Postherpetic neuralgia is more common with older age. Recommended treatments include topical agents (lidocaine or capsaicin) and systemic agents (in particular, gabapentin, pregabalin, or tricyclic antidepressants), but their efficacy tends to be suboptimal. The latest Clinical Practice article is on this topic, and comes from University of Bristol’s Dr. Robert Johnson and Imperial College London’s Dr. Andrew Rice.
Postherpetic neuralgia is the most frequent chronic complication of herpes zoster and the most common neuropathic pain resulting from infection.
•What are the epidemiology of and risk factors for postherpetic neuralgia?
Postherpetic neuralgia is conventionally defined as dermatomal pain persisting at least 90 days after the appearance of the acute herpes zoster rash. The incidence and prevalence of postherpetic neuralgia vary depending on the definition used, but approximately a fifth of patients with herpes zoster report some pain at 3 months after the onset of symptoms, and 15% report pain at 2 years. Analysis of data from the United Kingdom General Practice Research Database showed that the incidence of postherpetic neuralgia (as defined by pain at 3 months) rose from 8% at 50 to 54 years of age to 21% at 80 to 84 years of age. Risk factors for postherpetic neuralgia include older age and greater severity of the prodrome, rash, and pain during the acute phase. The incidence is also increased among persons with chronic diseases such as respiratory disease and diabetes, and it may be increased among immunocompromised patients, although the evidence is sparse and inconsistent.
•What is the typical clinical presentation and appropriate evaluation of a patient with postherpetic neuralgia?
Although a history of herpes zoster often cannot be confirmed with absolute certainty, the disorder has a characteristic clinical presentation, and thus postherpetic neuralgia rarely presents a diagnostic challenge. Clinical assessment of the patient with postherpetic neuralgia should follow the general principles of assessment of patients with peripheral neuropathic pain. Features of pain and associated sensory perturbations (e.g., numbness, itching, and paresthesias) should be assessed. Pain associated with postherpetic neuralgia occurs in three broad categories: spontaneous pain that is ongoing (e.g., continuous burning pain), paroxysmal shooting or electric shock-like pains, and evoked sensations that are pathologic amplifications of responses to light touch and other innocuous stimuli (mechanical allodynia) or to noxious stimuli (mechanical hyperalgesia). The physical examination should include a comparison of sensory function in the affected dermatome with that on the contralateral side. Loss of sensory function in response to both mechanical and thermal stimuli is common in patients with postherpetic neuralgia, as are pathologic sensory amplifications (e.g., allodynia and hyperalgesia). In most cases, no additional evaluation is needed beyond the history taking (with concomitant disease and medications noted) and physical examination.
Morning Report Questions
Q: What is the appropriate treatment for postherpetic neuralgia?
A: Topical therapy alone is reasonable to consider as first-line treatment for mild pain. It is sometimes used in combination with systemic drugs when pain is moderate or severe, although data are lacking from randomized trials comparing combination topical and systemic therapy with either therapy alone. Patches containing 5% lidocaine are approved for the treatment of postherpetic neuralgia in Europe and the United States. However, evidence in support of their efficacy is limited. There is evidence to support the use of tricyclic antidepressants (off-label use) and the antiepileptic drugs gabapentin and pregabalin (Food and Drug Administration-approved) for the treatment of postherpetic neuralgia. Opioids, including tramadol, should generally be considered as third-line drugs for postherpetic neuralgia after consultation with a specialist and should be prescribed only with appropriate goals and close monitoring.
Q: What is the evidence for the effectiveness of preventive therapy for postherpetic neuralgia?
A: Placebo-controlled trials of antiviral drugs for acute herpes zoster have shown that they reduce the severity of acute pain and rash, hasten rash resolution, and reduce the duration of pain. These trials were not designed to assess the subsequent incidence of postherpetic neuralgia. Two randomized trials have shown that the addition of systemic glucocorticoids to antiviral drugs during the acute phase of herpes zoster does not reduce the incidence of postherpetic neuralgia. In one placebo-controlled trial, low-dose amitriptyline, started soon after the diagnosis of herpes zoster and continued for 90 days, significantly reduced the incidence of pain at 6 months. Further studies are required to confirm this finding. The only well-documented means of preventing postherpetic neuralgia is the prevention of herpes zoster. A live attenuated VZV [varicella-zoster virus] vaccine has been available since 2006; it was initially licensed for immunocompetent persons 60 years of age or older but now is approved for persons 50 years of age or older. In a randomized trial in the older age group, its use reduced the incidence of herpes zoster by 51% and the incidence of postherpetic neuralgia by 66%. In patients 70 years of age or older as compared with those 60 to 69 years of age, the vaccine was less effective in reducing the risk of herpes zoster (38% reduction) but conferred similar protection against postherpetic neuralgia (67% reduction).