• L Feller, Y Jadwat, and M Bouckaert.
• Department of Periodontology and Oral Medicine, Medunsa Oral Health Centre, Faculty of Dentistry, University of Limpopo, Medunsa Campus. lfeller@ul.ac.za
• SADJ. 2005 Nov 1; 60 (10): 432, 436-7.

AbstractPost-herpetic neuralgia (PHN) is the most frequent complication of herpes zoster and often results in significant morbidity and a reduction in the patient's quality of life. The peripheral nerve injury that occurs during the acute phase of herpes zoster (HZ) leads to an abnormal tonic impulse discharge from primary nociceptive afferent neurons which induce slow temporal summation. This "wind-up" phenomenon is responsible for continuous partial depolarisation of second-order neurons with increased spontaneous impulse discharge and expanded receptive fields within the dorsal horn nociceptive neurons. The abnormal central processing involves the activation of N-methyl-D-aspartate (NMDA) receptors resulting in neuropathic pain, characterized by spontaneous pain, hyperalgesia and allodynia which is typical of PHN. In addition, tonic input from non-nociceptive AB afferent neurons, maintained by sympathetic efferent activity, contribute to the development and maintenance of neuropathic pain in general, and a burning sensation in particular.

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