Guilleminault C, Stoohs R, Quera-Salva M A
Stanford Sleep Research Center, Palo Alto, CA 94304.
Neurology. 1992 Jul;42(7 Suppl 6):53-60.
Daytime breathing problems caused by neurologic lesions always worsen during sleep, and in certain cases abnormal breathing patterns are only seen during sleep or specific sleep states. The first clinical manifestation of maltase deficiency, myopathy, or myotonic dystrophy is often a sleep-related complaint, such as unexplained waking from sleep (insomnia) or daytime somnolence. Thus, systematic investigation during sleep of disorders impairing the loop involved in breathing is strongly encouraged. Lesions may involve sensory receptors, sensory pathways, brainstem-controlling neurons, upper motor neurons, descending motor pathways, lower motor neurons, motor nerves, neuromuscular junctions, or respiratory muscles. Most of these lesions lead to a decrease in or absence of inspiratory efforts (diaphragmatic apnea or hypopnea) during sleep. These events differ from the classic obstructive sleep apnea syndrome and the recently described upper airway resistance syndrome, which usually involve mild or significant anatomic abnormalities of the upper airway and craniofacial region. The treatment of abnormal breathing during sleep has been improved by the development of nasal ventilation methods: continuous positive airway pressure, intermittent positive pressure, and volume ventilation. These therapeutic approaches can prevent tracheostomy and diaphragmatic pacing and are more efficacious than drug treatments. Long-term compliance is generally much better in breathing disorders secondary to neurologic impairments than in cases of mild to moderate obstructive sleep apnea.
