Postherpetic neuralgia is an exceptionally drug-resistant neuropathic pain. To investigate the pathophysiological mechanisms underlying postherpetic neuralgia we clinically investigated sensory disturbances, pains and itching, with an 11-point numerical rating scale in 41 patients with ophthalmic postherpetic neuralgia. In all the patients we recorded the blink reflex, mediated by non-nociceptive myelinated A beta-fibers, and trigeminal laser evoked potentials (LEPs) related to nociceptive myelinated A delta- and unmyelinated C-fiber activation. We also Sought possible correlations between clinical sensory disturbances and neurophysiological data. Neurophysiological testing yielded significantly abnormal responses on the affected side compared with the normal side (P < 0.001). The blink reflex delay correlated with the intensity of paroxysmal pain, whereas the A delta and C-LEP amplitude reduction correlated with the intensity of constant pain (P < 0.01). Allodynia correlated with none of the neurophysiological data. Our study shows that postherpetic neuralgia impairs all sensory fiber groups. The neurophysiological-clinical correlations suggest that constant pain arises from a marked loss of nociceptive afferents, whereas paroxysmal pain is related to A beta-fiber demyelination. These findings might be useful for a better understanding of pain mechanisms in postherpetic neuralgia. (C) 2008 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Truini, A., Galeotti, F., Haanpaa, M., Zucchi, R., Albanesi, A., Biasiotta, A., et al. (2008). Pathophysiology of pain in postherpetic neuralgia: A clinical and neurophysiological study. PAIN, 140(3), 405-410 [10.1016/j.pain.2008.08.018].

Pathophysiology of pain in postherpetic neuralgia: A clinical and neurophysiological study

GATTI, ANTONIO;
2008-01-01

Abstract

Postherpetic neuralgia is an exceptionally drug-resistant neuropathic pain. To investigate the pathophysiological mechanisms underlying postherpetic neuralgia we clinically investigated sensory disturbances, pains and itching, with an 11-point numerical rating scale in 41 patients with ophthalmic postherpetic neuralgia. In all the patients we recorded the blink reflex, mediated by non-nociceptive myelinated A beta-fibers, and trigeminal laser evoked potentials (LEPs) related to nociceptive myelinated A delta- and unmyelinated C-fiber activation. We also Sought possible correlations between clinical sensory disturbances and neurophysiological data. Neurophysiological testing yielded significantly abnormal responses on the affected side compared with the normal side (P < 0.001). The blink reflex delay correlated with the intensity of paroxysmal pain, whereas the A delta and C-LEP amplitude reduction correlated with the intensity of constant pain (P < 0.01). Allodynia correlated with none of the neurophysiological data. Our study shows that postherpetic neuralgia impairs all sensory fiber groups. The neurophysiological-clinical correlations suggest that constant pain arises from a marked loss of nociceptive afferents, whereas paroxysmal pain is related to A beta-fiber demyelination. These findings might be useful for a better understanding of pain mechanisms in postherpetic neuralgia. (C) 2008 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
2008
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/41 - ANESTESIOLOGIA
English
Blink reflex; Laser evoked potentials; Neuropathic pain; Postherpetic neuralgia
Truini, A., Galeotti, F., Haanpaa, M., Zucchi, R., Albanesi, A., Biasiotta, A., et al. (2008). Pathophysiology of pain in postherpetic neuralgia: A clinical and neurophysiological study. PAIN, 140(3), 405-410 [10.1016/j.pain.2008.08.018].
Truini, A; Galeotti, F; Haanpaa, M; Zucchi, R; Albanesi, A; Biasiotta, A; Gatti, A; Cruccu, G
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/38486
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