Sleep disturbances among older adults following traumatic brain injury.
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ABSTRACT:
SUBMITTER: Albrecht JS
PROVIDER: S-EPMC6986451 | biostudies-literature | 2020 Feb
REPOSITORIES: biostudies-literature
Publications
Sleep disturbances among older adults following traumatic brain injury.
Albrecht Jennifer S JS Wickwire Emerson M EM
International review of psychiatry (Abingdon, England) 20190923 1
Sleep disturbances are common sequelae of traumatic brain injury (TBI) that are associated with poorer recovery. This is important among older adults, who fare worse following TBI relative to younger adults and have a higher prevalence of sleep disorders. The objective of this study was to assess the risk of newly-diagnosed sleep disorders following TBI among adults ≥65 years. Using a large commercial insurance database, older adults diagnosed with TBI between 2008-2014 (<i>n</i> = 78,044) and n ...[more]
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Project description:Study objectivesSleep disturbances are frequently reported following traumatic brain injury (TBI); however, the exact disturbances remain unclear. This meta-analysis aimed to characterize sleep disturbance in community dwelling patients with TBI as compared to controls.MethodsTwo investigators independently conducted a systematic search of multiple electronic databases from inception to May 27, 2015. Studies were selected if they compared sleep in community dwelling individuals with TBI relative to a control population without head injury. Data were pooled in meta-analysis with outcomes expressed as the standard mean difference (SMD) and 95% confidence interval (CI). The primary outcomes were derived from polysomnography and secondary outcomes were derived from subjective sleep measures.ResultsSixteen studies were included, combining 637 TBI patients and 567 controls, all of whom were community dwelling. Pooled polysomnography data revealed that TBI patients had poorer sleep efficiency (SMD = -0.47, CI: -0.89, -0.06), shorter total sleep duration (SMD = -0.37, CI: -0.59, -0.16), and greater wake after sleep onset time (SMD = 0.60, CI: 0.33, 0.87). Although sleep architecture was similar between the groups, a trend suggested that TBI patients may spend less time in REM sleep (SMD = -0.22, CI: -0.45, 0.01). Consistent with polysomnographic derangement, TBI patients reported greater subjective sleepiness and poorer perceived sleep quality.ConclusionsThe evidence suggests that TBI is associated with widespread objective and subjective sleep deficits. The present results highlight the need for physicians to monitor and address sleep deficits following TBI.
| S-EPMC4773614 | biostudies-literature
Project description:OBJECTIVE:This prospective longitudinal study investigated sleep disturbance (SD) and internalizing problems after traumatic injury, including traumatic brain injury (TBI) or extracranial/bodily injury (EI) in children and adolescents, relative to typically developing (TD) children. We also examined longitudinal relations between SD and internalizing problems postinjury. METHOD:Participants (N = 87) ages 8-15 included youth with TBI, EI, and TD children. Injury groups were recruited from a Level 1 trauma center after sustaining vehicle-related injuries. Parent-reported SD and internalizing problems were assessed at preinjury/baseline, and 6 and 12 months postinjury. Linear mixed models evaluated the relation of group and time of assessment on outcomes. RESULTS:Controlling for age, the combined traumatic injury group experienced significantly higher postinjury levels of SD (p = .042) and internalizing problems (p = .024) than TD children; however, TBI and EI injury groups did not differ from each other. Injury severity was positively associated with SD in the EI group only, but in both groups SD was associated with additional postinjury sequelae, including fatigue and externalizing behavior problems. Internalizing problems predicted subsequent development of SD but not vice versa. The relation between injury and SD 1 year later was consistent with mediation by internalizing problems at 6 months postinjury. CONCLUSIONS:Children with both types of traumatic injury demonstrated higher SD and internalizing problems than healthy children. Internalizing problems occurring either prior to or following pediatric injury may be a risk factor for posttraumatic SD. Consequently, internalizing problems may be a promising target of intervention to improve both SD and related adjustment concerns. (PsycINFO Database Record
| S-EPMC5851286 | biostudies-literature
