Postherpetic neuralgia

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Postherpetic neuralgia
Classification and external resources
ICD-10B02.2, G53.0, G44.847 Mm
ICD-9053.19
MedlinePlus007423
eMedicineneuro/317
Patient UKPostherpetic neuralgia
 
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"PHN" redirects here. For the Spanish National Water Plan (Plan Hidrológico Nacional), see Water supply and sanitation in Spain.
Postherpetic neuralgia
Classification and external resources
ICD-10B02.2, G53.0, G44.847 Mm
ICD-9053.19
MedlinePlus007423
eMedicineneuro/317
Patient UKPostherpetic 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 it can begin in the absence of herpes zoster, in which case zoster sine herpete is presumed (see Herpes zoster).

Treatment options for postherpetic neuralgia include antidepressants, anticonvulsants (such as gabapentin, pregabalin, or topiramate), gabapentin enacarbil (a prodrug of gabapentin) and topical agents such as lidocaine patches or capsaicin lotion. Opioid analgesics may also be appropriate in many situations. There are some sporadically successful experimental treatments, such as rhizotomy (severing or damaging the affected nerve to relieve pain) and TENS (a type of electrical pulse therapy).

Pathophysiology[edit]

Postherpetic neuralgia is thought to be 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.

Frequency[edit]

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.

Predisposing factors[edit]

Signs and symptoms[edit]

Symptoms:

Signs:

Lab and imaging studies[edit]

Lab Studies:

Imaging studies:

Treatment[edit]

Treatment for postherpetic neuralgia depends on the type and characteristics of pain experienced by the patient. Pain control is essential to quality patient care; it ensures patient comfort. Possible options include:

In some cases, treatment of postherpetic neuralgia brings complete pain relief. But most people still experience some pain, and a few do not receive any relief. Although some people must live with postherpetic neuralgia the rest of their lives, most people can expect the condition to gradually disappear on its own within five years.

Prognosis[edit]

The natural history of postherpetic neuralgia involves slow resolution of the pain syndrome. In those patients who develop postherpetic neuralgia, most respond to agents such as the tricyclic antidepressants. A subgroup of patients may develop severe, long-lasting pain that does not respond to medical therapy. Continued research for new agents is necessary.

Prevention[edit]

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.[8] The CDC recommends use of this vaccine in all persons over 60 years old.[9]

Secondary prevention[edit]

An April 2013 Cochrane Collaboration meta-analysis of 6 Randomized Control Trials (RCTs) investigating PO antiviral medications given within 72 hours after the onset of Herpes Zoster (HZ) rash in immunocompetent people for preventing postherpetic neuralgia (PHN) found no significant difference between placebo and aciclovir. Combining four RCTs, 44.1% of the aciclovir 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%. Nor was a 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). If patients are prescribed PO antiviral agents after the onset of rash, they should be informed that their chances of developing PHN are no different than those not taking PO antiviral agents. [10]

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).[11]

Research directions[edit]

References[edit]

  1. ^ a b Gharibo, Christopher; Kim, Carolyn (December 2011). "Neuropathic Pain of Postherpetic Neuralgia". 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.". J Am Osteopath Assoc 109 (6 (Suppl 2)): S2–6. PMID 19553632. Retrieved 6 October 2014. 
  4. ^ De Benedittis G, Besana F, Lorenzetti A (1992). "A new topical treatment for acute herpetic neuralgia and post-herpetic neuralgia: the aspirin/diethyl ether mixture. An open-label study plus a double-blind controlled clinical trial". Pain 48 (3): 383–90. doi:10.1016/0304-3959(92)90088-S. PMID 1594261. 
  5. ^ Chen N, Yang M, He L, Zhang D, Zhou M, Zhu C (2010). He, Li, ed. "Corticosteroids for preventing postherpetic neuralgia". Cochrane Database Syst Rev (12): CD005582. doi:10.1002/14651858.CD005582.pub3. PMID 21154361. 
  6. ^ Doble S (2008). "Spinal Management of patients with post-herpetic neuralgia". Nursing Standard 22 (39): 49–56. doi:10.7748/ns2008.06.22.39.49.c6569. PMID 18578133. 
  7. ^ Harke H, Gretenkort P, Ladleif HU, Koester P, Rahman S (2002). "Spinal cord stimulation in postherpetic neuralgia and in acute herpes zoster pain". Anesthesia & Analgesia 94 (3): 694–700. doi:10.1097/00000539-200203000-00040. PMID 11867400. 
  8. ^ Chen N, Li Q, Zhang Y, Zhou M, Zhou D, He L (2011). He, Li, ed. "Vaccination for preventing postherpetic neuralgia". Cochrane Database Syst Rev (3): CD007795. doi:10.1002/14651858.CD007795.pub2. PMID 21412911. 
  9. ^ http://www.cdc.gov/vaccines/vpd-vac/shingles/default.htm
  10. ^ Chen N, Li Q, Yang J, et al. (2014). He, Li, ed. "Antiviral treatment for preventing postherpetic neuralgia". Cochrane Database Syst Rev 2 (2): CD006866. doi:10.1002/14651858.CD006866.pub3. PMID 24500927. 
  11. ^ 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. 
  12. ^ Bernstein, L.R. (2013). "Gallium, therapeutic effects". In Kretsinger, R.H.; Uversky, V.N.; Permyakov, E.A. Encyclopedia of Metalloproteins. New York: Springer. pp. 823–835. ISBN 978-1-4614-1532-9. 

External links[edit]