(169) Isolated Sleep Paralysis Associated with Gabapentin for Alcohol Use Disorder: A Case Report

Abstract: Background/Significance: Gabapentin has many applications including alcohol use disorder, seizures, neuropathic pain, restless leg syndrome, and anxiety. Gabapentin has been shown to affect sleep architecture including an increase in slow-wave sleep and reduction in N1 sleep; however, reported effects on REM sleep vary. There are no reported cases of gabapentin use associated with sleep paralysis, a REM parasomnia. We report a case of recurrent isolated sleep paralysis following gabapentin dose escalation with subsequent resolution of sleep paralysis symptoms with dose reduction.

Case: Mr. B, a 30-year-old male patient with a history of alcohol use disorder and post-traumatic stress disorder was voluntarily admitted for subacute alcohol withdrawal. He was initiated on gabapentin 300mg three times daily, prazosin 1mg nightly for nightmares, and divalproex 500mg nightly. To address his ongoing anxiety and cravings, gabapentin was increased to 400mg/400mg/600mg dosing. After this change, every night thereafter Mr. B reported paralysis upon awakening, in which he felt fully awake and aware of his surroundings, but unable to move his body. Mr. B had never experienced any similar event in the past, does not have a history of parasomnias, and did not experience any increased daytime sleepiness, cataplexy, or hallucinations. Prazosin was discontinued without any change. Gabapentin was decreased back to 300mg three times daily. The next day, he did not report any recurrence of sleep paralysis symptoms overnight, and did not endorse it again, despite uptitrating divalproex later in his course.

Discussion: Sleep paralysis is a REM parasomnia characterized by an inability to initiate voluntary movement of the trunk and limbs. This involves the extension of muscle atonia, typically present only during REM sleep, into the awake state (Stefani, 2021). Several variables have been shown to be associated with sleep paralysis, including substance use, trauma history, hereditary factors, other sleep disturbances, and psychiatric illness. Mechanistically, gabapentin is believed to act on presynaptic voltage-gated ion channels, including calcium and sodium, to enhance GABAergic inhibitory signals. Animal studies have shown that simultaneous inhibition of GABAA/GABAB/glycine prevents REM atonia, suggesting that co-activation of these pathways are involved in generating atonia (Brooks, 2012). It may be postulated whether an up-regulation of GABA and associated inhibitory effects secondary to gabapentin use could be associated with the onset of isolated sleep paralysis, a REM parasomnia. Both alcohol use disorder and PTSD have been shown to decrease baseline levels of GABA. Therefore, it follows that for Mr. B, the relative increase in GABA from dose escalation of gabapentin could have played a significant role in triggering ISP in an already susceptible individual.

Conclusion/Implications: This case is significant because it adds to the limited and indeterminate research on the effects of gabapentin on REM sleep, as well as reporting occurrence of ISP.

1. Stefani A, Högl B. Nightmare Disorder and Isolated Sleep Paralysis. Neurotherapeutics. 2021 Jan;18(1):100-106. doi: 10.1007/s13311-020-00966-8. Epub 2020 Nov 23. PMID: 33230689; PMCID: PMC8116464.


2. Brooks PL, Peever JH. Identification of the transmitter and receptor mechanisms responsible for REM sleep paralysis. J Neurosci. 2012 Jul 18;32(29):9785-95. doi: 10.1523/JNEUROSCI.0482-12.2012. PMID: 22815493; PMCID: PMC6621291.

Presentation Eligibility: Not previously published or presented. Prefer virtual format.

Diversity, Equity, and Inclusion: Individuals from historically marginalized groups are more likely to suffer from sleep disorders. Therefore disseminating knowledge on psychopharmacology will improve healthcare within this group vs other privileged groups. However, this work was not specifically designed to advance DEI.