The Relationship between Sleep Architecture and Symptoms of Sleep Disturbance in Individuals with Traumatic Brain Injury

Objective: To measure sleep architecture in individuals with TBI and determine its relationship with self-reported sleep quality, fatigue, and daytime sleepiness. Design: Participants: completed self-report measures and underwent two nights of in-laboratory nocturnal polysomnography. Setting: General community. Participants: 46 individuals with mild to severe TBI. Inclusion criteria included age between 18 years to 65 years and a documented TBI as a result of a blow to the head with a loss of consciousness or period of being dazed and confused (e.g., EMS report, hospital record, physician record, or a positive screen on the Brain Injury Screening Questionnaire). Participants: were required to be at least one year post injury (SD Z 13.33 years, range 1.17 years e 56.33 years), English-speaking, and have at least a sixth-grade reading level. No use of Modafinil, amphetamines or soporific medications (e.g., zolpidem, zolpidem MR, eszopiclone, zaleplon, sedating antidepressants, melatonin, valerian root, Benedryl, Ramelteon or chloral hydrate) was allowed 72 hours prior to polysomnography. Use of medications known to cause hypersomnolence (e.g. barbiturates, benzodiazepines, opiates) was not allowed for seven days prior to study. Exclusion criteria included active hepatic or renal failure (which may lead to hypersomnia), active substance abuse disorder, prior or current psychotic disorder, pre-existing neurological disorder or a brain injury with an etiology other than trauma, untreated hypothyroidism and any medical condition or reason that, in the investigator’s opinion, might make the participant unsuitable to participate. All participants were recruited through flyer postings in the Mount Sinai Medical Center and through healthcare provider referrals. The study was approved by the institutional review board of Icahn School of Medicine at Mount Sinai. Informed consent was obtained prior to screening to determine whether or not they met inclusion/exclusion criteria. Interventions: Not applicable. Main Outcome Measure(s): The measures included self-report measures of sleep quality (Pittsburgh Sleep Quality Index; PSQI), fatigue (Multidimensional Assessment of Fatigue; MAF), daytime sleepiness (Epworth Sleepiness Scale; ESS), and nocturnal polysomnography (NPSG) from which sleep efficiency, sleep onset latency, REM latency, wake time after sleep onset, and percentage of stage 1, 2, 3, and REM 4 sleep were extracted. Results: Pearson product-moment correlation coefficients were used to analyze the association between responses on self-report questionnaires. Hierarchical linear regression was used to analyze the association between NPSG sleep parameters and self-report questionnaires, adjusting for age, sex, body mass index, sleep apnea, and TBI severity. Poor sleep quality as measured by the PSQI was associated with fatigue as measured by the MAF. Poor sleep quality was associated with poor sleep efficiency, short duration of stage 2 sleep, and long duration of rapid eye movement sleep. There was a weak association between high levels of fatigue and poor sleep efficiency. Daytime sleepiness as assessed was not associated with any NPSG sleep parameters. Conclusions: In this sample of TBI survivors, those who reported poor sleep quality evidenced shorter time spent in stage 2 sleep compared to those who reported better sleep quality. These findings suggest that disruptions in stage 2 sleep might underlie the symptoms of sleep disturbance experienced following TBI.