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  • Updated 09.12.2021
  • Released 09.14.2000
  • Expires For CME 09.12.2024

Stimulant-dependent sleep disorder



CNS stimulant medications, as well as stimulant drug abuse, have adverse effects on sleep, causing insomnia and hypersomnia. Use of stimulants as symptomatic therapy may also obscure underlying sleep disorders. In this article, the author discusses advances in the understanding of the underlying pathophysiology and treatment of stimulant-dependent sleep disorder. Newer CNS stimulants used for the treatment of daytime drowsiness and narcolepsy have fewer adverse effects. Management of stimulant-dependent sleep disorders is also outlined.

Key points

• CNS stimulants used for treatment of hypersomnia or excessive daytime sleepiness, as well as abuse of substances that have CNS stimulant action, may cause insomnia.

• Chronic abstinence from stimulants is also associated with sleep disorders, including drowsiness.

• Chronic abstinence from cocaine may lead to occult insomnia.

• Understanding the mechanisms of rebound hypersomnia may help improve efficacy and reduce adverse effects of CNS stimulant medications.

• Although there is no established approach to the management of stimulant-dependent sleep disorders, preventive measures are important and some drugs are available for the management of symptoms.

Historical note and terminology

Stimulant-dependent sleep disorder was originally defined as a "reduction of sleepiness or suppression of sleep by CNS stimulants and resultant alterations in wakefulness following drug abstinence. The International Classification of Sleep Disorders, 3rd edition, (ICSD-3) mentions "sleep disorders resulting from a drug or substance" under the following categories: (1) central sleep apnea; (2) sleep-related hypoventilation; (3) central disorders of hypersomnolence; (4) insomnia; (5) parasomnia; and (6) sleep-related movement disorders (02). Drug or substance can be a prescription medication, recreational drug, caffeine, alcohol, or food item. The ICSD-3 defines insomnia as a repeated difficulty with sleep initiation, duration, consolidation or quality that occurs despite adequate opportunity and circumstances for sleep and results in some type of daytime impairment. This includes insomnia due to drugs or substances, which is secondary to substance abuse or withdrawal. The scope of this article is limited to sleep disorders resulting from the use of CNS stimulants.

CNS stimulants, now classified as sympathomimetic (amphetamine and cocaine) and nonsympathomimetic (caffeine or theophylline), have been used medicinally for centuries. Amphetamines, introduced for human use in the 1930s, were used extensively in World War II to combat fatigue. Subsequently, systematic electrophysiologic studies revealed that use of amphetamines not only increases wakefulness, but also reduces total sleep time as well as the time spent in REM sleep through the night. Amphetamine use also increases the time to the first REM sleep period while asleep (increased REM sleep latency). On "stimulant withdrawal," the time spent sleeping increases. In the setting of stimulant abuse, withdrawal occasionally results in total sleep times ranging from 18 to 48 hours, and "REM sleep rebound," with REM sleep occupying an abnormally high percentage of total sleep time and latencies to the first REM sleep period much shorter than normal (27). These REM sleep effects are occasionally not seen until after 1 or 2 nights following stimulant withdrawal. In the 1970s, medical use of these drugs was restricted due to high abuse potential. Only dextroamphetamine and methylphenidate were available for medical use.

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