Gabapentin for Sleep
Gabapentin (Neurontin) increases slow-wave sleep and is a safe, effective treatment for insomnia. It is a widely prescribed medication in neurology and psychiatry. In neurology, it is used for seizures, neuropathic pain, migraines, and restless legs syndrome. In psychiatry, it is used for insomnia, anxiety, and alcohol dependence. It is also helpful for hot flashes, fibromyalgia, and teeth-grinding.
Benefits of Gabapentin
It improves sleep quality by increasing slow-wave sleep
It is not a controlled substance
It does not cause respiratory depression
It can be combined safely with alcohol
It has a wide safety margin
It is not metabolized by the liver (may need to be reduced with impaired kidney functioning)
Few drug interactions
OBJECTIVES: The prevalence of insomnia is very high in our society. Although pharmacological treatment of insomnia is available, most hypnotics have been shown to alter sleep architecture and have many adverse effects. Gabapentin was originally designed for antiepileptic therapy; however, some studies reported that its use increases slow-wave sleep in healthy volunteers or patients. Our goal was to evaluate the benefits of gabapentin in the treatment of primary insomnia in patients.
METHODS: Eighteen patients with primary insomnia participated in the study. They received gabapentin treatment for at least 4 weeks. All patients received polysomnography, a biochemical blood test, and neuropsychological tests before and after the treatment period. All measures were analyzed with Student t test to examine the treatment effects of gabapentin, except that the measures of heart rate variability were analyzed with analysis of variance.
RESULTS: Polysomnographic study revealed increased sleep efficiency and slow-wave sleep, decreased wake after sleep onset, and spontaneous arousal index after gabapentin treatment. The biochemical blood test revealed decreased prolactin levels in the morning after treatment. Electroencephalographic power spectral analysis showed increased delta-2 and theta power in sleep stage 1 and decreased sigma activity power in sleep stages N2 and N3 after gabapentin treatment. Heart rate variability analyses also showed a significant increase in normalized high-frequency percentage in sleep stages N2 and N3 and low frequency-high frequency ratio in sleep stage N2 after treatment. In addition, neuropsychological tests revealed the elevation of visual motor processing speed after gabapentin treatment.
CONCLUSIONS: Gabapentin enhances slow-wave sleep in patients with primary insomnia. It also improves sleep quality by elevating sleep efficiency and decreasing spontaneous arousal. The results suggest that gabapentin may be beneficial in the treatment of primary insomnia.
OBJECTIVE: Residual sleeping disturbances after improvement of depression in major depressed patients are associated with more functional problems, increased relapses and more risk of becoming resistant to treatment. The aim of this study was to compare the efficacy of gabapentin with clonazepam for treating residual sleeping disturbances. METHODS: This comparative trial was designed as a randomized, controlled, double-blind study. Sixty-three patients with a DSM-IV diagnosis of major depressive disorder (MDD) who had been treated with one of the selective serotonin reuptake inhibitors (SSRIs; fluoxetine, citalopram or sertraline) were included in the study. The patients’ depression had improved [Hamilton Depression Rating Scale (HDRS) <10] but they were complaining of sleeping problems [Pittsburgh Sleep Quality Index (PSQI) >5; Insomnia Severity Index (ISI) >8]. Patients were randomized to receive a flexible dose of gabapentin (100-600 mg/day) or clonazepam (0.5-2 mg/day) beside their current antidepressant medication for a period of 4 weeks. Outcome measures were PSQI, ISI and Clinical Global Impression (CGI). RESULTS: Our results demonstrated that similar to the clonazepam group, sleeping problems improved significantly in the gabapentin group at the end of the trial.The two groups did not show a significant difference in treating residual sleep disturbances. CONCLUSION: This study revealed that gabapentin is comparable to clonazepam for treating sleeping problems associated with major depression.
