[Drug therapy of sleep-related respiration disorders].
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Because sleep apnoea syndrome is often associated with arterial hypertension, it has been suggested that sleep apnoea might be responsible for hypertension. This hypothesis is mainly based on epidemiological studies showing a statistically significant association between snoring and arterial hypertension; this association remains true even after data correction to take into account the increased frequency of snoring with age and overweight. However, this statistical link is no evidence of a cause-effect relationship, and the mechanism through which sleep apnoea syndrome could produce arterial hypertension remains unknown. Yet treatment of sleep apnoea syndrome seems to improve arterial hypertension, and this alone would justify a search for sleep apnoea syndrome in all patients presenting with arterial hypertension.
Sleep affects, and is in turn affected by, cardiovascular, thermal, respiratory, endocrine, circadian, and sensory processes. Integrative areas of the basal forebrain play a crucial role, as does interaction with cholinergic and aminergic areas of the brain stem. AD, which affects a wide range of structures and functions, alters sleep in a manner distinguishable from depressive pseudodementia and may involve changes in autonomic function. Sleep apnea occurs with a high incidence in patients with AD, and the possibility should be explored that treating sleep apnea might be beneficial to their cognitive and affective status. Long-acting hypnotics can adversely affect daytime functioning. This might occur because of either direct effects on structures mediating sleep and cognition or, alternatively, exacerbation of sleep-related respiratory dysfunction. Studies of the benzodiazepine receptor complex may lead to the development of new drugs to aid sleep and wakefulness.
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We hope that the reader is impressed with the relatively limited amount of information available about the effects of drugs on breathing during sleep in both normal subjects and patients with sleep-disordered breathing. Although more reports are appearing, well-controlled evaluations remain limited in number. We believe that this information gap will quickly close because it is now increasingly appreciated that either spontaneous or drug-induced breathing abnormalities measured during wakefulness may be strikingly magnified during sleep. Therefore, this area of investigation is exciting. Finally, we hope the reader shares our view that, to date, drug therapy for sleep apnea has limited efficacy.
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Antidepressants are recommended by some clinicians as therapy for irritable colon even when there is no evidence of clinical depression, since this syndrome may represent a type of chronic masked depression. Antidepressants may be a good alternative in elderly patients with peptic ulcer disease, particularly in those with concurrent depression. Advantages include once-a-day administration, lower cost, and ease of serum monitoring.
The recent advances in our understanding of breathing in sleep include an evolution in the selection and surgical therapy of patients with the sleep apnea syndrome. Recent work suggests that shorter polysomnographic studies may be adequate for diagnostic purposes in many sleep apnea patients. It is now clear that central apnea may occur, paradoxically, in patients with either very blunted chemical drives to breathe or increased drives to breathe.
Sleep apnea syndrome is estimated to affect as many as 2 to 3 percent of the adult male population. Excessive snoring and daytime sleepiness are but a few of the many clues to diagnosis. The hypoxemia occurring as a result of apnea may lead to pulmonary hypertension. Depressed respiratory center neural output or upper airway occlusion during sleep may cause the apnea. There are a number of treatment options available.
Tricyclic antidepressants and some structurally related compounds were tested for their ability to antagonize histamine H1 and muscarinic acetylcholine receptors of cultured mouse neuroblastoma cells. As a group, tertiary amine tricyclic antidepressants tended to be more potent than secondary amine drugs at both receptors. The most potent antihistamine, doxepin hydrocholoride, was about 4 times more potent than amitriptyline hydrochloride, about 800 times more potent than diphenhydramine hydrochloride, and about 8,000 times more potent than desipramine hydrochloride, the least potent tricyclic antidepressant at both the histamine H1 and the muscarinic acetylcholine receptors. All tricyclic drugs except desipramine hydrochloride were more potent as antihistamines than as anticholinergics. Doxepin hydrochloride and amitriptyline hydrochloride may be the most potent antihistamines known, and the antihistaminic potencies of these and the other tricyclic antidepressant drugs may relate directly to their ability to cause sedation and drowsiness in patients.
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Narcolepsy is characterized by excessive daytime sleepiness and cataplexy, which may be accompanied by hypnogogic or hypnopompic hallucinations and sleep paralysis. Automatic behavior is a relatively newly recognized symptom of the narcolepsy syndrome. This case report describes a particularly troublesome sort of automatic behavior--shoplifting--in a narcoleptic patient. It illustrates how a sleep-laboratory evaluation was used to confirm the diagnosis of narcolepsy and considers aspects of the treatment of the problem.
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