Sleep-related movement disorder

Buskova J, Vorlova T, Pisko J, Sonka K. Severe sleep-related movement disorder induced by sertraline. Sleep Med 2012 13(6) 769-70. Lange-Asschenfeldt C, Grohmann R, Lange-Asschenfeldt B, Engel RR, Ruther E, Cordes J. Cutaneous adverse reactions to psychotropic drugs data from a multicenter surveillance program. J CKn Psychiatry 2009 70(9) 1258-65. 

Sleep-wake state alterations in PD can be broadly classified into disturbances of (1) thalamocortical arousal state and (2) excessive nocturnal movement (Rye and Bliwise 2004 Rye and Iranzo 2005). The former includes the loss of sleep spindles and SWS, daytime sleepiness, and intrusion of REM sleep into daytime naps (i.e. sleep onset REM periods, or SOREMs), and the latter encompass periodic leg movements of sleep (PLMs) and REM sleep behavior disorder (RBD). The pathophysiological basis of sleepiness and SOREMs appears to be dopaminergic cell loss in PD, though excessive nocturnal movements are not as clearly related to dopaminergic deficits. 

Sleep disorders are common, and are generally underdiagnosed. The two major complaints related to sleep are insomnia ( I can t sleep ) and excessive daytime sleepiness (EDS, I can t stay awake ). EDS is a relatively nonspecific symptom. It can be the end result of any factor that causes sleep disruption, and it can be caused by primary or intrinsic sleep disorders. Insomnia of any cause can result in sleep deprivation and subsequent EDS. The most common cause of EDS in the general population is self-imposed sleep deprivation, or insufficient sleep syndrome. By contrast, the most common causes of EDS seen in a sleep center are primary (intrinsic) disorders of EDS. The American Academy of Sleep Medicine (AASM, formerly the American Sleep Disorders Association) classification of sleep disorders includes over 80 diagnoses that are associated with EDS, but the majority of patients evaluated at sleep centers have sleep apnea, narcolepsy, idiopathic hypersomnia, or periodic limb movements of sleep. 

Nefazodone is unusual amongst antidepressants in that it does not reduce and in fact may increase rapid eye movement (REM) sleep or dream sleep. In a controlled study in depressed patients nefazodone 400 mg/day increased REM sleep, while fluoxetine 20 mg/day produced the opposite effect (3). In addition, nefazodone increased sleep efficiency, while fluoxetine reduced it. The patients subjective assessments of sleep improved more with nefazodone than with fluoxetine. However, the overall antidepressant effects of the drugs were similar. The function of REM sleep and its relation to depressive disorders is not clear, so it is uncertain whether preservation of REM sleep by nefazodone is likely to be of clinical consequence. 

Patients wdth major depressive disorder are reported to have decreased latency to first episode of rapid eye movement (REM) sleep (Kupfer and Foster, 1972). This finding may relate to the hypothesized dysregulation in circadian rhythms found in mood disorders. This interest in circadian rhythms has lead to development of some specific treatments for depression, including sleep deprivation and light therapy. 

A sleep disorder that is not endogenous or due to a medical condition or substance-related condition is categorized as not otherwise specified. Restless leg syndrome and periodic limb movements are two sleep disturbances that do not meet criteria for any of the other sleep disorders. 

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