Postherpetic Neuralgia

Abstract

FigureThe intense pain following a shingles outbreak is the after effect of a stealth attack from the release of the herpesvirus that lies dormant in the dorsal root ganglia of the spinal cord along the neuroaxis including the cervical, thoracic, and lumbosacral segments, which supply sensory nerve efferent and afferent pathways to the corresponding peripheral nerves in the face, trunk, and pelvis. Varicella zoster, or the chickenpox virus, is part of the herpesvirus family. Herpes Zoster Manifestations Nearly all Americans older than 60 years are at risk for the development of shingles as 95% of the population carries antibodies against the varicella zoster virus from exposure to the virus through an active infection or a live vaccine for children. The virus lies dormant and is usually suppressed by an immunocompetent person. But when immunosuppression, stress, surgery, or hospitalization occurs in older adults, the virus may spontaneously reactivate with prodromal symptoms quickly followed by a vesicular painful eruption.2,3 Postherpetic Neuro Pain The exactmechanisms for the phenomena of neuropathic pain mechanisms postherpetic neuralgia (PHN) are unclear; however, Dworkin1 codifies what he calls a useful approach is to distinguish processes that involve the following mechanisms: increased primary afferent nociceptor firing (eg, as a result of abnormal collections of sodium channels in damaged peripheral nerve fibers, causing ectopic discharges) decreased inhibition of neuronal activity in central structures (eg, due to loss of inhibitory neurons) alterations in central processing (central sensitization) so that normal sensory input has an amplified and sustained irritability. A continuum that has been explored in PHN has “irritability” of the nociceptive system at one end and deafferentation at the other. Contributions of other peripheral processes as they relate to PHN remain poorly understood. For example, the sympathetic nervous system may facilitate persistent abnormal primary afferent nociceptor (aberrant pain generators) activity following nerve injury. In addition, nerve injury and inflammation during the acute phase of herpes zoster may be followed by a mixture of abnormal regeneration and receptor expression and permanent cutaneous afferent loss in patients with PHN.1 In other words, the sensory input is abnormally highly receptive to light touch and noxious stimuli, sending abnormal and aberrant pain signals and generators to the central nervous system and brain. These signals are perceived as intense, sharp burning pain that may be hypersensitized by the inflammatory process in the acute stage of a PHN viral attack on the peripheral sensory nerves and the dorsal root ganglion. Treatment Strategies Of the 1 million annual cases of herpes zoster in the United States, it is estimated that between 9% and 34% will develop PHN, and 3 of 4 will experience persistent pain after the shingles episode. In the acute phase, shingles is typically treated with acyclovir, but its efficacy is difficult to demonstrate. Steroid tapers are also used; however, the use of such strategies is limited to a trained medical specialist, and steroids should be used with caution in immunocompromised patients and those with diabetes, as well as in patients with herpes infections of the eye. The World Health Organization’s analgesic ladder should be used to manage the pain. Pregabalin has been shown to be efficacious in reducing the burning pain and allodynia. Chemical counterirritants, such as capsaicin, are thought to reduce substance P, and low-dose selective serotonin reuptake inhibitors are thought to have a synergistic influence on the peripheral nerve pain. When practical, lidocaine topical anesthetics may be effective. The wound care practitioner, as a team member, should be aware of the adverse effect profile of these treatment options for patients. Patients with advanced age should be screened by their primary care practitioner to determine the risk and benefit of the shingles vaccine.2–4 Complications Complications of shingles include superimposed infections that could lead to Streptococcus and Staphylococcus infections, central nervous system infections, Ramsay Hunt syndrome, and infection of the facial ganglia, including the eyes, ears, and nose including hemifacial paralysis. Viral encephalopathies and myelopathies are life threatening and may cause permanent paralysis, brain injury, and disability. Chest and abdominal pain associated with PHN can mimic pulmonary emboli, myocardial infarction, gallbladder disease, and acute abdomen. In patients with advanced age, shingles and PHN are associated with a rapid functional decline, nonrestorative sleep, and an increased risk for falls.FigureRichard “Sal” Salcido, MD