Disrupted rapid eye movement sleep predicts poor declarative memory performance in post-traumatic stress disorder.

Successful memory consolidation during sleep depends on healthy slow-wave and rapid eye movement sleep, and on successful transition across sleep stages. In post-traumatic stress disorder, sleep is disrupted and memory is impaired, but relations between these two variables in the psychiatric condition remain unexplored. We examined whether disrupted sleep, and consequent disrupted memory consolidation, is a mechanism underlying declarative memory deficits in post-traumatic stress disorder. We recruited three matched groups of participants: post-traumatic stress disorder (n = 16); trauma-exposed non-post-traumatic stress disorder (n = 15); and healthy control (n = 14). They completed memory tasks before and after 8 h of sleep. We measured sleep variables using sleep-adapted electroencephalography. Post-traumatic stress disorder-diagnosed participants experienced significantly less sleep efficiency and rapid eye movement sleep percentage, and experienced more awakenings and wake percentage in the second half of the night than did participants in the other two groups. After sleep, post-traumatic stress disorder-diagnosed participants retained significantly less information on a declarative memory task than controls. Rapid eye movement percentage, wake percentage and sleep efficiency correlated with retention of information over the night. Furthermore, lower rapid eye movement percentage predicted poorer retention in post-traumatic stress disorder-diagnosed individuals. Our results suggest that declarative memory consolidation is disrupted during sleep in post-traumatic stress disorder. These data are consistent with theories suggesting that sleep benefits memory consolidation via predictable neurobiological mechanisms, and that rapid eye movement disruption is more than a symptom of post-traumatic stress disorder.

The implications of sleep disruption for cognitive and affective processing in methamphetamine abuse.

Sleep is disrupted during active use of methamphetamine (MA), during withdrawal from the drug, and during abstinence from its use. However, relatively little is known about possible mediatory functions of disrupted sleep in the emergence, manifestation, and maintenance of cognitive and affective symptoms of MA abuse. We hypothesise that sleep functions as a mediator for stimulant drug effects. Specifically, we propose that objectively-measured sleep parameters can be used to explain some of the variability in the experience and presentation of memory deficits and emotion dysregulation in MA abusers. After describing how important healthy sleep is to unimpaired cognitive and affective functioning, we review literature describing how sleep is disrupted in MA abuse. Then, we provide a conceptual framework for our hypothesis by explaining the relationship between MA abuse, sleep disruption, memory deficits, emotion dysregulation, and changes in reward-related brain networks. We conclude by discussing implications of the hypothesis for research and treatment.