Postherpetic neuralgia

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Postherpetic neuralgia
Classification and external resources
Specialty neurology
ICD-10 B02.2, G53.0, G44.847 Mm
ICD-9-CM 053.19
MedlinePlus 007423
eMedicine neuro/317
Patient UK Postherpetic neuralgia

Postherpetic neuralgia is a nerve pain due to damage caused by the varicella zoster virus. Typically, the neuralgia is confined to a dermatomic area of the skin, and follows an outbreak of herpes zoster (commonly known as shingles) in that same dermatomic area. The neuralgia typically begins when the herpes zoster vesicles have crusted over and begun to heal, but can begin in the absence of herpes zoster—a condition called zoster sine herpete (see Herpes zoster).

Signs and symptoms[edit]


  • With resolution of the herpes zoster eruption, pain that continues for three months or more is defined as postherpetic neuralgia.
  • Pain is variable, from discomfort to very severe, and may be described as burning, stabbing, or gnawing.


  • Area of previous herpes zoster may show evidence of cutaneous scarring.
  • Sensation may be altered over the areas involved, in the form of either hypersensitivity or decreased sensation.
  • In rare cases, the patient might also experience muscle weakness, tremor, or paralysis if the nerves involved also control muscle movement.


Postherpetic neuralgia is thought to be due to nerve damage caused by herpes zoster. The damage causes nerves in the affected dermatomic area of the skin to send abnormal electrical signals to the brain. These signals may convey excruciating pain, and may persist or recur for months, years, or for life.[1]

A key factor in the neural plasticity underlying neuropathic pain is altered gene expression in sensory dorsal root ganglia neurons. Injury to sensory nerves induces neurochemical, physiological and anatomical modifications to afferent and central neurons, such as afferent terminal sprouting and inhibitory interneuron loss.[1] Following nerve damage, NaCl channel accumulation causes hyperexcitability, and downregulation of the TTX-resistant Nav1.8 (sensory neuron specific, SNS1) channel and upregulation of TTX-sensitive Nav1.3 (brain type III) and TRPV1 channels. These changes contribute to increased NMDA glutamate receptor-dependent excitability of spinal dorsal horn neurons and are restricted to the ipsilateral (injured) side. A combination of these factors could contribute to the neuropathic pain state of postherpetic neuralgia.


In the United States each year approximately 1,000,000 individuals develop herpes zoster.[2] Of those individuals approximately 10-18% develop postherpetic neuralgia.[3]

Less than 10 percent of people younger than 60 develop postherpetic neuralgia after a bout of herpes zoster, while about 40 percent of people older than 60 do.


Lab Studies:

  • No laboratory work is usually necessary.
  • Results of cerebrospinal fluid evaluation are abnormal in 61%.
    • Pleocytosis is observed in 46%, elevated protein in 26%, and VZV DNA in 22%.
  • These findings are not predictive of the clinical course of postherpetic neuralgia.
  • Viral culture or immunofluorescence staining may be used to differentiate herpes simplex from herpes zoster in cases that are difficult to distinguish clinically.
  • Antibodies to herpes zoster can be measured. A 4-fold increase has been used to support the diagnosis of subclinical herpes zoster (zoster sine herpete). However, a rising titer secondary to viral exposure rather than reactivation cannot be ruled out.

Imaging studies:

  • Magnetic resonance imaging lesions attributable to herpes zoster were seen in the brain stem and cervical cord in 56% (9/16) of patients.
  • At three months after onset of herpes zoster, 56% (5/9) of patients with an abnormal magnetic resonance image had developed postherpetic neuralgia.
  • Of the seven patients who had no herpes-zoster-related lesions on the magnetic resonance image, none had residual pain.


Primary prevention[edit]

In 1995, the Food and Drug Administration (FDA) approved the Varicella vaccine to prevent chickenpox. Its effect on postherpetic neuralgia is still unknown. The vaccine—made from a weakened form of the varicella-zoster virus—may keep chickenpox from occurring in nonimmune children and adults, or at least lessen the risk of the chickenpox virus lying dormant in the body and reactivating later as shingles. If shingles could be prevented, postherpetic neuralgia could be completely avoided.

