Slowed reaction time in HIV-1-infected patients without AIDS Mellgren A Ê , Norkrans G, Hagberg L, Dunlop O, Wejsta Êl R, Gissle Ân M. Slowed reaction time in HIV-1-infected patients without AIDS. Acta Neurol Scand 2000: 102: 169±174. # Munksgaard 2000. Objectives ± To investigate if HIV-1-infected patients without acquired immunode®ciency syndrome (AIDS) have cerebral dysfunction as re¯ected by impaired reaction times compared to patients with chronic hepatitis C. Material and methods ± Forty-one HIV-1-infected patients not ful®lling the AIDS criteria, were tested with three reaction time tests and compared to controls with chronic hepatitis C, matched according to gender and age. Results ± HIV-1-infected individuals had, in mean, 5±47 ms longer reaction time than patients with hepatitis C (statistically signi®cant in two of three tests). All but 9 HIV-1-infected individuals had, however, reaction times within the normal range de®ned by the control group (meant2 SD). No correlation was found between reaction time and immune status measured as CD4-cell count. Conclusion - This study indicates that a subgroup of HIV-1-infected individuals have slower reaction time compatible with cerebral deterioration early in the course of the infection. A Ê . Mellgren 1 , G. Norkrans 1 , L. Hagberg 1 , O. Dunlop 2 , R. Wejsta Êl 1 , M. Gissle Ân 1 1 Department of Infectious Diseases, Sahlgrenska University Hospital, Go Èteborg, Sweden and 2 Department of Infectious Diseases, Ulleva Êl University Hospital, Oslo, Norway Key words: HIV-1; reaction time; neuropsychological tests; hepatitis C Magnus Gissle Ân, Department of Infectious Diseases, Sahlgrenska University Hospital, SE-416 85 Go Èteborg, Sweden e-mail: magnus.gisslen@infect.gu.se Accepted for publication May 16, 2000 Human immunode®ciency virus type 1 (HIV-1) infects the central nervous system (CNS) early in the course of the disease and establishes a chronic pro- gressive CNS infection (1). Approximately 5±10% of HIV-1-infected patients experience neurological symptoms before any systemic symptoms (2), and up to 80±90% of patients with AIDS show neuro- pathological changes at autopsy (3). Neurological complications are caused either by opportunistic infections and neoplasms, such as cryptococcal meningitis, cerebral toxoplasmosis, progressive multifocal leukoencephalopathy (PML), and CNS lymphoma, or by the HIV-1 infection itself. HIV-1-associated dementia is an AIDS-de®ning condition and the most common neurologic complication caused by HIV-1. Frequencies vary according to the diagnostic criterias used, and reported prevalences have varied from 7% to 40% (4, 5). Many studies have reported a prevalence between 15 and 20% (6±8), but after the introduction of zidovudine treatment, the incidence has decreased to below 10% (5, 9). The incidence of HIV-1-associated dementia among patients on highly active antiretroviral therapy (HAART) is not known, but recent results indicate that HAART does not reduce the incidence of HIV-1-associated dementia as effectively as it reduces the incidence of other AIDS-de®ning ill- nesses (10). HIV-1-associated dementia has three key features, but all three must not be present to indicate the diagnosis. Cognitive impairment, the ®rst feature, includes decline in memory, decreased concentration and attention span, and problems with visual-spatial functions. The second feature is central motor problems, where the ®rst sign may be subtle motor slowing of rapid eye and limb move- ments. Later symptoms include walking dif®culties, action tremor, ataxia, and loss of balance. The third criteria, behavioural changes on an organic basis, is the most dif®cult clinical feature to assess in HIV- 1-associated dementia. It includes a general loss of interest in usual activities, a loss of drive, irritability, apathy, and a sense of ``slowing down'' (11). It is not yet clear if HIV-1 causes functional cerebral impairment in otherwise asymptomatic patients. Neuroradiological, neurological, and psy- chological examinations/investigations give fairly rough measures. To understand the pathogenesis Acta Neurol Scand 2000: 102: 169±174 Printed in UK. All rights reserved Copyright # Munksgaard 2000 ACTA NEUROLOGICA SCANDINAVICA ISSN 0001-6314 169