Herpes zoster (shingles) is a viral infection that mainly affects the elderly. About 20% of people experience a herpes zoster infection during their lifetime. In contrast to other herpes infections, herpes zoster recurs relatively seldom. Only a small percentage of patients are referred to hospital by their GP, and these are usually patients with severe pain or with postherpetic neuralgia.

There is no consensus on the definition of postherpetic neuralgia (PHN). PHN is usually defined as a zoster-related pain that is still present one month after the vesicles have appeared. A period of three to six months has sometimes been seen. Although only a small percentage of herpes zoster patients have longstanding and severe pain, the consequences are serious. Their quality of life is seriously affected, not only by the pain, but also indirectly by fatigue, decreased mobility and social contacts.


Herpes zoster is caused by reactivation of the varicella zoster virus (VZV), which is seen in children and leads to chickenpox. After recovery from chickenpox, the virus settles into the sensory ganglia. As people grow older, virus-specific cellular immunity gradually decreases and, at a certain moment, the virus overcomes the immunity. The virus then spreads from the ganglion via the axon to the skin and leads to the characteristic unilateral shingles rash in one or sometimes several dermatomes. The vesicles contain the virus and are therefore infectious to people who have not yet built up any natural immunity. It is possible that grandparents are the source of their grandchildren's chickenpox. The other way around is impossible because, through contact with chickenpox, immunity is reinforced and the risk of shingles is decreased. The pain accompanying shingles occurs primarily due to inflammation of the sensory nerve. The pathophysiology of PHN is not yet completely understood. At least two processes play a role: sensitisation and deafferentation.

Peripheral sensitization occurs when inflammatory mediators such as substance P, histamines and cytokines reduce the threshold of nociceptors. Central sensitization is associated with an increasing response of neurons in the dorsal horn due to constant stimulation by nociceptive C fibres. Deafferentation can occur by replication of the virus in the cells and/or by the subsequent inflammation reaction. Due to the swelling associated with inflammation, the sensory ganglion is pinched in the intervertebral foramen, resulting in ischemia and damage to the nervous tissue.

Signs and symptoms

Patients with herpes zoster present unilateral symptoms in the dermatomes corresponding to the affected spinal ganglion. As well as pain, they experience paraesthesia, dysesthesia and itching. Moreover, general malaise, fever and headache can occur. These symptoms usually start as a prodrome several days before the appearance of the rash. Dermatome-related pain is described as being burning, throbbing, dull and itchy. Patients with postherpetic neuralgia describe their pain as being a sharp, burning, aching or shooting pain constantly present in the dermatome corresponding to the previous rash. Stimulus-evoked pain, allodynia and hyperalgesia are often present. In these patients, the wearing of clothes is very uncomfortable or even painful.


Physical Examination

In the acute phase, the patient has a typical rash with redness and vesicles in the painful dermatome(s). The healing vesicles show crustae. The rash is generally unilateral and never crosses the midline of the body. Additional sensory abnormalities, such as hypesthesia, hyperalgesia and allodynia, frequently occur. Rarely do patients show a motor deficit. In postherpetic neuralgia, the painful area increases in size and can cross the boundaries of the affected dermatome. In cases of cranial herpes zoster, the neurological examination can determine whether an essential trigeminal neuralgia is involved.

Additional Somatic Diagnostics

In atypical presentation of the skin rash and reoccurring rash in the same zone, an additional blood examination is indicated in order to exclude or confirm the presence of the herpes simplex virus. If dermatome-related pain is present without vesicles, a significant increase in antibodies of the so-called zoster sine herpete can be confirmed.


The aim of the treatment of herpes zoster is: (1) to reduce the severity and duration of pain; (2) to promote recovery of the skin lesions and to prevent secondary infections; and (3) to reduce or prevent postherpetic neuralgia.

The objective of postherpetic neuralgia pain relief treatment is primarily and indirectly related to improved quality of life.

Somatic Treatment

Pharmacological treatment:

Herpes zoster:

  • Antiviral drugs
  • Corticosteroids
  • Analgesics
  • Adjuvant analgesics

Postherpetic neuralgia:

  • Tricyclic anti-depressants
  • Anti-epileptics
  • Tramadol
  • Opioids
  • Local anaesthetics
  • Capsaicin cream

Combination therapies:

  • There is a tendency to use more than one therapeutic class of drug together because of a possible additive or synergistic effect.

Other treatment

Interventional Pain Treatments

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