Sleep disturbances are associated with a variety of gastrointestinal disorders, including gastroesophageal reflux disease, ulcer disease, inflammatory bowel disease, and irritable bowel syndrome. Of particular interest in the last few years is the association of obstructive sleep apnea, use of continuous positive airway pressure, and gastroesophageal reflux disease. The author reviews the current literature on these topics as well as a comparison of sleep patterns among patients with irritable bowel syndrome to those with inflammatory bowel disease.
• Nocturnal gastrointestinal symptoms, including heartburn, pain, diarrhea, and fecal incontinence, may disrupt sleep in a large proportion of patients with various gastrointestinal disorders.
• Sleep, in turn, may exacerbate conditions such as reflux by delaying clearance of potentially injurious materials from vulnerable segments of the gastrointestinal tract.
• There is emerging evidence that infants with comorbid apparent life-threatening events and reflux have altered autonomic activity compared with infants with histories of apparent life-threatening events alone.
• Therapies, such elevating the head of the bed, proton pump inhibitors, H2-receptor antagonists, and Nissen fundoplication, have been shown to alleviate nocturnal heartburn symptoms and improve subjective measures of sleep quality.
Historical note and terminology
The enteric nervous system coordinates both intrinsic and responsive motor activity throughout the gastrointestinal tract. This complex neuronal network, first proposed by Langley, constitutes a third division of the autonomic nervous system (Langley 1921). Although influenced by both sympathetic and parasympathetic input (brain-gut axis), enteric neural activity is also mediated by a vast array of other substances (bombesin, prostaglandins, dopamine, serotonin, opioids, and nitric oxide). This later evidence confirmed Langley's original theory.
Early studies of gastric acid secretion revealed circadian rhythmicity. In 1924, Johnston and Washeim reported that acid volume was lower during sleep and that gastric acidity gradually rose prior to sleep then fell to baseline levels within 1 1/2 hours after the onset of sleep (Johnston and Washeim 1924). Increased nocturnal acid secretion was observed in most patients with active duodenal ulcer disease (Winklestein 1935). Refinement in small pH electrodes has made it possible to measure gastric acidity continuously throughout an entire 24-hour period.
Gastrointestinal activity can also affect breathing during sleep. The earliest report of prolonged apnea related to gastroesophageal reflux in infants is a description of 2 infants who died from aspiration of vomitus (Forshall 1955). Several investigators, noting a high frequency of chronic pulmonary disorders in patients with gastroesophageal reflux and improvement in asthma after surgical repair for gastroesophageal reflux, established a more definite link between gastroesophageal reflux and nocturnal asthma. However, the causative mechanism is still not fully understood. For example, the peak incidence of nocturnal asthma occurs late in the night (usually between 5:00 and 6:00 am), whereas episodes of gastroesophageal reflux are more likely to occur earlier. Gastric surgery is, therefore, recommended only to a small fraction of patients with nocturnal asthma.
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