suppression, resulting in increased nocturnal arousal responses, or constantly occurring waking or a reduced relaxation function (Weeß et al. 1998a/b) and cognitive damage caused by intermittent hypoxia (Montplaisir et al. 1992). As the main symptom is excessive daytime sleepiness (EDS) is considered.
It is also assumed that the OSAS accompanying Insomnia and sleepiness influence cognitive functions (Jennum et al. 1993). As reported by Schwarzenberger et al. (1987) that patients with EDS have complaints and problems in situations of physical rest and during prolonged monotonous concentration tasks. A study by Kales (1985) showed that 76% of OSAS patients have cognitive deficits in the areas of thinking, learning ability, memory, communication and the ability to learn new information. Naegele et al. (1995) were able to establish in Sleep Apnea Syndrome patients that they were reduced at executive functions when these tasks involve the acquisition of information to memory processing. Another study by Cassel et al. (1995) showed that Sleep Apnea Syndrome patients have a reduced non-verbal performance and processing speed. Regarding the central nervous system activation (alertness), selective attention and sustained attention in Sleep Apnea Syndrome patients Kotterba et al. (1998) found, that they were impaired, and that they have a reduced vigilance (Barbe et al. 1998). The cause of cognitive and neuropsychological deficits in the EDS itself, the sleep fragmentation and arousals and nocturnal hypoxemia are discussed (Findley et al. 1986, Greenberg et al. 1987, Guilleminault et al. 1988, Colt et al, 1991, Bedard et al. 1991, Roehrs et al. 1995).
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