Genetic Factors and Sleep

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Alyssa Musa Ali
Reaction Paper #4
4/17/2013

Parkes (1999) reviewed the genetic factors in various human sleep disorders. Specifically, he reviewed the Norrie disease, Prader-Willi syndrome and Moebius syndrome. He suggested how damage to particular neuroanatomical structures in these sleep disorders plays a role in sleep disturbances. Norrie disease is a deletion or point mutation of Xp 11.3-11.4, which leads to a possibility of cataplexy and REM sleep abnormalities by changes in serotonin and peripheral catecholamine levels. Prader-Willi syndrome is a deletion of 15q 11-q13 which results in a failure of hypothalamic development. With the damaged hypothalamus and also damage to the suprachiasmatic nucleus excessive sleepiness during the daytime occurs and many naps at inappropriate times. Lastly, the Moebius syndrome is a deletion of 13q12 caused by teratogen factors that results in a failure of mid-brain development and damage to the high medulla. In addition, Parkes (1999) presents a detail study on a female subject with Moebius syndrome to review the distribution of sleep-wake problems associated with Moebius syndrome. His findings suggest a genetic basis of sleeping and waking. Parkes (1999) suggests that lesions determined by genes result in sleep disturbances. Specifically, thalamic lesions result in insomnia, hypothalamic lesions in central disturbances, mid-brain lesions in parasomnia, and pontine lesions in narcolepsy and loss of REM sleep. The damaged lesions caused by genetic disorders can be related to sleep disturbances because of the projections of specific systems in the reticular formation and the lateralization of functions to certain neuroanatomical structures. The reticular formation is a mass of neurons and nerve fibers that makes the core of the brain stem. It runs through the medulla oblongata, pons and midbrain. One of its many functions is to regulate wakefulness and arousal. Through its ascending arousal system the reticular...
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