Axonal excitability in viral polyneuropathy and nucleoside neuropathy in HIV patients
- 1Royal North Shore Hospital, University of Sydney, Sydney, Australia
- 2St Vincent's Hospital, University of New South Wales, Sydney, Australia
- 3Royal Prince Alfred Hospital, University of Sydney, Sydney, Australia
- Correspondence to Dr Karl Ng, Department of Neurology and Clinical Neurophysiology, Royal North Shore Hospital, St Leonards, Sydney, NSW 2065, Australia;
Contributors All authors contributed to the conception, collection of data, analysis and write-up.
- Received 13 December 2009
- Revised 31 March 2010
- Accepted 5 May 2010
- Published Online First 16 July 2010
HIV infection is associated with several forms of peripheral neuropathy, the most common being a distal symmetrical polyneuropathy due to HIV infection (‘DSP’). Direct viral effects are an important cause (hereafter termed viral neuropathy (VN)), but sometimes, it is due to nucleoside antiretroviral drug therapy (nucleoside neuropathy (NN)). Mechanisms of disease are incompletely understood, with some evidence implicating HIV envelope glycoprotein gp120 mediated neuronal apoptosis for the former and mitochondrial toxicity±DNA polymerase γ involvement in the latter. The authors studied 16 HIV positive patients, 14 of whom had neuropathy (10 VN; 4 NN), clinically, with conventional nerve-conduction studies (NCS), and with measurements of the excitability of motor and sensory axons in the median nerve. Clinically neuropathic patients were all symptomatic, and 12 had abnormalities in NCS. There were no changes in the excitability of sensory or motor axons in VN, but there were in the NN group. These were consistent with depolarisation of the internodal membrane (‘fanned in’ threshold electrotonus, increased resting current–voltage slope, reduced superexcitability) but with sparing of nodal properties (absolute threshold, strength–duration properties, refractoriness). Membrane abnormalities in VN are not diffuse and are likely to result from a more focal process, presumably proximal, while those in NN most likely relate to mitochondrial dysfunction. Confirmation of these findings may allow neurophysiological distinction between these entities.
Funding National Health and Medical Research Council of Australia, Pfizer Australia Neurosciences Research Grant; The Brain Foundation of Australia.
Competing interests None.
Patient consent Obtained.
Ethics approval Ethics approval was provided by the Northern Sydney Central Coast Health Human Research Ethics Committee.
Provenance and peer review Not commissioned; externally peer reviewed.