Sleep architecture parameters as a putative biomarker of suicidal ideation in treatment-resistant depression

- Suicidal ideation in treatment-resistant depression is linked with less deep sleep.
- The same group had increased nocturnal wakefulness and decreased sleep efficiency.
- Effect sizes were greater for those with bipolar than major depressive disorder.
- Sleep architecture may be a key putative biomarker in suicide prevention.

BackgroundDisturbed sleep may confer risk for suicidal behaviors. Polysomnographic (PSG) sleep parameters have not been systematically evaluated in association with suicidal ideation (SI) among individuals with treatment-resistant depression (TRD).MethodsThis secondary data analysis included 54 TRD individuals (N=30 with major depressive disorder (MDD) and N=24 with bipolar depression (BD)). PSG sleep parameters included Sleep Efficiency (SE), Total Sleep Time (TST), Wakefulness After Sleep Onset (WASO), REM percent/latency, and non-REM (NREM) Sleep Stages 1-4. The Hamilton Depression Rating Scale (HAM-D) was used to group participants according to presence or absence of SI. Sleep abnormalities were hypothesized among those with current SI. ANOVA analyses were conducted before (Model 1) and after adjusting for depression (Model 2) and diagnostic variables (Model 3).ResultsSignificant differences in PSG parameters were observed in Model 1; those with SI had less NREM Stage 4 sleep (p<.05). After adjusting for central covariates, Models 2 and 3 revealed significantly less NREM Stage 4 sleep, lower SE (P<.05), and higher WASO (P<.05) among those with SI. BD participants with SI also had less NREM Stage 4 and more NREM Stage 1 sleep.Limitations1) a predominantly white sample; 2) exclusion of imminent suicide risk; 3) concomitant mood stabilizer use among BD patients; and 4) single-item SI assessment.ConclusionsIndependent of depression severity, SI was associated with less NREM Stage 4 sleep, and higher nocturnal wakefulness across diagnostic groups. Sleep may warrant further investigation in the pathogenesis of suicide risk, particularly in TRD, where risk may be heightened.