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Post-herpetic neuralgia

Created: 14/9/2005
Herpes zoster results from reactivation of the varicella zoster virus. Unlike varicella, herpes zoster is a sporadic disease, with an estimated lifetime incidence of 10 to 20 per cent. The incidence of herpes zoster increases sharply with advancing age, roughly doubling in each decade past the age of 50 years. Herpes zoster is uncommon in persons less than 15 years old.

The normal age-related decrease in cell-mediated immunity is thought to account for the increased incidence of varicella zoster virus reactivation. Patients with disease states that affect cell-mediated immunity, such as HIV infection and certain malignancies, are also at increased risk. Chronic corticosteroid use, chemotherapy and radiation therapy may increase the risk of developing herpes zoster.

About 20 per cent of patients with herpes zoster develop post-herpetic neuralgia. The most established risk factor is age; this complication occurs nearly 15 times more often in patients more than 50 years of age. Other possible risk factors for the development of post-herpetic neuralgia are ophthalmic zoster, a history of prodromal pain before the appearance of skin lesions and an immunocompromised state.


Varicella zoster virus is a highly contagious DNA virus. Varicella represents the primary infection in the non-immune or incompletely immune person. During the primary infection, the virus gains entry into the sensory dorsal root ganglia. How the virus enters the sensory dorsal root ganglia, and whether it resides in neurones or supporting cells are not completely understood. The varicella zoster virus genome has been identified in the trigeminal ganglia of nearly all seropositive patients.

The virus remains latent for decades because of varicella zoster virus-specific cell-mediated immunity acquired during the primary infection, as well as endogenous and exogenous boosting of the immune system periodically throughout life. Reactivation of the virus occurs following a decrease in virus-specific cell-mediated immunity. The reactivated virus travels down the sensory nerve and is the cause for the dermatomal distribution of pain and skin lesions.

The pathophysiology of post-herpetic neuralgia remains unclear. However, pathological studies have demonstrated damage to the sensory nerves, the sensory dorsal root ganglia and the dorsal horns of the spinal cord in patients with this condition.

Clinical presentation

Herpes zoster typically presents with a prodrome consisting of hyperaesthesia, paraesthesias, burning dysaesthesias or pruritus along the affected dermatome(s). The prodrome generally lasts 1-2 days but may precede the appearance of skin lesions by up to 3 weeks. Some patients may have prodromal symptoms without developing the characteristic rash. This situation, known as "zoster sine herpete", may further complicate the eventual diagnosis. The prodromal phase is followed by development of the characteristic skin lesions of herpes zoster. The skin lesions begin as a maculopapular rash which follows a dermatomal distribution, commonly referred to as a "belt-like pattern". The maculopapular rash evolves into vesicles with an erythematous base. The vesicles are generally painful, and their development is often associated with the occurrence of anxiety and flu-like symptoms.

Pain is the most common complaint for which patients with herpes zoster seek medical care. The pain may be described as "burning" or "stinging" and is generally unrelenting. Some patients may have insomnia because of the severe pain. Although any vertebral dermatome may be involved, T5 and T6 are most commonly affected. The most frequently involved cranial nerve dermatome is the ophthalmic division of the trigeminal nerve. Twenty or more lesions outside the affected dermatome reflect generalised viraemia. Of these patients, approximately one half manifest other neurological or visceral involvement, and as many as one in seven with viraemia may die. The vesicles eventually become haemorrhagic or turbid and crust over within 7-10 days. As the crusts fall off, patients are generally left with scarring and pigmentary changes.

Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve. These complications include mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility.

The most common chronic complication of herpes zoster is post-herpetic neuralgia. Pain that persists for longer than 1-3 months after resolution of the rash is generally accepted as the sign of post-herpetic neuralgia. Patients usually report constant burning, lancinating pain, which may be radicular in nature. Patients may also complain of pain in response to non-noxious stimuli. Even the slightest pressure from clothing, bedsheets or wind may elicit pain.

Post-herpetic neuralgia is generally a self-limiting disease. Symptoms tend to abate over time. Less than one quarter of patients still experience pain at 6 months after the herpes zoster eruption, and fewer than one in 20 has pain at 1 year.

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