In May 2006 the Advisory Committee on Immunization Practices approved a new vaccine by Merck (Zostavax) against shingles. This vaccine is a more potent version of the chickenpox vaccine, and evidence shows that it reduces the incidence of postherpetic neuralgia.[4] The CDC recommends use of this vaccine in all persons over 60 years old.[5]

Secondary prevention[edit]

An April 2013 Cochrane Collaboration meta-analysis of 6 randomized controlled trials (RCTs) investigating oral antiviral medications given within 72 hours after the onset of herpes zoster rash in immunocompetent people for preventing postherpetic neuralgia (PHN) found no significant difference between placebo and acyclovir. Combining four RCTs, 44.1% of the acyclovir treatment group developed herpetic neuralgia whereas 53.3% of the placebo group developed herpetic neuralgia. Heterogeneity between the four RCTs was moderate: Chi2 =3.36, df = 2 (P=0.19); I2 = 40%. Additionally, there was no significant difference in preventing the incidence of PHN found in the one RCT included in the meta-analysis that compared placebo to PO famciclovir treatment within 72 hours of HZ rash onset. Studies using valaciclovir treatment were not included in the meta-analysis. PHN was defined as pain at the site of the dermatomic rash at 120 days after the onset of rash, and incidence was evaluated at 1, 4, and 6 months after rash onset. There was a slight reduction in the incidence of pain at 4 weeks after the onset of rash in the aciclovir group (153 study participants with pain out of 347 study participants in the aciclovir group) versus the placebo group (184 study participants with pain out of 345 study participants in the placebo group). Patients who are prescribed PO antiviral agents after the onset of rash should be informed that their chances of developing PHN are no different than those not taking PO antiviral agents.[6]

A randomized controlled trial found that amitriptyline 25 mg per night for 90 days starting within two days of onset of rash can reduce the incidence of postherpetic neuralgia from 35% to 16% (number needed to treat is 6).[7]


The natural history of postherpetic neuralgia involves slow resolution of the pain syndrome. Most people who develop postherpetic neuralgia respond to agents such as tricyclic antidepressants.[citation needed] A subgroup of affected individuals may develop severe, long-lasting pain that does not respond to medical therapy.


  1. ^ a b Gharibo, Christopher; Kim, Carolyn (December 2011). "Neuropathic Pain of Postherpetic Neuralgia" (PDF). Pain Medicine News. McMahon Publishing. Retrieved 6 October 2014. 
  2. ^ Brian J. Hall; John C. Hall. "Infectious diseases in the skin". Sauer's Manual of Skin Diseases. Lippincott Williams & Wilkins, 2010. p. 232. 
  3. ^ Weaver, B A (2009). "Herpes zoster overview: natural history and incidence" (PDF). J Am Osteopath Assoc. 109 (6 (Suppl 2)): S2–6. PMID 19553632. Retrieved 6 October 2014. 
  4. ^ Chen N, Li Q, Zhang Y, Zhou M, Zhou D, He L (2011). He L, ed. "Vaccination for preventing postherpetic neuralgia". Cochrane Database Syst Rev (3): CD007795. doi:10.1002/14651858.CD007795.pub2. PMID 21412911. 
  5. ^
  6. ^ Chen N, Li Q, Yang J, et al. (2014). He L, ed. "Antiviral treatment for preventing postherpetic neuralgia". Cochrane Database Syst Rev. 2 (2): CD006866. doi:10.1002/14651858.CD006866.pub3. PMID 24500927. 
  7. ^ Bowsher D (1997). "The effects of pre-emptive treatment of postherpetic neuralgia with amitriptyline: a randomized, double-blind, placebo-controlled trial". Journal of Pain and Symptom Management. 13 (6): 327–31. doi:10.1016/S0885-3924(97)00077-8. PMID 9204652. 

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