Project description:ObjectivesSleep disturbances commonly follow traumatic brain injury (TBI) and contribute to ongoing disability. However, there are no conclusive findings regarding specific changes to sleep quality and sleep architecture measured using polysomnography. Possible causes of the sleep disturbances include disruption of circadian regulation of sleep-wakefulness, psychological distress, and a neuronal response to injury. We investigated sleep-wake disturbances and their underlying mechanisms in a TBI patient sample.MethodsThis was an observational study comparing 23 patients with TBI (429.7 +/- 287.6 days post injury) and 23 age- and gender-matched healthy volunteers on polysomnographic sleep measures, salivary dim light melatonin onset (DLMO) time, and self-reported sleep quality, anxiety, and depression.ResultsPatients with TBI reported higher anxiety and depressive symptoms and sleep disturbance than controls. Patients with TBI showed decreased sleep efficiency (SE) and increased wake after sleep onset (WASO). Although no significant group differences were found in sleep architecture, when anxiety and depression scores were controlled, patients with TBI showed higher amount of slow wave sleep. No differences in self-reported sleep timing or salivary DLMO time were found. However, patients with TBI showed significantly lower levels of evening melatonin production. Melatonin level was significantly correlated with REM sleep but not SE or WASO.ConclusionsReduced evening melatonin production may indicate disruption to circadian regulation of melatonin synthesis. The results suggest that there are at least 2 factors contributing to sleep disturbances in patients with traumatic brain injury. We propose that elevated depression is associated with reduced sleep quality, and increased slow wave sleep is attributed to the effects of mechanical brain damage.
| S-EPMC3462582 | biostudies-literature
Project description:Sleep-wake disturbances following traumatic brain injury (TBI) are increasingly recognized as a serious consequence following injury and as a barrier to recovery. Injury-induced sleep-wake disturbances can persist for years, often impairing quality of life. Recently, there has been a nearly exponential increase in the number of primary research articles published on the pathophysiology and mechanisms underlying sleep-wake disturbances after TBI, both in animal models and in humans, including in the pediatric population. In this review, we summarize over 200 articles on the topic, most of which were identified objectively using reproducible online search terms in PubMed. Although these studies differ in terms of methodology and detailed outcomes; overall, recent research describes a common phenotype of excessive daytime sleepiness, nighttime sleep fragmentation, insomnia, and electroencephalography spectral changes after TBI. Given the heterogeneity of the human disease phenotype, rigorous translation of animal models to the human condition is critical to our understanding of the mechanisms and of the temporal course of sleep-wake disturbances after injury. Arguably, this is most effectively accomplished when animal and human studies are performed by the same or collaborating research programs. Given the number of symptoms associated with TBI that are intimately related to, or directly stem from sleep dysfunction, sleep-wake disorders represent an important area in which mechanistic-based therapies may substantially impact recovery after TBI.
| S-EPMC6251652 | biostudies-literature
Project description:Traumatic brain injury (TBI) is a major cause of disability worldwide. Post-TBI sleep and wake disturbances are extremely common and difficult for patients to manage. Sleep and wake disturbances contribute to poor functional and emotional outcomes from TBI, yet effective therapies remain elusive. A more comprehensive understanding of mechanisms underlying post-TBI sleep and wake disturbance will facilitate development of effective pharmacotherapies. Previous research in human patients and animal models indicates that altered hypocretinergic function may be a major contributor to sleep-wake disturbance after TBI. In this study, we further elucidate the role of hypocretin by determining the impact of TBI on sleep-wake behavior of hypocretin knockout (HCRT KO) mice. Adult male C57BL/6J and HCRT KO mice were implanted with electroencephalography recording electrodes, and pre-injury baseline recordings were obtained. Mice were then subjected to either moderate TBI or sham surgery. Additional recordings were obtained and sleep-wake behavior determined at 3, 7, 15, and 30 days after TBI or sham procedures. At baseline, HCRT KO mice had a significantly different sleep-wake phenotype than control C57BL/6J mice. Post-TBI sleep-wake behavior was altered in a genotype-dependent manner: sleep of HCRT KO mice was not altered by TBI, whereas C57BL/6J mice had more non-rapid eye movement sleep, less wakefulness, and more short wake bouts and fewer long wake bouts. Numbers of hypocretin-positive cells were reduced in C57BL/6J mice by TBI. Collectively, these data indicate that the hypocretinergic system is involved in the alterations in sleep-wake behavior that develop after TBI in this model, and suggest potential therapeutic interventions.
