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NEUROLOGY 1994;44:2174
© 1994 American Academy of Neurology

Cytomegalovirus multifocal neuropathy in AIDS

Analysis of 15 consecutive cases

E. Roullet, MD, V. Assuerus, MD, J. Gozlan, MD, A. Ropert, MD, G. Saïd, MD, PhD, M. Baudrimont, MD, PhD, M. El Amrani, MD, C. Jacomet, MD, C. Duvivier, MD, G. Gonzales-Canali, MD, M. Kirstetter, MD, M.-C. Meyohas, MD, O. Picard, MD and W. Rozenbaum, MD

Departments of Neurology (Drs. Roullet, Assuerus, and El Amrani), Infectious Diseases (Drs. Kirstetter and Meyohas), Virology (Dr. Gozlan), Internal Medicine (Drs. Duvivier, Gonzales-Canali, and Picard), Pathology (Dr. Baudrimont), and Neurophysiology (Dr. Ropert), Hôpital Saint-Antoine, and the Department of Infectious Diseases (Drs. Jacomet and Rozenbaum), Hôpital Rothschild, Paris; and the Department of Neurology (Dr. Saïd), Hôpital Bicêtre, Le Kremlin-Bicêtre, France.

A severe multifocal neuropathy caused by cytomegalovirus (CMV-MN) can occur in the late stage of human immunodeficiency virus (HIV) infection. In a retrospective study, we identified 15 consecutive HIV-positive patients with a diagnosis of CMV-MN based on (1) markedly asymmetric neuropathy, (2) fewer than 100 CD4+ cells per mm3, (3) exclusion of other causes of neuropathy, and (4) characteristic CMV cytopathic changes on neuromuscular biopsy (2 patients), positive CSF culture for CMV (2 patients), or clinical improvement on anti-CMV therapy given for concurrent extraneurologic CMV disease (8 patients) or neuropathy (3 patients). All patients were men and had severe immunosuppression (mean CD4+ cell count, 18 per mm3). The initial symptoms were numbness and painful paresthesias showing a patchy, multifocal distribution. After a mean of 11 weeks (range, 1 to 10 months), the patients developed moderate or severe sensorimotor asymmetric neuropathy. Extraneurologic CMV infection occurred in 10 patients before diagnosis. Electrophysiologic studies showed axonal neuropathy and CMV DNA was present in CSF by the polymerase chain reaction (PCR) technique in 90% of patients tested. Fourteen patients showed a marked improvement 1 to 4 weeks after starting ganciclovir or foscarnet therapy. During follow-up on maintenance therapy (13 patients), the neuropathy relapsed in three patients and probable or confirmed CMV encephalitis occurred in five. Twelve patients died during follow-up, at a mean interval of 9.5 months after their first symptoms. These results extend the clinical spectrum of CMV-MN and show that PCR detection of CMV DNA in CSF may be a useful diagnostic marker.

Address correspondence and reprint requests to Dr. E. Roullet, Service de Neurologie, Hôpital Tenon, 4 rue de la Chine, 75020 Paris, France.

Supported by grants 93010 and 93039 from the Agence Nationale de Recherche sur le SIDA.

Received February 18, 1994. Accepted in final form May 11, 1994.




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