Herpes Zoster (shingles) has a 10% to 20% lifetime incidence that increases with age. The incidence doubles with each decade after the age of 50 years. Shingles occurs from the reactivation of the varicella-zoster virus. The normal decrease in cell mediated immunity with age and diseases that affect cell mediated immunity (such as malignancy, HIV, and chronic corticosteroid use) are thought to be reasons for developing herpes zoster.
The varicella-zoster virus is a highly contagious DNA virus that enters the sensory dorsal root ganglion during the primary infection and remains dormant for decades. Virus reactivation occurs when there is a decrease in the virus specific cell mediated immunity. The reactivated virus travels down the sensory nerve leading to a rash and pain within the dermatomal distribution of the nerve.
A maculopapular rash evolves into vesicles with an erythmatous base. The vesicles eventually crust over in 7 to 10 days. Scars and pigment changes occur when the crusts fall off. Shingles pain is described as burning, stinging, and unrelenting. The T5 and T6 spinal nerves are the most commonly affected vertebral dermatomes and the ophthalmic division of the trigeminal nerve is the most commonly affected cranial nerve dermatome.
Post herpetic neuralgia (PHN) occurs in 20% of those with herpes zoster. Age is the most established risk factor for PHN with an incidence 15 times more often in those over age 50. Other risk factors include ophthalmic zoster, prodromal pain, and an immunocompromised state. Prodromal pain presents as hyperesthesias, paresthesias, burning dysethesias, or pruritis along the affected dermatome lasting one to two days and up to three weeks before the rash. PHN tends to be self-limited over time with 25% having pain at six months and five percent having pain at one year.
Shingles treatment is aimed at the acute viral infection, pain, and preventing post herpetic neuralgia. Oral antiviral agents (acyclovir, famciclovir, valacyclovir) decrease the duration and pain of the rash if used within the first 72 hours and can reduce the incidence of PHN. Oral prednisone has variable results for the acute viral infection, but reduces the acute pain when combined with acyclovir. Prednisone can diminish the onset of PHN and is often recommended in those over the age of 50 who are at a greater risk for PHN.
Treatment of the acute pain associated with Shingles includes the use of OTC medications, calamine lotion on vesicles, capsaicin cream for crusted lesions, opioids, prednisone, steroid injections of vesicles, epidurals and nerve root blocks. The same medications used for acute Shingles pain are used to treat PHN along with anticonvulsants and tricyclic antidepressants. Peripheral nerve stimulation is an effective last resort if other measures for pain control fail.