3% and at 3 months is about 5%. At 1 year, 3% continue to have severe pain.
Family history as a risk factor for herpes zoster has been described. In a case-control study of 504 patients and 523 controls, Hicks et al found that the patients were more likely to report blood relatives with herpes zoster than the controls (39% vs 11%, p< .001). This risk was higher in patients with multiple blood relatives with herpes zoster compared with those with a single blood relative with herpes zoster. [3]
A study from Iceland demonstrated variations in risk of PHN associated with different age groups. No patient younger than 50 years described severe pain at any time. Patients older than 60 years described severe pain: 6% at 1 month and 4% at 3 months from the onset of shingles. [4]
Mortality/Morbidity
Postherpetic neuralgia is not fatal. Patients may experience significant pain for a prolonged period of time.
Sex
No predilection for developing PHN is known. Although 65% of patients in a study by Watson et al were women, this was believed to mirror the usual predominance of women in this age group.
Age
The association between greater age and PHN is strong. [5] Older age appears to be the most significant risk factor for developing PHN. At age 60 years, approximately 60% of patients with shingles develop PHN, and at age 70 years, 75% develop PHN.
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Hypopigmented rash in thoracic dermatome of postherpetic lesion.
