Postherpetic Neuralgia

The most common sites associated with postherpetic neuralgia are the cranial nerve and cervical and thoracic spine most predominantly the fourth to sixth dermatomes. The pain may range from sharp, stabbing to burning. Many patients also complain of allodynia. The other sensory modalities are usually affected within the dermatome, with diminished vibration, tactile and thermal sensation. There are usually scars along the affected dermatome, making the diagnosis less complicated [6].

Laboratory tests

The diagnosis is usually straight forward with no need for many laboratory studies. There is usually a history of preceding herpes zoster with persistence of the pain after resolution of the rash. It may be necessary to find out the predisposing factors such as suspected human immunodeficiency virus infection, but the cause may also be obvious such as age or chemotherapy.

Imaging

Magnetic resonance imaging of the spinal level of the affect dermatome may reveal lesions, but these lesion are present even in patients whose pain does not persist [7].

A number of medications have been used to treat the pain in postherpetic neuralgia including tricyclic antidepressants such as amitriptyline. Anticonvulsants, particularly gabapentin and pregabalin have also been tried and shown to be effective in controlling the pain.

Opioids have been shown to work well but the prolonged use has the risk of addiction, physical and psychological dependence. Topical agents such as capsaicin have been used with poor results currently due to its intolerability. Other tropical agents used include topical lidocaine, but data is sparse, but the little that is there shows it may be of some benefit.

Intrathecal glucocorticoids, have been used when other modalities have failed (in non-cranial neuralgia). The last options include cryotherapy of the affected nerves and surgery with variable results [8] [9] [10].

Postherpetic neuralgia is a condition that is slow to resolve, but most of the patients will respond to first line treatment with tricyclic antidepressants. A few will have refractory pain requiring more radical measures.

The virus is called human herpesvirus-3, more commonly known as varicella zoster virus or VZV. It is a double-stranded DNA virus of the herpesvirales order. After initial infection the virus remains dormant within the dorsal root ganglia until it reactivates causing herpes zoster. Most common areas of latency being the trigeminal nerve, cervical and thoracic spine [2].

The incidence rates increase with age, and with increasing impairment of immunity. The incidence in people below 20 years of age is low with a rate of 1 per 1000 and the rates in the above 80 group reaching 1 per 100. It is very common in immunocompromised patients such as patients on steroids and chemotherapy. It is also has high rates in patients suffering from human immunodeficiency virus (HIV) infection. Severe emotional stress and malnutrition are also recognised risk factors [3].

Herpes zoster (shingles) is caused by reactivation of the latent varicella zoster virus after persistence within the dorsal root ganglia. The reason for the reactivation being decreased immunity (primarily cellular immunity) due to various causes with age being the most common.

The activated virus uses the nerves transport system causing a painful neuritis, associated with a characteristic rash along the dermatome of the supplying nerve. After resolution of the rash the pain usually subsides. In those who the pain persists it is thought that there are changes to the dorsal root ganglion nerves, sensitizing them and resulting in spontaneous activity thus maintaining the continuing pain. There have been theories that persistent viral replication within the neurons causes the persistent pain [4] [5].

Early treatment of the acute herpes zoster with antivirals has shown to be beneficial. Vaccination against the varicella zoster virus to prevent initial infection has been shown to reduce the incidence of the condition.

The neuropathic pain of postherpetic neuralgia may be severe and persistent enough to significantly decrease the quality of life, with interference of normal daily activity and sleep. The pain may persist from months to years and may recur even in successfully treated patients. Postherpetic neuralgia may be very challenging to treat.

There is variability in the definitions of postherpetic neuralgia, but the most agreed upon is persistence or recurrence of pain after the acute rash of herpes zoster subsides. Others defined it as pain persisting for four months from the initial onset of the rash.

Definition: Postherpetic neuralgia is a disease that occurs after a shingles attack. Shingles is a painful rash that occurs along a nerve and usually looks like a band. The pain may be persistent and last up to years. It is common in the older population.

Cause: It is caused by the chicken pox virus (varicella zoster virus). After the initial infection with chicken pox usually in childhood, the virus goes into a dormant state and hides within the nerves usually near spinal cord. When there is a drop in immunity the virus reactivates and causes shingles which may then cause postherpetic neuralgia.

Symptoms: The predominant symptom is pain which may range from burning to stabbing in nature and this pain may persist for years and affect daily activities and sleep.

Diagnosis: The diagnosis may be made by a doctor after listening to the history and usually does not require many investigations to confirm the diagnosis. The doctor may ask for a magnetic resonance imaging (MRI) of the spine to rule out other causes.

Treatment: The treatment includes medications to control the pain. Some of the medications used are the same medications used to treat depression and epilepsy. Most patients respond to these medications, but the response may be slow and more than one type of medication may have to be used to control the pain.

1. Dworkin RH, Portenoy RK. Pain and its persistence in herpes zoster. Pain 1996; 67:241.
2. Burke BL, Steele RW, Beard OW, et al. Immune responses to varicella-zoster in the aged. Arch Intern Med 1982; 142:291.
3. Helgason S, Petursson G, Gudmundsson S, Sigurdsson JA. Prevalence of postherpetic neuralgia after a first episode of herpes zoster: prospective study with long term follow up. BMJ 2000; 321:794.
4. Woolf CJ. Recent advances in the pathophysiology of acute pain. Br J Anaesth 1989; 63:139.
5. LaMotte RH, Shain CN, Simone DA, Tsai EF. Neurogenic hyperalgesia: psychophysical studies of underlying mechanisms. J Neurophysiol 1991; 66:190.
6. Gilden D, Nagel MA, Mahalingam R, et al. Clinical and molecular aspects of varicella zoster virus infection. Future Neurol. Jan 1 2009;4(1):103-117
7. Haanpaa M, Dastidar P, Weinberg A, et al. CSF and MRI findings in patients with acute herpes zoster. Neurology. Nov 1998;51(5):1405-11
8. Argoff CE. Review of current guidelines on the care of postherpetic neuralgia. Postgrad Med 2011; 123:134.
9. Moore RA, Wiffen PJ, Derry S, McQuay HJ. Gabapentin for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2011
10. Dubinsky RM, Kabbani H, El-Chami Z, et al. Practice parameter: treatment of postherpetic neuralgia: an evidence-based report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2004; 63:959.