Obstructive sleep apnea and the prefrontal cortex: towards a comprehensive model linking nocturnal upper airway obstruction to daytime cognitive and behavioral deficits

Abstract

Obstructive sleep apnea (OSA) is accompanied by significant daytime cognitive and behavioral deficits that extend beyond the effects of sleepiness. This article outlines a causal model by which to understand these psychological effects among OSA patients. The model proposes that sleep disruption and blood gas abnormalities prevent sleep‐related restorative processes, and further induce chemical and structural central nervous system cellular injury. This, in turn, leads to dysfunction of prefrontal regions of the brain cortex (PFC), manifested behaviorally in what neuropsychologists have termed `executive dysfunction'. Executive dysfunction is proposed to markedly affect the functional application of cognitive abilities, resulting in maladaptive daytime behaviors. The proposed model (1) accounts for the specific psychological phenotype associated with OSA, (2) accommodates developmental components in this phenotype, (3) bridges between physical and psychological phenomena, (4) suggests mechanisms by which the nocturnal disorder might have effects on daytime functioning, (5) is empirically testable, (6) generates unique research hypotheses, and (7) has practical implications. The model is intended to act as a catalyst for future research and as a preliminary guide for clinicians.

The contribution of fatigue and sleepiness to depression in patients attending the sleep laboratory for evaluation of obstructive sleep apnea

“…Individuals who visit sleep laboratories generally complain of excessive daytime somnolence (EDS), fatigue [17][18] and neurocognitive dysfunction [2,[19][20][21]; symptoms which are also hallmarks of depression [22]. A number of Diagnostic and…”

Obstructive sleep apnea syndrome and cognition in Down syndrome

“…[8][9][10] Individuals with persistent OSAS have a neurocognitive profile similar in many respects to that of individuals with Down syndrome. 11,12 This overlap suggests the possibility that OSAS, by virtue of its destabilizing effects on sleep architecture or its reduction of oxygen, might account for some of the cognitive variability seen in individuals with Down syndrome.…”

Effects of mandibular advancement on brain activation during inspiratory loading in healthy subjects: a functional magnetic resonance imaging study

“…Moreover, the prefrontal cortex forms the so-called frontal-subcortical neuronal circuit with both the putamen and cingulate cortex, which mediate motor activity and behavior (52). It is notable that the prefrontal cortex displays reduced activity across all sleep stages and appears to be functionally disconnected during sleep from such a neuronal circuit, since this area is commonly regarded as the "hardest working" region of the brain during wakefulness, necessitating some time for recovery during sleep, with "recalibration" of the circuits that requires a lack of input interference from other brain regions (6). On the other hand, most other structures of the brain are active at some point during sleep.…”

“…A loss of gray matter (36) and less activity compared with healthy subjects (35) have been reported in the prefrontal cortex in subjects with OSA, suggesting some degree of impairment of psychophysiological function, such as amnesia, attention deficits and learning disabilities, daytime cognitive and behavioral deficits, etc. (3,6,32).…”