Neuroimaging studies have produced seemingly contradictory findings in regards to the pathophysiology of insomnia. Although most study results are interpreted from the perspective of a “hyperarousal” model, the aggregate findings from neuroimaging studies suggest a more complex model is needed. We provide a review of the major findings from neuroimaging studies, then discuss them in relation to a heuristic model of sleep-wake states that involves three major factors: wake drive, sleep drive, and level of conscious awareness. We propose that insomnia involves dysregulation in these factors, resulting in subtle dysregulation of sleep-wake states throughout the 24 h light/dark cycle.

Objectives: Parkinson's disease (PD) is a multisystem movement disorder associated with sleep disturbance and depression. Sleep disturbances and depression severity share a bidirectional association. This association may be greater in individuals who are more vulnerable to the deleterious consequences of sleep disturbance and depression severity. We investigated whether the association between sleep disturbances and depression severity is greater in patients with PD than in matched controls (MC).Materials and Methods: The study sample (N = 98) included 50 patients with idiopathic PD and 48 age‐, race‐, sex‐, and education‐matched controls. Sleep disturbances were assessed using self‐reported total sleep time (TST) on the Pittsburgh Sleep Quality Index, the sleep item on the Beck Depression Inventory, 2nd ed. (BDI‐II), and the Insomnia Severity Index total score. Depression severity was assessed using the BDI‐II total score, excluding the sleep item. Spearman's correlations, chi‐squared tests, and multiple regression were used to assess associations between sleep disturbances and depression severity in PD and MC. Fisher's Z transformation was used to test whether the association between sleep disturbances and depression severity was stronger in patients with PD.Results: Shorter TST, sleeping less than usual, and insomnia severity were associated with depression severity in the total sample, r_s(94) = −0.35, p = .001; r_s(71) = 0.51, p < .001; r_s(78) = −0.47, p < .001; r_s(98) = 0.46, p < .001, respectively. The association between shorter TST and depression severity was greater in patients with PD than it was in MC, p < .05.Conclusion: Short TST may be an important marker, predictor, or consequence of depression severity in patients with Parkinson's disease.

Sleep discrepancies are common in primary insomnia (PI) and include reports of longer sleep onset latency (SOL) than measured by polysomnography (PSG) or “negative SOL discrepancy.” We hypothesized that negative SOL discrepancy in PI would be associated with higher relative glucose metabolism during nonrapid eye movement (NREM) sleep in brain networks involved in conscious awareness, including the salience, left executive control, and default mode networks. PI (n = 32) and good sleeper controls (GS; n = 30) completed [¹⁸F]fluorodeoxyglucose positron emission tomography (FDG-PET) scans during NREM sleep, and relative regional cerebral metabolic rate for glucose (rCMR_glc) was measured. Sleep discrepancy was calculated by subtracting PSG-measured SOL on the PET night from corresponding self-report values the following morning. We tested for interactions between group (PI vs. GS) and SOL discrepancy for rCMR_glc during NREM sleep using both a region of interest mask and exploratory whole-brain analyses. Significant group by SOL discrepancy interactions for rCMR_glc were observed in several brain regions (p_corrected < .05 for all clusters). In the PI group, more negative SOL discrepancy (self-reported > PSG-measured SOL) was associated with significantly higher relative rCMR_glc in the right anterior insula and middle/posterior cingulate during NREM sleep. In GS, more positive SOL discrepancy (self-reported < PSG-measured SOL) was associated with significantly higher relative rCMR_glc in the right anterior insula, left anterior cingulate cortex, and middle/posterior cingulate cortex. Although preliminary, these findings suggest regions of the brain previously shown to be involved in conscious awareness, and the perception of PSG-defined states may also be involved in the phenomena of SOL discrepancy.

Insomnia is a risk factor for suicidal behavior including attempts and death by suicide. We investigated whether insomnia symptom severity was associated with suicidality and death by suicide in patients with psychiatric disorders. The sample included 180 deceased patients with psychiatric disorders seen at Weber Human Services between 2008 and 2018 who completed the Outpatient Questionnaire-45.2 (OQ) prior to death. Insomnia symptom severity was assessed using item 41 from the OQ. Manner of death was determined by death records and autopsy reports. History of suicidality was determined through electronic medical records. Cases were grouped into 4 lifetime categories: non-suicidal (n=30), suicidal ideation (n=36), suicide attempt (n=95), and death by suicide (n=19). Demographic, medical, and psychiatric features of each group were compared using linear regression. Logistic regression was used to determine whether insomnia symptom severity was associated with lifetime suicidality severity grouping, adjusting for psychiatric disorders commonly linked to suicidality. Lifetime suicidality was associated with sleep problems, fatigue, headaches, and psychiatric disorders (i.e., depressive, personality, and trauma-related disorders). Referenced to the non-suicidal group, greater insomnia symptom severity was significantly associated with suicide attempts and death by suicide, with odds ratios (OR) of OR=2.67, p=0.011, and OR=5.53, p=0.002, respectively, even after adjusting important psychiatric diagnoses. Results suggest that insomnia symptom severity endorsed during a clinical visit is associated with heightened suicidality, especially suicidal behavior. The presence of insomnia symptoms in patients with psychiatric disorders may indicate risk for suicide and is a target for suicide prevention.

Parkinson’s disease (PD) is associated with cognitive and sleep impairments. The presence of rapid eye movement (REM) sleep behavior disorder (RBD) symptoms may represent a worse disease prognosis for PD individuals. We investigated cognitive functioning and self-reported sleep in early-stage PD individuals with (n = 19) or without (n = 31) probable RBD. Probable RBD was defined as >5 on the REM Sleep Behavior Disorder Screening Questionnaire. Inhibition, visuospatial cognitive abilities, working memory, sustained visual attention, verbal fluency, and episodic memory were assessed. Sleep impairments were assessed using the Pittsburgh Sleep Quality Index, Insomnia Severity Index, Epworth Sleepiness Scale, and Patient-Reported Outcomes Measurement Information System questionnaires. Chi-squared, Mann-Whitney U, and independent sample t-tests were employed to assess group differences. Participants with PD and probable RBD performed significantly worse on word reading and switching verbal fluency tasks than PD participants without probable RBD (p < 0.05). No significant differences were found in mood, PD severity, or sleep measures between PD individuals with or without probable RBD. Cognitive tasks that involve verbal or switching components may be most impaired in PD individuals with probable RBD. Larger samples are needed to determine whether other cognitive domains and sleep features are significantly associated with RBD in PD.