INTRODUCTION HUMAN AFRICAN TRYPANOSOMIASIS (HAT), KNOWN AS SLEEPING SICKNESS, HAS REEMERGED IN 36 COUNTRIES THROUGHOUT SUB-SAHARAN AFRICA AND IS AN IMPOR- TANT CAUSE OF HUMAN MORTALITY AND MORBIDITY.1 It

HUMAN AFRICAN TRYPANOSOMIASIS (HAT), KNOWN AS SLEEPING SICKNESS, HAS REEMERGED IN 36 COUNTRIES THROUGHOUT SUB-SAHARAN AFRICA AND IS AN IMPORTANT CAUSE OF HUMAN MORTALITY AND MORBIDITY.1 It results from the infectious bite of tsetse flies (genus Glossina), which inoculate protozoan parasites of the Trypanosoma species. The East African form is provoked by Trypanosoma brucei (T. b.) rhodesiense; the West African form by T. b. gambiense. It is estimated that about 50 million people worldwide are at risk of being infected.2 Both diseases affect the central nervous system, with T. b. rhodesiense causing an acute form of neurologic disease, and T. b. gambiense, a more chronically evolutive meningoencephalitis.3 In HAT, the involvement of the nervous system occurs at a late stage of the disease, with the disease being invariably fatal if untreated. The meningoencephalitic stage of HAT is characterized by a number of distinct neurologic symptoms. These include altered sleep patterns and diverse neuropsychiatric disorders including dysesthesia, extrapyramidal motor disturbances, mood disturbances, etc.4,5 Humans suffering from African trypanosomiasis at the stage of meningoencephalitis exhibit 2 specific disturbances: (1) a major disruption of the 24-hour sleep-wake distribution, which worsens with the severity of the disease6-9 and (2) the occurrence of sleep-onset rapid-eyemovement (REM) sleep episodes (SOREM), proportional to the severity of the illness.8,10 A recent report11 postulated that both alterations might be triggered by a serotonergic dysfunction impacting the circadian timing system. Experimental animal infection has been used to investigate the neuropathologic alterations of African trypanosomiasis. However, the correlation with clinical symptoms remains to be clarified, especially regarding sleep and wake alterations. In order to understand such disturbances, a few experimental studies have been conducted in rats.12-15 Continuous 24-hour recordings have revealed a considerable sleep fragmentation during the second week following infection12: changes in sleep-wake stages were numerous, the number of wakefulness and slowwave sleep (SWS) episodes increased, and the infection produced a progressive disruption of the sleep-wake cycle. However, the extent of the disturbances observed in patients with HAT has not been attained in the rat model. More recently, a considerable fragmentation of SWS and a consequent disruption of the SWS-paradoxical sleep (PS) sequence were described 3 weeks after infection.13-15 The purpose of this study was to specify the time course of the disturbances in the sleep-wake cycle and that of the alteration of sleep architecture in infected rats. Electrophysiologic recordings were per-