Polysomnographic recordings during acute

intoxication with stimulants demonstrate Increased sleep latency, decreased TST, Increased spontaneous awakenings with Increased body movements during sleep, prolonged REM latency, and reduced total REM time. Stimulant withdrawal Is associated with reduced sleep latency and Increased TST with hypersomnia and prolongation of nocturnal sleep duration.7’13 REM and SWS may rebound to greater than baseline values. MSLT during the withdrawal phase shows Increased sleepiness with mean sleep latency <10 min. Sedative-, hypnotic-, and anxiolytic-dependent sleep disorder The Inverse of stimulant abuse Is abuse of sedative-hypnotic agents. Inhibitors,research,lifescience,medical Hypnotic-dependent sleep disorder Inhibitors,research,lifescience,medical presents with excessive sleepiness or Insomnia associated with tolerance to or withdrawal from sedative-hypnotic medications. Sleep complaints and objective measures of sleep

are affected by the differences In duration of action and half -life of the various sedative-hypnotic agents.7 During Inhibitors,research,lifescience,medical acute Intoxication, sedative-hypnotic drugs produce hypersomnolence and decrease wakefulness.7 Chronic usage, however, may lead to tolerance, with return of underlying Insomnia, and, If the dose is Increased, daytime hypersomnia, sluggishness, ataxia, slurred speech, and visual-motor AMPK inhibition problems with late-afternoon restlessness and nervousness, can occur.13 Polysomnography In subjects using hypnotic agents demonstrates disrupted sleep architecture with an Increase In stage 2 NREM sleep, reduction In stages 1, 3, and 4 NREM Inhibitors,research,lifescience,medical sleep, and reduction In REM sleep.22 Both NREM and REM sleep are fragmented, with frequent sleep-stage transitions. Increased 14 to 18 Hz spindles are seen together with Increased alpha and beta activity. Sedative-hypnotics can

also aggravate underlying breathing disorders. Inhibitors,research,lifescience,medical Abrupt discontinuation of chronic sedative-hypnotic use can result In withdrawal insomnia, decreased sleep duration, Increased anxiety, tremulousness, and ataxia.7 Although sleep architecture rapidly Improves, subjective complaints of sleep quality and quantity will be deemed greater than before hypnotic therapy commenced.13 Abrupt discontinuation of chronic use of barbiturates and the older nonbarbiturate, nonbenzodlazepine drugs Thymidine kinase Is associated with a higher Incidence of withdrawal seizures compared to benzodiazepines. Shorter-duration sedative-hypnotic drugs can result In withdrawal Insom- nia, while longer-duration sedative-hypnotic agents can cause daytime hypersomnia during active use. However, any sedative-hypnotic agent can produce either withdrawal Insomnia or daytime sedation. Polysomnography during withdrawal demonstrates reduced sleep duration, increased sleep disruption, and REM sleep rebound.