Obstructive sleep apnea (OSA) is a sleep disorder with no widely accepted pharmacological therapy. Cannabinoids have been suggested to reduce OSA severity in small human studies. The purpose of this retrospective cohort study was to explore the association of self-reported cannabis use on OSA severity and sleep parameters in a large cohort of adults undergoing in-laboratory polysomnography.

Sleep and medication data were collected for all consecutive adults who completed diagnostic polysomnography at Sunnybrook Health Sciences Centre from 2010 to 2022. Multivariable linear regression models were employed that adjusted for age, sex, and BMI (minimally adjusted model), as well as medication and comorbidity data (maximally adjusted model). An exploratory subgroup analysis was additionally run in patients with moderate to severe OSA.

Of 6,958 individuals (mean age 54.7 ± 16.3, BMI 29.1 ± 6.8, 51.0% female), 71 reported cannabis use. In our minimally adjusted models, cannabis use predicted a reduced respiratory disturbance index (RDI) (β: −4.8 [95% CI: −9.4, −0.2]; p = 0.042); this association became nonsignificant in the fully adjusted models. In an exploratory analysis of patients with moderate to severe OSA (n = 613), cannabis use (n = 7) predicted increased stage N3 sleep (β: 33.5 [95% CI: 15.6, 51.4]; p < 0.001) and decreased REM sleep (β: 16.0 [95% CI: 0.3, 31.7]; p = 0.046).

Self-reported cannabis use was not associated with OSA severity after adjusting for confounders. In an exploratory subgroup analysis of patients with moderate to severe OSA, cannabis use impacted sleep architecture. Future studies should further explore these findings.

Obstructive sleep apnea (OSA) is prevalent after stroke and associated with recurrent stroke, prolonged hospitalization, and decreased functional recovery. Sex differences in post-stroke OSA remain underexplored. The objective of this study was to evaluate sex differences in functional outcomes, stroke and OSA severity, and clinical manifestations of OSA in stroke patients with OSA.

We retrospectively evaluated data from three previously conducted studies. Study patients had an imaging-confirmed stroke and had been found to have OSA (apnea–hypopnea index [AHI] ≥ 5) on either in-laboratory polysomnography or home sleep apnea testing performed within 1 year of their stroke. Linear regression models were used to evaluate study outcomes.

In total, 171 participants with post-stroke OSA (117 males [68.4%] and 54 females [31.6%]) were included. Female sex was an independent predictor for greater functional impairment (β = 0.37, 95% CI 0.029–0.71, p = 0.03), increased stroke severity (β = 1.009, 95% CI 0.032–1.99, p = 0.04), and greater post-stroke depressive symptoms (β = 3.73, 95% CI 0.16–7.29, p = 0.04). Female sex was associated with lower OSA severity, as measured by the AHI (β = –5.93, 95% CI –11.21– –0.66). Sex was not an independent predictor of specific symptoms of OSA such as daytime sleepiness, snoring, tiredness, and observed apneas.

Females with post-stroke OSA had poorer functional outcomes and more severe strokes compared to males, despite having lower OSA severity. Females with post-stroke OSA also exhibited more depressive symptoms. Understanding sex differences in patients with post-stroke OSA will likely facilitate better recognition of OSA and potentially improve clinical outcomes.

To characterize 1) the relationship between laxative use and objective sleep metrics, and 2) the relationship between laxative use and self-reported insomnia symptoms in a convenience sample of middle-aged/elderly patients who completed in-laboratory polysomnography.

We cross-sectionally analyzed first-night diagnostic in-laboratory polysomnography data for 2946 patients over the age of 40 (mean age 60.5 years; 48.3% male). Laxative use and medical comorbidities were obtained through self-reported questionnaires. Patient insomnia symptoms were based on self-report. Associations between laxative use and objective sleep continuity were analyzed using multivariable linear regression models. Associations between laxative use and insomnia were assessed using multivariable logistic regression models.

After adjusting for age, sex, body mass index, total recording time, and relevant comorbidities, laxative users had a 7.1% lower sleep efficiency (p < 0.001), 25.5-minute higher wake after sleep onset (p < 0.001), and a 29.4-minute lower total sleep time (p < 0.001) than patients not using laxatives. Laxative users were found to be at greater odds of reporting insomnia symptoms (OR = 1.7, p = 0.024) than patients not using laxatives.

Laxative use is associated with impairments in objective sleep continuity. Patients using laxatives were also at greater odds of reporting insomnia symptoms.

The amplitude of the cortically generated somatosensory evoked potential (SSEP) is used to predict outcome in comatose patients. The relationship between epileptiform discharges and SSEP amplitude has not been elucidated in those patients.

Bilateral median nerve SSEP and electroencephalograph (EEG) studies were performed in a comatose patient (patient 1) 1 day after cardiac surgery and repeated 4 days later. He had tranexamic acid administered before and during surgery. Another comatose patient (patient 2) had the same studies performed 1 day after sustaining 10 minutes of pulseless electrical cardiac activity.

Both comatose patients had epileptiform discharges (on EEG) that were coincident with giant cortically generated SSEPs. In patient 1, the EEG and SSEP studies repeated 5 days postoperatively showed no epileptiform discharges, and the cortically generated SSEP amplitude was decreased (normalized) compared with that obtained one day postoperatively. He emerged from coma and had a good recovery. Patient 2 died shortly after EEG and SSEP testing.

Epileptiform discharges were associated with giant cortically generated median nerve SSEP amplitude (tranexamic acid was implicated in patient 1 and anoxic brain injury in patient 2). Accordingly, those who use the amplitude of cortically generated SSEPs for predicting outcome in comatose patients should consider the presence of epileptiform discharges (detected by EEG) as a potential confounding factor.