Articles: neuralgia.
-
A double-blind, randomized, placebo-controlled trial was conducted to study the analgesic efficacy of the NMDA (N-methyl-D-aspartate) receptor antagonist memantine (1-amino-3,5-dimethyladamantane hydrochloride) in relieving postherpetic neuralgia (PHN). Memantine (or an identical-looking placebon=12/group) was administered at a dose of 10 mg/day for one week, and 20 mg/day for an additional 4 weeks. All patients were required to record their pain level twice daily during the entire study period, with the use of a 0-10 numerical pain scale (NPS). ⋯ Although three patients were withdrawn from the memantine group and only one from the control group, no differences in incidence of adverse effects between the two groups were found. Study results show that memantine is ineffective in reducing spontaneous and evoked pain in patients with PHN. Copyright 1998 European Federation of Chapters of the International Association for the Study of Pain.
-
Comparative Study Clinical Trial
[Neuralgia and zovirax treatment of patients with herpes zoster].
To estimate the occurrence of postherpetic neuralgia (PHN) arising after acute period of herpes zoster (HZ) and determination of zovirax efficiency in PHN prevention. ⋯ Zovirax is effective and safe in preventing PHN in HZ patients.
-
Several pathophysiological mechanisms may be responsible for initiation and maintenance of chronic postherpetic pain. (1) Peripheral nociceptive fibers can develop abnormal sensitization. Secondary to this, central nociceptive "second-order" neurons in the spinal cord dorsal horn can also be sensitized, i.e. they become hyperexcitable and start responding to non-noxious stimuli. (2) Degeneration of nociceptive neurons may trigger anatomical sprouting of low-threshold mechanosensitive terminals to form connections with central nociceptive neurons and may subsequently induce functional synaptic reorganization in the dorsal horn. According to these mechanisms theoretical possibilities of therapeutical interventions to prevent postherpetic neuralgia are (1) adequate analgesia in the acute phase (analgesics, antidepressants, sympathetic blocks) and (2) prevention of C-fiber degeneration by reducing the inflammatory reaction (antiviral drugs, corticosteroids, neurotrophins). ⋯ Although there is no clear evidence in favor of a prevention of postherpetic neuralgia for any of the interventions, it is definitely reasonable to perform the best analgesia possible during the acute phase of herpes zoster.
-
To our knowledge, this is the first report on pain-related abnormalities of the eye blink reflex (BR) in a clinical pain patient population. The objective of this study was to evaluate the possible neuropathic mechanisms underlying the burning mouth syndrome (BMS), by means of objective electrophysiological examination of the trigemino-facial system. We studied the BR with stimulation of the supraorbital nerve (SON) with particular emphasis on the occurrence of the pain-related ultralate R3 components, and the habituation response of the R2 components. ⋯ In two of these patients, the findings were segmental (i.e., unilateral), coinciding with the side of the subjective BM symptoms. The abnormalities of the BR tests appeared to be related to longer disease duration. Our results suggest a possible pathologic involvement of the nervous system in chronic BMS.
-
Clinical Trial Controlled Clinical Trial
Afferent large fiber polyneuropathy predicts the development of postherpetic neuralgia.
Acute zoster infection may be followed by a chronic pain syndrome, i.e., postherpetic neuralgia (PHN). Besides older age, the intensity of pain and neuronal damage within the acutely affected body region are regarded as predictors or risk factors for PHN. As an alternative approach an underlying peripheral polyneuropathy may be considered as potential co-factor. ⋯ Nociceptive C-fiber and parasympathetic fiber function demonstrated no significant differences in both groups. Acute zoster pain was slightly more intense in the PHN group. We concluded that (i) a mild generalized impairment of afferent A beta-fiber function (A beta-polyneuropathy) seems to be an important co-factor in the development of PHN and (ii) impairment of vibration sense, i.e., impairment of afferent A beta-fiber function, may be used as a predictor of PHN.