Results show stage related prevalence of distal symmetric polyneuropathy already in early stages. In late stages of HIV-infection prevalence of distal symmetric polyneuropathy seems to be directly correlated to immunodeficiency syndrome. The pathogenesis of distal symmetric polyneuropathy during HIV-infection is up to now incompletely understood, but results indicate a clear dependency between progressive immunological dysfunction and neuropathy. High active antiretroviral therapy in patients suffering from distal symmetric polyneuropathy is a main topic of future studies.

OBJECTIVES—A total of 670 patients were screened for distal symmetric HIV‐associated polyneuropathy during CDC stages 1–3 and its correlation to immunological deterioration. MATERIAL AND METHODS—Clinical examinations of 670 patients admitted to the neurological outpatient clinic at the Department of Neurology, University of Munster. Neurophysiological investigations were performed on the sural and peroneal nerve for detection of axonal and myelin lesion. RESULTS—Clinical examination proved progressive clinical signs and symptoms indicating distal symmetric polyneuropathy from CDC 1 (32%) to CDC 3 (55%). At least one neurophysiological result was impaired in CDC 1 in 25% and in CDC 3 in 45%. Significant correlation between neurophysiological changes and CDC 4(+)‐cells and beta‐microglobuline were detected for stage CDC 3 C. CONCLUSION—Results show stage related prevalence of distal symmetric polyneuropathy already in early stages. In late stages of HIV‐infection prevalence of distal symmetric polyneuropathy seems to be directly correlated to immunodeficiency syndrome. The pathogenesis of distal symmetric polyneuropathy during HIV‐infection is up to now incompletely understood, but results indicate a clear dependency between progressive immunological dysfunction and neuropathy. High active antiretroviral therapy in patients suffering from distal symmetric polyneuropathy is a main topic of future studies.

In up to 50% of all human immunodeficiency virus (HIV) patients, the nervous system is clinically involved. Primary or secondary manifestations of the nervous system have been found in even 90% by neuropathological investigations. We present a retrospective analysis of cerebrospinal fluid (CSF) and serum data of 238 HIV patients. Data of cross-sectional analysis in 208 patients and longitudinal analysis in 30 patients are given. In addition, the viral load in CSF and serum was determined in 29 patients. The HIV patients without opportunistic infections showed increased levels of immunoglobulins and more oligoclonal bands. In later stages of the infection, beta-2 microglobulin as a marker of HIV-associated encephalopathy was increased. In the longitudinal study with an observation period of 1 year, an increase could be observed in total CSF proteins of patients who did not receive antiretroviral treatment. In patients with new opportunistic infections of the central nervous system, similar changes in CSF parameters were noted as in comparison to patients not infected by HIV but with the same opportunistic infections. Analysis of CSF is mandatory for the diagnosis and control of opportunistic infections.

Only some patients with HIV-infection receive an adequate pain therapy. In later stages of HIV-infection up to 50% 6 of patients perform extraordinary doctor visits because of pain. Principally primary and secondary neuromanifestations of HIV-infection have to be differentiated. Rare forms of HIV-associated polyneuropathies represent mononeuropathy or mononeuritis multiple acute and chronic inflammatory demyelinating polyneuropathy and polyneuropathy caused by opportunistic infections. HIV-associated distal-symmetric polyneuropathy represents the most common form during HIV-infection with a prevalence up to 50%. Typical clinical symptoms and signs are pain, hyp- and dysaesthesia, diminuted deep tendon reflexes, motor deficits and autonomic disturbances. Always neurological examination and neurophysiologic investigation on the sural and peronaeal nerve are necessary for monitoring progression of polyneuropathy and as basics before starting antiretroviral therapy with neurotoxic substances. According to momentary opinion, HIV-associated distal-symmetric polyneuropathy represents no indication for antiretroviral therapy. Symptomatic therapy includes antiepileptic medication as gabapentine, antidepressive drugs as amitiptyline and additionally retarded opiates. Depressive disorders ma y accentuate pain problems a n d need psychotherapeutic and thymoleptic therapy. Special problems occur when neurotoxic substances evoke or deteriorate polyneuropathy. In these cases an individual therapeutic proceeding about continuation or discontinuation of neurotoxic medication is necessary. Symptoms of myopathy during HIV-infection are muscle pain, elevation of CK and typical changes of motor units detected by electromyography. In most cases biopsy is necessary for diagnosis of specific forms of HN-associated myopathy. HIV-associated polymyositis is treated by non-steroid analgetics, corticoids, immunoglobulines and plasmapheresis, myopathy induced by neurotoxic medication analogous to polyneuropathy.

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