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.