Development of laryngeal function: etiologic significance in the sudden infant death syndrome.
Recent clinical evidence implicates transient upper airway obstruction as a cause of potentially fatal cardiorespiratory disturbances. This investigation identifies age-related neurologic mechanisms which may be pertinent to the production of abnormal laryngeal closure as a possible cause of unexpected infant death. A period of transient laryngeal hyper-excitability is identified in pups 50--75 days post-natally. The mechanism of the hyper-excitable state resulting in increased risk of laryngeal spasm, appears related to: 1. the completion of central synaptic maturation: 2. transient reduction in central latency; and 3. a reduction in central inhibition. Such observations provide clues to neurologic vulnerability occurring not immediately after birth, but during a discrete time period thereafter, prior to complete neurologic maturation. As such, these observations fulfill a criterion of utmost importance in the search for etiologic significance in the Sudden Infant Death Syndrome, and, in a broad sense, support the concept of selective maturational failure as a possible cause for age-dependent, unexpected infant death.
D000367:Age Factors; D000402:Airway Obstruction / Q000150:complications*; D000818:Animals; D000831:Animals, Newborn; D002415:Cats; D004285:Dogs; D006801:Humans; D007223:Infant; D007823:Laryngeal Nerves / Q000254:growth & development / Q000503:physiopathology; D007830:Larynx / Q000503:physiopathology*; D009431:Neural Conduction; D012018:Reflex / Q000502:physiology; D013398:Sudden Infant Death / Q000209:etiology* / Q000503:physiopathology; D013569:Synapses