Postherpetic neuralgia (PHN) is neuropathic pain that occurs due to damage to a peripheral nerve caused by the reactivation of the varicella zoster virus (herpes zoster, also known as shingles). PHN is defined as pain in a dermatomal distribution that lasts for at least 90 days after an outbreak of herpes zoster. Several types of pain may occur with PHN including continuous burning pain, episodes of severe shooting or electric-like pain, and a heightened sensitivity to gentle touch which would not otherwise cause pain or to painful stimuli. Abnormal sensations and itching may also occur. Postherpetic neuralgia is the most common long-term complication of herpes zoster, and occurs in approximately 20% of patients with shingles. Risk factors for PHN include older age, severe prodrome or rash, severe acute zoster pain, ophthalmic involvement, immunosuppression, and chronic conditions such as diabetes mellitus and lupus. The pain from postherpetic neuralgia can be very severe and debilitating. There is no treatment which modifies the course of the disease and management primarily aims to control symptoms. Affected individuals often experience a decrease in their quality of life. Shingles vaccination is the only way for adults to be protected against both shingles and postherpetic neuralgia, with the vaccine Shingrix providing 90% protection from postherpetic neuralgia. The chickenpox vaccine is approved for infants to prevent chickenpox, which also protects against PHN from a herpes zoster infection.
Overview Postherpetic neuralgia (PHN) is neuropathic pain that occurs due to damage to a peripheral nerve caused by the reactivation of the varicella zoster virus (herpes zoster, also known as shingles). Typically, the nerve pain (neuralgia) is confined to an area of skin innervated by a single sensory nerve, which is known as a dermatome. PHN is defined as dermatomal nerve pain that persists for more than 90 days after an outbreak of herpes zoster affecting the same dermatome. Several types of pain may occur with PHN including continuous burning pain, episodes of severe shooting or electric-like pain, and a heightened sensitivity to gentle touch which would not otherwise cause pain (mechanical allodynia) or to painful stimuli (hyperalgesia). Abnormal sensations and itching may also occur. The nerve pain of PHN is thought to result from damage in a peripheral nerve that was affected by the reactivation of the varicella zoster virus. PHN 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. There is no treatment that modifies the disease course of PHN; therefore, controlling the affected person's symptoms is the main goal of treatment. Medications applied to the skin such as capsaicin or topical anesthetics (e.g., lidocaine) are used for mild pain and can be used in combination with oral medications for moderate to severe pain. Oral anticonvulsant medications such as gabapentin and pregabalin are also approved for treatment of PHN. Tricyclic antidepressants reduce PHN pain, but their use is limited by side effects. Opioid medications are not generally recommended for treatment except in specific circumstances. Such cases should involve a pain specialist in patient care due to mixed evidence of efficacy and concerns about potential for abuse and addiction. Shingles vaccination is the only way for adults to be protected against both shingles and postherpetic neuralgia, with the vaccine Shingrix providing 90% protection from postherpetic neuralgia. The chickenpox vaccine is approved for infants to prevent chickenpox, which also protects against PHN from a herpes zoster infection. PHN is the most common long-term complication of herpes zoster. The incidence and prevalence of PHN are uncertain due to varying definitions. Approximately 20% of people affected by herpes zoster report pain in the affected area three months after the initial episode of herpes zoster, and 15% of people similarly report this pain two years after the herpes zoster rash. Since herpes zoster occurs due to reactivation of the varicella zoster virus, which is more likely to occur with a weakened immune system, both herpes zoster and PHN occur more often in the elderly. Risk factors for PHN include older age, severe prodrome or rash, severe acute zoster pain, ophthalmic involvement, immunosuppression, and chronic conditions such as diabetes mellitus and lupus. PHN is often very painful and can be quite debilitating. Affected individuals often experience a decrease in their quality of life.
Signs and symptoms
Symptoms:
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. Signs:
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.
Pathophysiology 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. 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. Following nerve damage, sodium 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.
Diagnosis
Lab Studies:
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