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NEUROLOGY 1990;40:938
© 1990 American Academy of Neurology

Steroid-responsive myeloneuropathy in a man dually infected with HIV-1 and HTLV-I

J. C. McArthur, MB, BS, MPH, J. W. Griffin, MD, D. R. Cornblath, MD, D. E. Griffin, MD, PhD, T. Tesoriero, MD, R. Kuncl, MD, PhD, C. J. Gibbs, PhD, H. Farzadegan, PhD and R. T. Johnson, MD

Johns Hopkins Medical Institutions (Drs. McArthur, J.W. Griffin, Cornblath, D.E. Griffin, Kuncl, Farzadegan, and Johnson), Baltimore, MD; Kaiser-Permanente (Dr. Tesoriero), Washington, DC; and National Institutes of Health (Dr. Gibbs), NINDS, Bethesda, MD.

Two human retroviruses, HIV-1 and HTLV-I, have been associated with myelopathies in addition to other neurologic disorders. We report an American dually infected with HIV-1 and HTLV-I who developed steroid-responsive myeloneuropathy. This 28-year-old bisexual man developed interstitial pneumonitis and a transient midthoracic sensory level followed by the evolution of a slowly progressive spastic paraparesis and sensorimotor neuropathy. Serologic studies demonstrated coinfection with both HIV-1 and HTLV-I. Peripheral blood absolute CD4 count was persistently within the normal range. Cranial MRI was normal and spinal MRI showed T3-T10 atrophy. Serial CSF analyses demonstrated marked intrathecal synthesis of anti-HTLV-I IgG, lymphocytic pleocytosis, elevated protein and immunoglobulin G, and oligoclonal bands. HIV-1 was isolated from CSF but not from peripheral nerve. Lymphoproliferative studies confirmed spontaneous proliferation in both blood and CSF. Soluble interleukin 2 receptor and soluble CD8 were greatly elevated in blood and CSF when compared with patients with HIV-related vacuolar myelopathy and seronegative patients with other causes of myelopathy. Nerve biopsy showed epi- and endoneurial CD8+ lymphocytic infiltration without vasculitis; muscle biopsy showed features of acute and chronic denervation. A 6-week course of prednisone produced sustained improvement in leg strength and walking times. We speculate that the myeloneuropathy was caused by HTLV-I in the setting of coinfection with HIV-1.

Address correspondence and reprint requests to Dr. Justin McArthur, Johns Hopkins Hospital, 600 N. Wolfe Street, Meyer 6-109C, Baltimore, MD 21205.

Supported by National Institutes of Health contract AI 72634, grants NS 23936 and NS 26643, and the OP GCRC 5M01RR00722.

Presented in part at the 41st annual meeting of the American Academy of Neurology, Chicago, IL, April 1989.






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