Creation of a shortened version of the Sleep Disorders Questionnaire (SDQ).

The 176-item Sleep Disorders Questionnaire (SDQ) was initially developed using canonical discriminant function analysis on 4 groups of sleep disorder patients, but it was never studied by factor analysis in its entirety. Several authors have criticized 2 of its subscales as being confounded with each other, and its narcolepsy scale as substantially over-diagnosing narcolepsy. This study describes its first exploratory factor analysis (EFA), the intent of which was to reassess item membership on the 4 existing subscales and to derive new scales to improve differential diagnosis between patient groups. It was also hoped that EFA could reduce the total number of questions, to increase speed of completion. The EFA was performed on the anonymized SDQ results from a retrospective review of the charts of 2131 persons from 7 sleep disorders clinics and research centers. Factors were assessed via scree plots and eigenvalues. The EFA identified four main factors: insomnia, daytime sleepiness, substance use, and sleep-disordered breathing. The insomnia factor had 3 subfactors: psychological symptoms of insomnia, subjective description of insomnia, and insomnia due to periodic limb movements. The sleepiness factor had two subfactors: daytime sleepiness and neurological symptoms of narcolepsy. The novel substance use factor was homogeneous, as was the sleep-disordered breathing factor. Importantly, the EFA reassigned items from the original SDQ's NAR, PSY, and PLM subscales to five of the new subscales. The Sleep Apnea (SA) subscale emerged mostly unchanged. The 7 resulting factors comprised only 66 items of the original 176-item SDQ. These results have allowed the creation of a new shorter questionnaire, to be called the SDQ-2. External validation of the SDQ-2 is currently underway. It will likely prove to be a superior differential diagnostic instrument for sleep disorders clinics, compared to the original SDQ.

A pilot study of serotonin-1A receptor genotypes and rapid eye movement sleep sensitivity to serotonergic/cholinergic imbalance in humans: a pharmacological model of depression.

RATIONALE: The serotonergic and cholinergic systems are jointly involved in regulating sleep but this system is theorized to be disturbed in depressed individuals. We previously reported that cholinergic and serotonergic agents induce sleep changes partially consistent with monoamine models of sleep disturbances in depression. One potential cause of disturbed neurotransmission is genetic predisposition. The G(-1019) allele of the serotonin-1A (5-HT1A) receptor promoter region predicts an increased risk for depression compared to the wild-type C(-1019) allele. OBJECTIVE: The goal of this study was to investigate how serotonin-1A receptor genotypes mediate sleep sensitivity to pharmacological probes modeling the serotonergic/cholinergic imbalance of depression. METHODS: Seventeen healthy female participants homozygous for either C (n=11) or G (n=6) alleles aged 18-27 years were tested on four nonconsecutive nights. Participants were given galantamine (an anti-acetylcholinesterase), buspirone (a serotonergic agonist), both drugs together, or placebos before sleeping. RESULTS: As reported previously, buspirone significantly increased rapid eye movement (REM) latency (P<0.001), as well as awakenings, percentage of time spent awake, and percentage of time asleep spent in stage N1 (P<0.019). Galantamine increased awakenings, percentage of time spent awake, percentage of time asleep spent in stage N1, and percentage of time asleep spent in REM, and decreased REM latency and percentage of time asleep spent in stage N3 (P<0.019). Galantamine plus buspirone given together disrupted sleep more than either drug alone, lowering sleep efficiency and percentage of time asleep spent in stage N3 and increasing awakenings, percentage of time spent awake, and percentage of time asleep spent in stage N1 (P<0.019). There was no main effect of genotype nor was there a significant multivariate interaction between genotype and drug condition. CONCLUSION: These findings are partially consistent with the literature about sleep in depression, notably short REM latency, higher percentage of total sleep time spent in REM, lower percentage of time asleep spent in stage N3, and increased sleep fragmentation. The C/G mutation in the serotonin-1A receptor promoter region does not appear to cause noticeable differences in the sleep patterns of a relatively small sample of healthy young females. Future studies with larger sample sizes are required.

The effects of galantamine and buspirone on sleep structure: Implications for understanding sleep abnormalities in major depression.

RATIONALE: The serotonergic and cholinergic systems are jointly involved in regulating sleep, but this balance is theorized to be disturbed in depressed individuals. OBJECTIVE: The goal of this study was to use biological probes in healthy participants, to model the serotonergic/cholinergic imbalance of depression and its associated abnormalities in sleep structure. METHODS: We tested 20 healthy female participants 18-30 years of age on four non-consecutive nights. Participants were given galantamine (a cholinergic agent), buspirone (a serotonergic agonist), both drugs together, or placebo before sleeping. RESULTS: Buspirone suppressed tonic rapid eye movement (REM): There was a significant increase in REM latency (p < 0.001). Galantamine increased tonic REM sleep, leading to more time spent in REM (p < 0.001) and shorter REM latency (p < 0.01). Galantamine and buspirone given together were not significantly different from the placebo night by REM sleep measures, but disrupted sleep more than either drug alone. CONCLUSIONS: These findings are partially consistent with the cholinergic literature about sleep in depression, notably short REM latency, higher percentage of total sleep time spent in REM and increased sleep fragmentation. The prolonged REM latency and reduced percentage of REM with buspirone resembled the effect of selective serotonin reuptake inhibitor antidepressants on REM sleep.