tion, 3% with paranodal demyelination, and 5% with seg- mental demyelination; and 8% of the fibers exhibited axonal degeneration, most at a late stage of wallerian degeneration. Prednisone, 1 mg/kg/day, was prescribed. zyxwvuts Six weeks later the patient walked better and his strength had improved. zyxwvu Discussion These observations show that peripheral nerves may be affected in HTLV-l-associated myelopathy, zyxwvu as sus- pected clinically when decreased Achilles tendon re- flexes coexist with spasticity of the legs and extensor plantar responses [4]. Our patient did not have clear clinical evidence of neuropathy, but electrophysiolog- ical study showed a mixture of axonal and demyelin- ating neuropathy with denervation, prolonged F-wave latency, reduced conduction velocity, and conduction block. The electrophysiological data, which suggest a multifocal mixed axonal and demyelinating process, are in agreement with the morphological data, which showed a slowly progressive, mixed, demyelinating and axonal neuropathy of inflammatory origin with cel- lular infiltrates predominating in the epineurium, espe- cially around blood vessels. The inflammatory lesions observed in the nerve specimen of this patient were similar to those found in the central nervous system of patients with tropical myelopathy (see review in [4}), and both probably result from infection with HTLV-I. These abnormalities are also comparable to those found in patients with inflammatory neuropathy associ- ated with infection with the human immunodeficiency virus zyxwvutsrqp {8], the agent causing the acquired immunodefi- ciency syndrome and a virus that belongs to the same family of retroviruses as HTLV-I. It is not clear whether the lesions observed in both the peripheral and the central nervous systems of some patients infected with HTLV-I result from the cyto- pathic effect of the virus itself or from the inflamma- tory and immune responses induced by penetration of the virus into the nervous system. The presence of lesions accessible to nerve biopsy in such patients may allow progress on the subject. Improvement of the patient's condition by treatment with steroids, a treat- ment that has also been found to be beneficial by others [5-71, indicates that the inflammatory lesions play an important role in HTLV-I-associated myelopa- thy. References 1. Gessain A, Barin F, Vernant JC, et al. Antibodies to human T-lymphotropic virus type I in patients with tropical spastic paraparesis. Lancet 1985;2:407-410 2. Rodgers-Johnson P, Gaidusek DC, Morgan OStC, et al. HTLV-I and HTLV-I11 antibodies in tropical spastic paraparesis. Lancet 3. Roman GC, Schoenberg BS, Madden DL, et al. Human T- lymphotropic virus type I antibodies in the serum of patients with tropical spastic paraparesia in the Seychelles. Arch Neurol 1985;2:1247- 1248 1987;44:605-607 4. Roman GC. Retrovims-associated myelopathies. Arch Neurol 1987;44:659-663 5. Osame M, Usuku K, Izumo S, et al. HTLV-I associated my- elopathy: a new clinical entity. Lancet 1986;1:1031-1032 6. Osame M, Matsumoto M, Koichiro U, et al. Chronic progressive myelopathy associated with elevated antibodies to human T- Lymphorropic virus type I and adult T-cell leukemialike cells. Ann Neurol 1987;21:117-122 7. Miyai I, Saida T, Fujita M, et al. Familial cases of HTLV-I- associated rnyelopathy. Ann Neurol 1987;22:601-605 8. Lipkin WI, Parry G, Kiprov D, Abrams D. Inflammatory neurop- athy in homosexual men with lymphadenopathy. Neurology 1985;35:1479-1483 Oligoclonal I& Bands in Cerebrospinal Fluid and Serum During Asvmmomatic Human z d I Immunodeficiency Virus Infection L. M. E. Grimaldi, MD,* A. Castagna, MD,t A. Lazzarin, MD,P R. Pristera, MD,S G. Bianchi, MD,$ M. Moroni, MD,t and R. P. Roos, MD" Serum and cerebrospinal fluid (CSF) samples from asymptomatic patients seropositive for human immuno- deficiency virus (HIV) showed frequent evidence of in- trathecal IgG synthesis and oligoclonal IgG bands, with different isoelectric focusing patterns in serum and CSF; 2 of 7 had zyxw a CSF pleocytosis. The results suggest fre- quent, early, chronic central nervous system infection following HIV infection. Grimaldi LME, Castagna A, Lazzarin A, Pristera R, Bianchi G, Moroni M, Roos RP. Oligoclonal IgG bands in cerebrospinal fluid and serum during asymptomatic human immunodeficiency virus infection. Ann Neurol 1988;24:277-279 Many questions remain concerning the pathogenesis of the neurological syndromes seen in acquired immuno- deficiency syndrome (AIDS), and especially AIDS de- mentia complex. We studied asymptomatic persons who tested positive for human immunodeficiency virus From the *Department of Neurology, University of Chicago, the ?Institute of Infectious Diseases, University of Milan, the SSezione Malattie Infettive, Ospedale Regionale Bolzano, and the §Laboratorio di Analisi, Istituto Neurologico C. Besta, Milan, Italy. Received Dec 7, 1987, and in revised form Mar 11, 1988. Accepted for publication Mar 12, 1988. Address correspondence to Dr Roos, Department of Neurology, Box 425, University of Chicago, 5841 South Maryland Ave, Chicago, IL 60637. Copyright zyxwv 0 1988 by the American Neurological Association 277