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In this chapter, we will review movement disorders in sleep. The disorders reviewed below encompass an extraordinarily wide range of movements and behaviors. For ease of presentation, we have divided this review into movement disorders known to be specific to sleep versus those movement disorders characteristic of wakefulness that may be modulated by sleep. Additionally, we will focus on practical guidelines for treatment that are, in part, driven by anatomic and physiological considerations of movement in sleep, using Parkinson's disease (PD) as the prototypical disorder. The similarity of the sleep-related manifestations of many of these disorders and their assumed common underlying pathophysiology lead to treatment considerations that are parallel, despite heterogeneity of waking clinical disease. It is our belief that the various states of sleep may represent an exquisitely sensitive window on the functional anatomy and pharmacology of the basal ganglia and related structures, which may enhance our knowledge of the mechanisms underlying these conditions.

Much of our knowledge of sleep and movement disorders derives from studies on small groups of patients, including many individual patient reports. There are sparingly few comprehensive studies that (1) evaluate the natural history of disordered sleep in various movement disorders; (2) control adequately for all variables that may confound clinical presentation, including aging, dementia, and affective state; and (3) evaluate response to treatment in a placebo-controlled fashion. This is not surprising, given the existence of multiple interacting variables that hinder identification of homogeneous patient populations. Moreover, complex combinations of pathology in brain regions such as the basal forebrain, raphe nuclei, locus ceruleus, and pedunculopontine nucleus occur in many movement disorders and would be expected to contribute appreciably to the manifestations of most of the conditions discussed below.

To define abnormal quantities or qualities of nocturnal movement, it is first necessary to establish the parameters of what constitutes normal movement during sleep. In some cases (e.g., paroxysmal nocturnal dystonia (PND) or rapid eye movement sleep behavior disorder (RBD)), the pattern and amplitude of movement is clearly abnormal. Conversely, in other cases, either by virtue of the widespread prevalence of a condition (e.g., periodic leg movements in sleep (PLMS)) or its transient expression during development (e.g., somnambulism), defining the limits of normality may be problematic. Undoubtedly, some of the complexity stems from the varying sensitivities of the techniques used to detect movements; that is, can they be documented videographically or do they require more sophisticated detection methods, such as accelerometers (e.g., actigraphy), surface, or even needle electromyography (EMG)? Muscle activity recorded from surface electrodes, as is used in most polysomnographic studies, for example, may reveal some information regarding individual motor units when those units are located closer to the skin surface, but in other situations involving higher threshold force or when the muscle group of interest is further from skin, such surface (EMGs may be insufficient.1 Additionally, determining whether movement in sleep is focal or is a manifestation of a more complex pattern of movement adds ...

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