The peculiarities of sleep in Parkinson disease have been extensively studied. Many patients in the early stages of the disease complain of fragmented and unrestful sleep, particularly in the early morning hours; some advanced cases have pathologic insomnia, and this is influenced also by medications used to treat the disease and by deep brain stimulation (see Chap. 39 for a discussion of the nonmotor effects of Parkinson disease). The loss of natural body movements and the alerting effects of l-dopa contribute to the insomnia. The directly acting dopaminergic agonist drugs used for the treatment of Parkinson disease may have the side effect of a pronounced and often rapid daytime sleepiness; however, a similar problem arises in some patients with advancing disease alone. The disturbed sleep patterns in patients with Alzheimer disease, Huntington chorea, olivopontocerebellar degeneration, and progressive supranuclear palsy have attracted attention by neurologists (Parkes). Dreaming is also said to be absent in some of these conditions.
In striatonigral degeneration (multiple system atrophy), Lewy-body disease, and other parkinsonian syndromes, there is often a characteristic REM sleep disorder, in which the patient moves and speaks violently and aggressively during dreaming. This “REM sleep behavior disorder” (RSBD, RBD) is discussed further on but here it is commented that the movements may be so extreme as to injure the bed partner and it is often that individual who reports the nighttime behavior. The sleep disorder is often a premonitory feature of the neurologic disease by months or years (see later in this chapter and Chap. 38).
Migraine, cluster headaches, and paroxysmal hemicrania all have been linked to certain sleep stages and are discussed in Chap. 9 in relation to other forms of “hypnic headaches.”
Disorders of Sleep Associated With Changes in Circadian Rhythm
Sleep is also disturbed and diminished when the normal circadian rhythm of the sleep–wake cycle is exogenously altered. This is observed most often in shift workers, who periodically change their work schedule from day to night, and as a result of transmeridian air travel—that is, jet lag (Baker and Zee). Eastbound travelers fall asleep late and face an early sunrise. The consequent fatigue is a product of both sleep deprivation and a phase change required by changing time zones. A review of the subject can be found by Sack. One antidote is to reset one’s watch on the plane and conform to the routine of the destination—that is, to stay awake all day until the usual evening hour for sleep—and to take a short-acting sedative at bedtime. Melatonin is also used for this purpose, and a meta-analysis by Herxheimer and Petrie of four trials suggests it is slightly effective. These measures facilitate the resetting of the circadian rhythm. Westbound travelers face a late sunset and a long night’s sleep and adjust more readily to resetting of the circadian rhythm than do those traveling east. Exposure to light during the extended day is helpful in entraining the sleep cycle; this adjustment is also accomplished more easily when traveling west than east. Shifting of the circadian rhythm in animals suggests that brief exposure to light at crucial times effectively resets the sleep–wake cycle; apparently, the period just before 4 a.m. is a nodal time for susceptibility to this phase change. The sleep problems caused by shift work are more complicated (see Monk).