I / Human Immunodeficiency Virus Type l-related Transient Neurological Deficits Bruce J. Brew, MBBS, MD, John Miller, RN, MN, Sydney, Australia PURPOSE: To characterize human immunodeficiency virus type 1 (HIV-1)-related transient neurological deficit (TND). DESIGN: A 3-year prospective study based at a tertiary referral center. METHODS: Patients with TND in the absence of an opportunistic infection, neoplasm, neurosyphilis, or seizure were recruited and further investigated. The frequency of hospital admission for these patients was compared with those who were HIV-1 seronegative and with those who were admitted for HIV-l-related thromboembolic events. RESULTS: Twenty-seven patients were identified: mean age of 39 ? 9 years; CD4+ cell count of 130 + 80/pL. Seven patients had no history of an AIDS-defining illness. Hemiparesis and hemisensory disturbance occurred in 23 patients (85%); 15 had preexisting ADC, 7 stage 1 and 8 stage 2; 3 developed ADC after 18 months. Thirteen patients had multiple attacks and 5 had more than 20; 2 patients developed a cerebral infarct. No cause for the TND was identified in 8 patients (30%). Anticardiolipin antibodies were found in 70% and low protein S levels in 53%, which was significantly more often than in a neurologically normal group with similarly advanced HIV-1 disease. The frequency of admission was 0.8% whereas the frequency for similar TND in HIV-l- seronegative patients was 0.4% and the frequency for HIV-l-related thromboembolic events was 0.9%. CONCLUSIONS: Transient neurological deficits occur in advanced HIV-1 disease and are often associated with ADC, elevated concentrations of anticardiolipin antibodies, and low protein S levels. Future studies will need to define the precise role of these associations in the I I From the Department of HIV Medicine, Centre for Immunology (JMI, Department of Neurology, St Vincent’s Hospital, and the Nahonal Centre In HIV Epidemrology and Clinical Research, Darlinghurst, Sydney, Austra- lia. Reauests for reorints should be addressed to Associate Professor B. J. Brew, National Centre in HIV Epidemiology and Clrnical Research, 376 Vrctoria St, Darlinghurst, Sydney, Australra 2010. Manuscript submrtted December 13, 1995 and accepted In rewed form May 9, 1996. ~C~l996 by Excerpta Medica, Inc. All rights reserved. pathogenesis of HIV-l-related TND. Am J Med. 1996;101:257-261. T ransient neurological deficit (TND) occurs oc- casionally in human immunodeficiency virus type 1 (HIV-l) infected patients. Commonly recog- nized causes include toxoplasmosis, cryptococcal meningitis, and lymphoma.’ However, in one retro- spective series more than half of the 25 patients had none of the latter causes identified.’ Thus far no study has prospectively focused on patients without an infective or neoplastic cause for the TND. More- over, the relationship between TND and AIDS de- mentia complex (ADC) has not been explored in viva despite autopsy evidence that approximately half of the patients with evidence of cerebral infarc- tion also had HIV-l -related multinucleated giant cell encephalitis,’ the pathological hallmark of moderate and severe ADC. We therefore embarked upon a pro- spective study to determine (1) the clinical charac- teristics of such TND in an HIV-l-infected popula- tion, including the relationship between TND and ADC; and (2) the frequency of TND among the HIV- l-infected patients who were admitted to hospital compared with TND in the non-HIV-l-infected pa- tients who were also admitted to hospital, and the frequency of thromboembolic phenomena in the same HIV-l -infected population. METHODS Patients were prospectively identified over a 3- year period. To be included in the study all of the following criteria had to be fulfilled: ( 1) occurrence of a neurological deficit lasting less than 24 hours, (2) no evidence of a seizure in relation to the TND as determined by history and electroencephalogram (EEG) , (3) no evidence of an abnormality on con- trast-enhanced computed tomography (CT) brain scan except for cerebral atrophy, (4) no evidence of a positive serum cryptococcal antigen, and (5) no evidence of syphilis by negative serology for VDRL and ETA. The characterisbcs of the TND were re- corded along with the degree of advancement of HIV-l disease by analysis of the CD4+ cell count in the peripheral blood and the presence and severity of ADC. Patients were diagnosed as having ADC if they had characteristic neurological symptoms, signs, and neuroimaging findings with other causes of dementia excluded.’ The severity of ADC was OOOZ-9343,'96/$15.00 257 PII SOOOZ-9343(96)00123-4