• Panagiotis Kokotis, Martin Schmelz, Georgios K Papadimas, Elias E Skopelitis, Kyriaki Aroni, Theodore Kordossis, and Nikolaos Karandreas.
• Department of Neurology, Aeginition Hospital, Medical School of Athens, Athens, Greece. pkokotis@med.uoa.gr
• Clin Neurophysiol. 2013 Jan 1;124(1):176-82.

ObjectiveTo investigate the underlying mechanisms of polyneuropathy induced by HIV infection or antiretroviral drugs.MethodsWe tested 100 HIV patients (59 with AIDS). Ninety-three patients received antiretroviral drugs. Forty-four were treated with neurotoxic compounds (ddI, ddC, d4T). Nerve conduction velocities and the sympathetic skin response (SSR) in palms and soles were measured in all patients. In skin biopsies (ankle and thigh), the intraepidermal nerve fiber density (IENFD) and the number of epidermal fibers without contact to the basal membrane (fragments) were quantified using PGP9.5 staining.ResultsSeverity of the disease (CD4 +count) correlated to conduction velocities of peroneal (p < 0.01, Spearmans rank correlation), sural (p < 0.01) and median nerves (p < 0.05/p < 0.001, sensory/motor). In contrast, the duration of neurotoxic treatment did not impair conduction velocities (p > 0.3) but correlated to reduced IENFD in the ankle (r = -0.24, p < 0.05). Despite their reduced IENFD, patients with long neurotoxic treatment had a high number of fragments irrespective of their CD4 +count.ConclusionsNeurotoxic treatment appears to primarily impair thin fiber conduction, whereas HIV neuropathy is linked to large fiber impairment and reduction of fragments of nerve fibers.SignificanceThese findings emphasize the differential pattern of polyneuropathy in HIV patients caused by the infection or induced by antiretroviral treatment.Copyright © 2012 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

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