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Disorders of Sleep Due to Neurologic Disease
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Many neurologic conditions seriously derange the total amount and patterns of sleep (see Culebras) Lesions in the upper pons, near the locus ceruleus, are particularly prone to do so Markand and Dyken have described cases of pontine infarction with involvement of the tegmental raphe nuclei; the clinical abnormality took the form of diminished NREM sleep and near abolition of REM sleep lasting for weeks or months Bilateral lacunar infarctions in the pontine tegmentum, demonstrable by magnetic resonance imaging (MRI), also appear to be the basis of some instances of the socalled REM sleep behavior disorder (Culebras and Moore) described further on, with the other parasomnias Bilateral paramedian thalamic infarctions are a potent cause of hypersomnia, the result of disruption of both arousal mechanisms and NREM sleep (Bassetti et al) Medullary lesions may affect sleep by altering automatic ventilation; the most extreme examples occur with bilateral tegmental lesions that may completely abolish breathing during sleep ( Ondine s curse, as described in Chap 26) Lesser degrees of tegmental damage as might occur with Chiari malformations, unilateral medullary infarction, syringobulbia, or poliomyelitis may cause sleep apnea and daytime drowsiness Patients with large hemispheric strokes may also be left with daytime lethargy on the basis of inversion of sleep-wake rhythm Certain instances of mesencephalic infarction that are characterized by vivid visual hallucinations (peduncular hallucinosis) may be associated with disruption of sleep Von Economo encephalitis, now an extinct illness, was usually associated with a hypersomnolent state but caused persistent insomnia in some instances The latter was related to a predominance of lesions in the anterior hypothalamus and basal frontal lobes, in distinction to hypersomnia, which was related to lesions mainly in the dorsal hypothalamus and subthalamus This subject and other forms of hypersomnia are elaborated further on, under Excessive Sleep A remarkable illness termed fatal familial insomnia has
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been described by Lugaresi and colleagues This disorder, with onset in middle age and a clinical course of 7 to 36 months, is characterized by a virtual incapacity to sleep and to generate EEG sleep patterns The cerebral changes consist mainly of profound neuronal loss in the anterior or anteroventral and mediodorsal thalamic nuclei These cases are thought to represent a familial form of prion disease similar to diseases that cause subacute spongiform encephalopathy and Gerstmann-Straussler-Scheinker disease (see Chap 33) Interestingly, the alcoholic form of the Korsakoff amnesic state, associated with less severe lesions in the same thalamic nuclei, is also characterized by a sleep disturbance, taking the form of an increased frequency of intermittent periods of wakefulness (Martin et al) Major head injury is an important cause of sleep disturbance The abnormalities, which may persist for months or years, consist mainly of a decrease in stages 1 and 2 of NREM sleep and less than the expected amounts of REM sleep and dreaming Some patients in the persistent vegetative state show a cycle of changes in the EEG, progressing from a picture of abortive spindles and K complexes with cyclic alterations in respiration and pupil size to the acquisition of a more normally structured sleep activity This sequence usually presages the change from a state of coma to one of wakefulness Organized sleep activity is absent in virtually all types of coma that are the result of anatomic damage to the brain A possible exception occurs in the unusual condition known as spindle coma, in which persistent coma and the electrographic features of sleep coexist This particular combination of events has been described after head trauma and rarely in association with profound metabolic encephalopathies Despite what appears to be a genuine comatose state (not simply hypersomnolence) from a lesion of the reticular activating system, the EEG displays frequent spindle activity and vertex waves, attesting to the integrity of thalamocortical pathways for sleep activity (see Nogueira de Melo et al) Disturbed sleep patterns have been described in patients with Alzheimer disease, Huntington chorea, olivopontocerebellar degeneration, and progressive supranuclear palsy (Parkes) Dreaming is absent in some of these conditions The peculiarities of sleep in Parkinson disease have been extensively studied; many patients in early stages of the disease complain of fragmented and unrestful sleep, particularly in the early morning hours The loss of natural body movements and the alerting effects of L-dopa contribute to the insomnia Also, 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 In striatonigral degeneration (multiple system atrophy), Lewy body disease, and other parkinsonian syndromes, REM sleep is particularly affected, although some of the effects may be the result of abnormal respiratory patterns and obstructive sleep apnea Migraine, cluster headaches, and paroxysmal hemicrania all have been linked to certain sleep stages Additionally, patients with epilepsy and myasthenia gravis and motor neuron disease may have sleep-related complaints; in the latter two the cause can be traced to mild respiratory failure or to pharyngeal weakness leading to apneic periods or aspiration A variety of sleep disturbances may accompany brain tumors or follow surgical resection of an intracranial tumor These include excessive daytime sleepiness, sleep apnea, and, rarely, nocturnal epilepsy The location of the lesion, rather than the tumor type, is predictive of such a disturbance; thus tumors affecting the hypo-
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thalamus and pituitary are associated with excessive daytime drowsiness, whereas medullary lesions cause respiratory disturbances that may affect sleep (Rosen et al) A symptomatic form of narcolepsy has been associated with tumors located adjacent to the third ventricle and midbrain (see below) Schwartz and associates have reported transient cataplexy following surgery for a craniopharyngioma, but a delirious state has been more common in the few cases we have followed
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