Middle Latency Auditory Evoked Potentials Sleep Apneics During Waking and as a Function of Arterial Oxygen Saturation During Apneas

Abstract

Summary: In adults with obstructive sleep apnea middle latency auditory evoked responses were recorded as a function of apnea-related arterial oxygen desaturation both before sleep onset and during nocturnal sleep. In waking, wave Pa latency was normal in five of six subjects, and Pa amplitude was normal in all. During sleep apneas, wave Pa remained stable even during intervals of severe oxygen desaturation (e.g., 45-90% and 50-84% saturation in two subjects). Furthermore, wave Pa recorded immediately on awakening in the morning was unaltered compared with the response recorded just prior to sleep onset, despite a high frequency of nocturnal apneas in all subjects. These data indicate that repetitive nocturnal oxygen desaturation associated with severe obstructive sleep apnea syndrome has neither immediate nor cumulative measurable effects on the functioning of neurons that sub serve the middle latency evoked response. These findings are discussed in relation to a possible cortical contribution to the middle latency response. Key Words: Evoked potentials-Sleep apnea-Middle latency auditory evoked potentials.. InPatients with sleep apnea syndrome exhibit a variable constellation of physiological, behavioral, and psychological manifestations (see 1, for review). These may include hypnagogic hallucinations, enuresis, nightmares, abnormal motor activity during sleep, and morning awakening with headache and/or confusional states with memory impairment and spatial and temporal disorientation. Daytime functioning can be further compromised by incapacitating sleepiness, excessive fatigability, dizziness, impaired concentration, automatic behaviors (often with retrograde amnesia), personality changes (irritability, anxiety, depression), impotence, and diminished libido. This spectrum of clinical findings raises the possibility that brain function may be compromised by the repeated episodes of oxygen deprivation that accompany sleep apneas, and/or that apneas are a manifestation of central nervous system (eNS) dysfunction. Transient apnea-related decreases in arterial oxygen