REM Sleep Suppression is a neurophysiological state characterized by a significant reduction in the duration, frequency, or intensity of the Rapid Eye Movement (REM) stage of sleep, which is the phase predominantly associated with dreaming, memory consolidation, and heightened brain activity. This suppression is often a side effect of certain pharmacological agents, alcohol consumption, or underlying sleep disorders, leading to impaired cognitive function, emotional dysregulation, and a failure to fully complete the essential restorative cycles of sleep.
Origin
This term originates from sleep medicine and neurobiology, following the discovery and characterization of the distinct stages of sleep via electroencephalography (EEG). The recognition of REM sleep as a vital, active phase led to studies on its disruption. The concept of “Suppression” highlights the clinical observation that various external and internal factors can inhibit the brain’s ability to enter or sustain this critical phase.
Mechanism
The mechanism of suppression typically involves the alteration of neurotransmitter balance in the brainstem and pontine nuclei, which govern the transition into REM sleep. Cholinergic activity is necessary for initiating REM, while monoaminergic neurotransmitters like serotonin and norepinephrine actively suppress it. Many common agents, such as selective serotonin reuptake inhibitors (SSRIs) and alcohol, increase the tonic activity of these monoaminergic systems, thereby preventing the necessary neural switch that allows for the onset of the REM state.
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