**1. Introduction**

116 Sleep Disorders

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> Sleep is a necessary and reversible behavioural state of perception, cognition, psyche and physical conditions. Abnormal sleep behaviours may include e.g. difficulties in falling asleep, breathing difficulties such as different kinds of apneas, sleep paralysis, hypnagogic hallucinations, sleep onset-REM, leg movements, sleepwalking, sleep talking, tooth grinding and other physical activities. These anomalies involving sleep processes also include sleep itself, dream imagery or muscle weakness.

> Within sleep there are two separate states, non-rapid eye movement (NREM) and rapid eyes movement (REM). REM sleep is defined by EEG activation, muscle atony, and episodic bursts of rapid eye movement. NREM (non-REM) sleep is subdivided into four stages (stages 1, 2, 3 and 4 – Rechtschaffen & Kales) or three stages (N1, N2 and N3 – AASM), which are defined by the electroencephalogram (EEG). The NREM stages are parallel to the depth of sleep continuum (lowest in stage 1 and highest in stage 4 sleep).

> NREM sleep and REM sleep continue to alternate through the night in cyclically. REM sleep episodes become longer across the night, stages 3 and 4 become shorter across the night.

> Sleep disorders have an impact on the structure and distribution of sleep. A distinction is important in diagnosis and in the choice of treatments. There are three very important sleep disorders: Insomnia, Narcolepsy and Sleep Apnea Syndrome.

> Altogether, in Western Europe already suffer more than 10 % of the population from *Sleep-Awake-Disturbances* which has to be treated urgently; 800,000 from Sleep Apnea Syndromes and 25,000 from Narcolepsy (PETER et al. 1995).


The Effects of Sleep-Related Breathing Disorders on Waking Performance 119

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

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. Naëgelé 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 (Barbè 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, Bédard et al. 1991, Roehrs et

Two concepts play a central role, first, the hypoxia and the other the disturbed sleep architecture in the causes of the neuropsychological and/or cognitive deficits in Sleep

Both factors appear usually occur together, so that it is hardly possible to separate the two. Several studies confirm the link between *nocturnal oxygen desaturation* and neuropsychological deficits. Greenberg et al. (1987) showed, for example, that the nocturnal hypoxia is the cause of the neuropsychological deficits and daytime sleepiness. In another study conducted by Findley et al. (1986) showed that there is a correlation between hypoxia during sleep and wakefulness with the degree of cognitive impairment, but not between sleep fragmentation and the cognitive functions. In a study of Kotterba et al. (1998), various neuropsychological parameters correlate with the degree of hypoxia, but not with the arousal index and AHI. Montplaisir et al. (1992) describe the nocturnal hypoxia as the best

For other investigators, the cause of the neuropsychological deficits such as those of daytime sleepiness exist in the *disruption of sleep patterns* or *sleep fragmentation*, accompanied by a reduction in the proportion of REM and slow wave sleep. According to Bonnet et al. (1985) healthy persons' sleep fragmentation leads to neuropsychological impairment. Other researchers such as Telakivi et al. (1988) and Guilleminault et al. (1988) find that sleep fragmentation has an important impact on neuropsychological deficits. This allowed Guilleminault et al. (1988) to conclude in a study that the sleep fragmentation would be the best predictor of the occurrence of daytime fatigue is, and that there is no relationship between daytime sleepiness and respiratory parameters such as RDI or oxygen desaturations. This could confirm also by Colt et al. (1991) in a study. Nocturnal hypoxias were induced during a night under nCPAP therapy and, no effect on daytime sleepiness

**2.1.2 Causes of neuropsychological deficits (Büttner 2001, 2009)** 

predictor for both daytime alertness as well as daytime sleepiness.

sleepiness (EDS) is considered.

al. 1995).

Apnea Syndrome patients.

The exact prevalence of the general population is unknown. Great differences exist in its appearance frequency. So the frequency of Japan is 0.16 % and of Israel 0.0002 %. Central Europe (0.006 %) and the USA (0.06-0.1 %) are located in the middle.

3. *Sleep Apnea Syndromes* (SAS) are common disorders, which are characterized by repeated oropharyngeal occlusions occurring during the sleep time (sleep-related breathing problems, intermittent hypoxemia) and may be associated with suppression of SWS sleep (disrupted and fragmentized sleep architecture). Due to intermittent hypoxemia and disrupted sleep architecture, SAS leads to impaired daytime functioning in various (neuro)psychological and affective domains and has been associated with increased morbidity and mortality, principally from adipositas, cardiovascular and neurological diseases.

The prevalence of moderate SAS (AHI >15/h) is 9% in male and 4% in female, respectively. 25-30 % Sleep Apnea Syndromes were described at patients with hypertension and 35-45 % with patients with on the left heart-failure. The SAS frequency increases with an advancing age and reaches their peak at the age from 50 to 70 years. 80% of the patients suffer under excessive daytime sleepiness and a reduced sustained attention. Resulting from this it comes to performance losses both professional and in the ability to drive motor vehicles.

*Fragmentation of sleep* and *increased frequency of arousals* occur in association with this three disorders and a number of other sleep disorders as well as with medical disorders involving physical pain or discomfort.

In this chapter, the author will describe neuropsychological dysfunctions/courses and neuropsychiatric syndromes due sleep disorders which were characterized by


There are wide varieties of difficulties in assessment, treatment and rehabilitation for cognitive impairment, psychiatric disorders and behavioural disability after sleep disorders.

In our studies we used neuropsychological and neuropsychiatric methods in different patient groups in a sleep laboratory. Over the past five years we have been testing and treating more than 2000 patients with different sleep disorders and more than 5000 neurological patients.

During admission to the clinic, all patients were selected according to their clinical diagnosis (ICD-10) and were examined neurologically, (neuro)psychologically, psychiatrically and medically. The test persons must not suffer from any severe psychiatric disorders. The study was carried out involving randomly selected patients with sleep disorders.
