A Review Of Postherpetic Neuralgia

Postherpetic neuralgia is one of the most feared complications of herpes zoster and one of the most painful conditions seen in pain practice. Both conditions occur much more commonly in elderly patients and immunosuppressed individuals, and stress may be an important instigator of both conditions. Early treatment of herpes zoster may however reduce the incidence of postherpetic neuralgia. Different clinical patterns of postherpetic neuralgia implying different underlying pain mechanisms, may explain the variation in response to treatment but may also lead to more logical choices in management. ACUTE HERPES ZOSTER INFECTION Herpes zoster (also known as shingles) is the clinical condition of the reactivation of a latent infection with varicella zoster virus usually contracted after an episode of chickenpox in childhood [1]. The virus tends to be reactivated only once in a lifetime, with the incidence of second attacks being less than 5% [1]. The connection between chickenpox and zoster was first suggested in 1892 by a Viennese physician, Janos Von Bokay, after observing several cases of chickenpox in persons exposed to zoster through household contact [2]. Herpes zoster most commonly affects a single dermatome, is frequently preceded by pain (preherpetic neuralgia) and is defined by the characteristic unilateral vesicular rash confined to that dermatome [3]. Prevalence of the condition is high, with an estimated 500,000 people per year suffering reactivation of the virus in the USA. Whereas the incidence in immunocompetent patients ranges from 1.2 to 3.4 per 1000 patient years, the incidence in the elderly is considerably higher, ranging from 3.9 to 11.8 per 1000 patient years [3]. This is because T cell immunity to the virus wanes in later life making advanced age the most significant risk factor for the occurrence of reactivated herpes zoster [1]. An additional major risk factor for herpes zoster reactivation is T cell immunosuppression as might occur in conditions such as human immunodeficiency virus (HIV) infection, certain cancers, and immunosuppression treatment after organ transplantation[1,3]. The rash and pain associated with shingles can be both dramatic and severe but in most cases the episode is transient lasting between 2 and 4 weeks [4]. PAINFUL COMPLICATIONS AND THEIR PREVENTION Although there are several serious complications of zoster (ophthalmic, splanchnic, cerebral, motor), the most common and feared in immunocompetent adults is postherpetic neuralgia (PHN). Its definition is controversial but recent data support the distinction between acute herpetic neuralgia (within 30 days of rash onset), subacute herpetic neuralgia (30-120 days after rash onset), and postherpetic neuralgia (defined as pain lasting at least 120 days from rash onset) [3]. However as PHN may arise at any time after the resolution of acute herpes zoster, a clinically useful definition of PHN is recurrent or persistent localized pain arising or persisting in areas affected by herpes zoster at least 3 months after healing of the skin lesion [5]. The most well established risk factors for PHN are older age, greater severity of acute herpetic neuralgia, more severe rash, and preherpetic neuralgia. Patients with all of these risk factors may have as much as a 50-75% risk of developing PHN [6]. As with other herpes virus infections, psychological distress and stressful life events appear to play an important role in instigating the onset of shingles as well as the development of PHN [3]. In treating the acute phase of herpes zoster, apart from keeping the patient comfortable, an attempt must be made to prevent the development of PHN. The mainstay of acute herpes zoster treatment is oral antiviral therapy and the most commonly used drugs are acyclovir, famciclovir, and A Review Of Postherpetic Neuralgia 2 of 7 valacyclovir. All of these agents have been shown to promote resolution of skin lesions and reduce the duration of viral shedding and pain [5,7]. Studies have indicated that antiviral treatment started within 48-72 hours of the development of the herpes zoster rash may also decrease the risk of PHN [8]. Antiviral therapy should be provided for patients at extreme risk for developing PHN, including the elderly and individuals with decreased cell-mediated immunity. Many adjunctive therapies are useful in the treatment of acute herpes zoster. Low-dose amitriptyline (25 mg daily) given within 1 month after the onset of zoster for a 90-day course can reduce the risk of PHN by one-half [9]. Corticosteroids added to antiviral therapy have been shown to accelerate healing of skin lesions, reduce analgesic requirement, improve sleep, and promote faster return to normal activity. They do not however affect the incidence of PHN [10]. Although acute pain will be reduced by antiviral and adjunctive drugs, patients will also require analgesics, sometimes strong opioids [6]. Sympathetic and regional blocks with long acting local anesthetics, and local infiltration with local anaesthetic and steroids have also been used to control pain, enhance healing, and prevent permanent nerve damage [11]. POST HERPETIC NEURALGIA