Obesity without sleep apnea is associated with daytime sleepiness.

BACKGROUND: Daytime sleepiness and fatigue is a frequent complaint of obese patients even among those who do not demonstrate sleep apnea. OBJECTIVE: To assess in the sleep laboratory whether obese patients without sleep apnea are sleepier during the day compared with healthy controls with normal weight. METHODS: Our sample consisted of 73 obese patients without sleep apnea, upper airway resistance syndrome, or hypoventilation syndrome who were consecutively referred for treatment of their obesity and 45 controls matched for age. All patients and healthy controls were monitored in the sleep laboratory for 8 hours at night and at 2 daytime naps, each for 1 hour the following day. RESULTS: Obese patients compared with controls were sleepier during the day and their nighttime sleep was disturbed. During both naps, sleep latency, wake time after onset of sleep, and total wake time were significantly lower, whereas the percentage of sleep time was significantly higher in obese patients compared with controls. In contrast, during the nighttime testing, obese patients compared with controls demonstrated significantly higher wake time after onset of sleep, total wake time, and lower percentage of sleep time. An analysis of the relation between nighttime and daytime sleep suggested that daytime sleepiness in obese patients is a result of a circadian abnormality rather than just being secondary to nighttime sleep disturbance. CONCLUSIONS: Daytime sleepiness is a morbid characteristic of obese patients with a potentially significant impact on their lives and public safety. Daytime sleepiness in individuals with obesity appears to be related to a metabolic and/or circadian abnormality of the disorder.

Afferent and efferent innervation of the rat esophagus. A tracing study with horseradish peroxidase and nuclear yellow.

The technique of retrograde labeling of nerve cells with HRP and nuclear yellow as well as transganglionic anterograde HRP-tracing of sensory projections into the CNS were used to establish the motor and sensory innervation pattern of two parts of the rat esophagus: the cervical and the abdominal segment. For comparison, also the innervation of the anterior wall of the stomach was studied. Application of HRP to the cervical part of the esophagus resulted in bilateral labeling of neurons in the nucleus ambiguus exclusively, while application of the tracer to the abdominal part was followed by labeling of cells in both the nucleus ambiguus and the dorsal motor nucleus of the vagus. Application of tracer to the wall of the stomach caused labeling of cells in the dorsal motor nucleus of the vagus exclusively. Labeling appeared always bilaterally. In all experiments there was a profuse labeling of primary afferent neurons with cell bodies in both nodose ganglia and endings in certain subnuclei of the solitary nucleus. Endings related to the cervical esophagus projected into the ventral subnuclei, projections from the abdominal esophagus were located in the ventral and medial subnuclei, those from the stomach in the medial subnucleus solely. The area postrema and the commissural nucleus received afferents from both organs, the esophagus and the stomach. Double labeling experiments with HRP and nuclear yellow provided no signs of overlap of sensory innervation areas of the sites investigated in this study. Within the wall of the esophagus no labeled intramural cells nor nerve fibers were found in sections beyond the injection sites.