Page 350 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
P. 350

Sleep Disorders
       Normal sleep requires the interplay of several  peptides that are broken down again during
       cerebral structures, among them the loci ceru-  sleep. It is possible that serotonin stimulates
       leus and subceruleus (norepinephrine being  the formation of sleep factors, because inhibit-
       the transmitter), the raphe nucleus (serotonin  ing serotonin formation, release or action (e.g.,
       as transmitter), tractus solitarius nucleus, and  by the antihypertensive drug reserpine) causes
    Systems  neurons in the hypothalamus. A lesion in the  insomnia.
       subceruleus nucleus results in rapid eye move-
                                        The sleep-inducing peptides cause “sleep
       ment (REM) insomnia (see below); lesions in
                                       pressure” (NREM sleep pressure or slow wave
                                       sleep [SWS]; → C1). The net sleep pressure is
       the raphe nuclei or the anterior hypothalamus
    Neuromuscular and Sensory  posterior hypothalamus cause narcolepsy. Ex-  and the reciprocal of the REM sleep pressure
                                       the difference between sleep pressure (violet)
       lead to (transient) insomnia; lesions in the
                                       (green) that follows a circadian rhythm essen-
       citation of the tractus solitarius nucleus (e.g.,
       by gastric distension) causes fatigue. Sleep is
                                       tially in parallel to body temperature and sim-
                                       ilar bodily parameters, such as “readiness for
       also very dependent on the circadian rhythm,
       in that destruction of the central rhythm gen-
                                       activity and effort”. The ability to fall asleep is
                                       a function of this net sleep pressure.
       erator, the suprachiasmatic nucleus (SCN)
                                        When experiencing a change of time zone
       leads to irregular periods of falling asleep and
                                       circadian rhythm at first continues to oscillate
       ated by the ascending reticular activating sys-
                                       in the original phase. When the day is short-
       tem (ARAS), a connection between the reticu-
    10  of difficulty in awakening. The latter is medi-  (jet lag; → C2) or when doing shift work, the
                                       ened, it is impossible to go to sleep at the local
       lar formation via intralaminar nuclei of the
       thalamus to large areas of the brain (→ A). De-  time because of the low net sleep pressure.
       struction of the intralaminar thalamic nuclei  When the day gets longer, the sleep pressure
       (e.g., by ischemia) leads to somnolence. De-  is increased by the longer waking period and
       synchronization between subcortical activity  falling asleep at the local time is no problem.
       and cortical sleep may be the cause of sleep-  The subsequent circadian rhythm, however,
       walking (somnambulism).         causes early awakening.
         Disorders of the regulation of breathing  Falling asleep is also disturbed by delayed
       during sleep have been held responsible for  sleep phase insomnia (→ C3), caused by an in-
       the sudden infant death syndrome (SIDS) and  flexible circadian rhythm that cannot be short-
       sleep apnea in adults. Metabolic alkalosis is  ened. When going to sleep too early the net
       thought to favor sleep apnea. In addition, de-  sleep pressure is too low. During chronother-
       creased muscle tone during sleep promotes  apy a lengthened daily rhythm (27 hours) is
       the collapse of the airways, apnea, and hypox-  forced upon the patient until the desired circa-
       ia.                             dian periodicity has been obtained.
         Normally  one  passes  through  several  Depression (→ C4) possibly reduces the for-
       phases of varying depth during sleep (→ B).  mation of sleep-inducing peptides through a
       During one night there are typically about 5  lack of serotonin (→ p. 350). This results in a
       phases of REM sleep (→ B, marked in red), dur-  decrease in net sleep pressure (red line) and
       ing which bursts of excitation from the brain  difficulty in falling asleep. The sleep pressure
       stem produce twitches in the otherwise hypo-  can be increased by sleep deprivation the next
       tonic musculature. Several phases of non-REM  day, and thus normal sleep can be achieved.
       (NREM) sleep must be passed through before  A raised level of excitement makes falling
       REM sleep is reached, whereby increasing  asleep more difficult and reduces the duration
       depth of sleep correlates with decreasing fre-  of sleep (→ C5). Anxiety about insomnia raises
       quency of the EEG waves. Chronic use of sleep-  this level and is thus counterproductive.
       ing pills leads to lighter NREM sleep and only
       occasional REM phases.
  340    During the awake phases endogenous sleep
       factors accumulate, such as the sleep-inducing
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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