OBJECTIVES: To evaluate the effects of single doses of gabapentin 250 and 500 mg on polysomnographic (PSG) and participant-reported sleep measures in a 5-h phase advance insomnia model. METHODS: Adults reporting occasional disturbed sleep received gabapentin 500 mg (n = 125), 250 mg (n = 125), or placebo (n = 127) 30 min prior to bedtime and were in bed from 17:00 to 01:00, ∼5 h before their habitual bedtime. Sleep was assessed by PSG, post-sleep questionnaire, and the Karolinska Sleep Diary (KSD). Next-day residual effects (Digit Symbol Substitution Test [DSST] and Stanford Sleepiness Scale [SSS]) and tolerability were assessed. RESULTS: Demographics were comparable among groups. Among PSG endpoints, wake after sleep onset (primary endpoint) (135.7 [placebo], 100.7 [250 mg], and 73.2 [500 mg] min) was significantly lower and total sleep time (TST) (311.4, 356.5, and 378.7 min) significantly greater in both gabapentin groups versus placebo. Latency to persistent sleep was not significantly different among groups. Percent slow wave sleep (12.6%, 15.4%, and 17.0%, respectively) was significantly greater and percent stage 1 (15.1%, 11.8%, and 10.8%, respectively) significantly lower relative to placebo. Gabapentin was associated with significantly higher values of KSD Sleep Quality Index and reported TST versus placebo; no other reported outcomes were significant. Neither gabapentin dose produced evidence of next-day residual effects as measured by DSST and SSS. Adverse events were infrequent (< 5%). CONCLUSION: Participants with occasional disturbed sleep treated with gabapentin showed significantly longer sleep duration and greater depth (versus placebo) in response to a phase advance manipulation known to disrupt sleep maintenance.
PURPOSE: This study aimed to determine if the use of gabapentin is more efficacious than a stabilization splint with regard to the intensity of masseter muscle contractions and/or sleep quality for patients experiencing sleep bruxism (SB). MATERIALS AND METHODS: Twenty patients with SB participated in this clinical study. They were randomly divided into two treatment groups: stabilization splint group (n = 10) and gabapentin group (n = 10). The first polysomnographic examination was performed before the beginning of the experiment for all the participants. At the end of a 2-month period of stabilization splint therapy or gabapentin usage, a second polysomnographic recording was made. RESULTS: Statistically significant reductions in the number of SB episodes per hour and per night, bruxism time index, total duration of SB episodes per night and number of SB episodes in stages NR I and NR II (p < 0.05) were observed in both groups after treatment. Both treatments significantly reduced the mean intensity of masseter muscle contractions during SB episodes. Moreover, the participants treated with gabapentin showed a significant improvement in total sleep time, slow wave sleep (stage III), and sleep efficiency (p < 0.05). CONCLUSIONS: Gabapentin could be an effective treatment modality in SBs, especially in those with poor sleep quality.
PURPOSE:The older antiepileptic drugs (AEDs) have a variety of effects on sleep, including marked reduction in rapid-eye-movement (REM) sleep, slow-wave sleep (SWS), and sleep latency, and an increase in light sleep. The effects of the newer AEDs on sleep are unknown. Our purpose was to study the effect of gabapentin (GBP) on sleep.METHODS: Ten healthy adults and nine controls were the subjects of this study. All underwent baseline and follow-up polysomnography (PSG) and completed sleep questionnaires. After baseline, the treated group received GBP titrated to 1,800 mg daily. Polygraphic variables and Epworth Sleepiness Scale (ESS) scores, a subjective measure of sleep propensity, were compared by using the Wilcoxon signed rank test. RESULTS: Nine of the treated subjects achieved the target dose; one was studied with 1,500 mg daily because of dizziness experienced at the higher dose. GBP-treated subjects had an increase in SWS compared with baseline. No difference in the ESS or other polygraphic variables was observed. However, a minor reduction in arousals, awakenings, and stage shifts was observed in treated subjects. CONCLUSIONS: Gabapentin for sleep appears to be less disruptive than are some of the older AEDs. These findings may underlie the drug’s therapeutic effect in the treatment of sleep disorders.