Secondary Sleep Disorders

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Psychogenic sleep disorders. Depression (of various types) can impair sleep, though paradoxically sleep deprivation can ameliorate depression. Depressed persons typically complain of early morning awakening, nocturnal restlessness, and difficulty in starting the day. Sleep disturbances are also common in patients suffering from psychosis, mania, anxiety disorders, alcoholism, and drug abuse.

Neurogenic sleep disorders. Sleep can be impaired by dementia, Parkinson disease, dys-tonia, respiratory disturbances secondary to neuromuscular disease (muscular dystrophy, amyotrophic lateral sclerosis), epilepsy (nocturnal attacks), and headache syndromes (cluster headaches, migraine). Fatal familial insomnia is a genetic disorder of autosomal dominant inheritance (p. 252). Sleep disorders due to systemic disease. Sleep can be impaired by pulmonary diseases (asthma, COPD), angina pectoris, nocturia, fibromyalgia, and chronic fatigue syndrome.

Secondary Sleep Disorders

Consciousness is an active process with multiple individual components, including wakefulness, arousal, perception of oneself and the environment, attention, memory, motivation, speech, mood, abstract/logical thinking, and goal-directed action. Psychologists and philosophers have long sought to understand the nature of consciousness.

Clinical assessment of consciousness tests the patients' perception of themselves and their environment, behavior, and responses to external stimuli. Findings are expressed in terms of three categories: level of consciousness (state/clarity of consciousness, quantitative level of consciousness, vigilance, alertness, arousability); content of consciousness (quality of consciousness, awareness); and wakefulness. Changes in any of these categories tend to affect the others as well. Morphologically, the level of consciousness is associated with the reticular activating system (RAS). This network is found along the entire length of the brain stem reticular formation (p. 26), from the medulla to the intralaminar nuclei of the thalamus. The RAS has extensive bilateral projections to the cerebral cortex; the cortex also projects back to the RAS. Neurotransmission in these systems is predominantly with acetylcholine, monoamines (norepinephrine, dopamine, serotonin), GABA (inhibitory), and glutamate (excitatory).

In the normal state of consciousness, the individual is fully conscious, oriented, and awake. All of these categories undergo circadian variation (depending on the time of day, a person may be fully awake or drowsy, more or less concentrated, with organized or disorganized thinking), but normal consciousness with full wakefulness can always be restored by a vigorous stimulus.

lucinations, restlessness, suggestibility, and au-tonomic disturbances (tachycardia, blood pressure fluctuations, hyperhidrosis). Somnolence is a mild reduction of the level of consciousness (drowsiness, reduced spontaneous movement, psychomotor sluggishness, and delayed response to verbal stimuli) while the patient remains arousable: he or she is easily awakened by a stimulus, but falls back asleep once it is removed. The patient responds to noxious stimuli with direct and goal-directed defensive behavior. Orientation and attention are mildly impaired but improve on stimulation. Stupor is a significant reduction of the level of consciousness. These patients require vigorous and repeated stimulation before they open their eyes and look at the examiner. They answer questions slowly and inadequately, or not at all. They may lie motionless or display restless or stereotyped movements. Confusion reflects concomitant impairment of the content of consciousness.

Disorders of arousal. Wakefulness normally follows a circadian rhythm (p. 112). Sleep apnea syndrome, narcolepsy, and parasomnia are disorders of arousal (dyssomnias, p. 114). Hyper-somnia is caused by bilateral paramedian thalamic infarcts, tumors in the third ventricular region, and lesions of the midbrain tegmen-tum (p. 70 ff). The level and content of consciousness may also be affected. In patients with bilateral paramedian thalamic infarction, for example, there may be a sudden onset of confusion, followed by somnolence and coma. After recovery from the acute phase, these patients are apathetic and their memory is impaired ("thalamic dementia").

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