| S-EPMC6387567 | biostudies-literature
Project description:ObjectivesThe objective of this study was to examine the effects of traumatic brain injury (TBI) and age on facial emotion recognition abilities in adults. Age and TBI were expected to have negative effects on emotion recognition and a TBI by age interaction was hypothesized such that older adults with TBI would have the lowest emotion recognition scores.MethodsA prospective cohort study was conducted. Participants were 26 adults with moderate-severe TBI (13 older and 13 younger) and 26 uninjured peers matched for age, sex, and education. Emotion recognition was measured using the Emotion Recognition Task, which is comprised of dynamically morphed facial expressions of the six basic emotions, presented at different intensity levels.ResultsTBI and older age were associated with poorer recognition of both subtle and intense expressions, but only for expressions of anger and sadness. There was no interaction of age and TBI.ConclusionsResults add to the growing evidence of emotion recognition impairments after TBI, particularly for select negative emotions, and extend this finding to adults over the age of 60. Further research is needed to better understand social cognitive effects of TBI across the adult lifespan.
| S-EPMC8351800 | biostudies-literature
Project description:ImportanceTraumatic brain injury (TBI), seizures, and dementia increase with age. There is a gap in understanding the associations of TBI, seizures, and medications such as antiseizure and antipsychotics with the progression of cognitive impairment across racial and ethnic groups.ObjectiveTo investigate the association of TBI and seizures with the risk of cognitive impairment among cognitively normal older adults and the role of medications in moderating the association.Design, setting, and participantsThis multicenter cohort study was a secondary analysis of the Uniform Data Set collected between June 1, 2005, and June 30, 2020, from the National Alzheimer's Coordination Center. Statistical analysis was performed from February 1 to April 3, 2024. Data were collected from participants from 36 Alzheimer's Disease Research Centers in the US who were 65 years or older at baseline, cognitively normal at baseline (Clinical Dementia Rating of 0 and no impairment based on a presumptive etiologic diagnosis of AD), and had complete information on race and ethnicity, age, sex, educational level, and apolipoprotein E genotype.ExposureHealth history of TBI, seizures, or both conditions.Main outcomes and measuresProgression to cognitive impairment measured by a Clinical Dementia Rating greater than 0.ResultsAmong the cohort of 7180 older adults (median age, 74 years [range, 65-102 years]; 4729 women [65.9%]), 1036 were African American or Black (14.4%), 21 were American Indian or Alaska Native (0.3%), 143 were Asian (2.0%), 332 were Hispanic (4.6%), and 5648 were non-Hispanic White (78.7%); the median educational level was 16.0 years (range, 1.0-29.0 years). After adjustment for selection basis using propensity score weighting, seizure was associated with a 40% higher risk of cognitive impairment (hazard ratio [HR], 1.40; 95% CI, 1.19-1.65), TBI with a 25% higher risk of cognitive impairment (HR, 1.25; 95% CI, 1.17-1.34), and both seizure and TBI were associated with a 57% higher risk (HR, 1.57; 95% CI, 1.23-2.01). The interaction models indicated that Hispanic participants with TBI and seizures had a higher risk of cognitive impairment compared with other racial and ethnic groups. The use of antiseizure medications (HR, 1.23; 95% CI, 0.99-1.53), antidepressants (HR, 1.32; 95% CI, 1.17-1.50), and antipsychotics (HR, 2.15; 95% CI, 1.18-3.89) was associated with a higher risk of cognitive impairment, while anxiolytic, sedative, or hypnotic use (HR, 0.88; 95% CI, 0.83-0.94) was associated with a lower risk.Conclusions and relevanceThis study highlights the importance of addressing TBI and seizures as risk factors for cognitive impairment among older adults. Addressing the broader social determinants of health and bridging the health divide across various racial and ethnic groups are essential for the comprehensive management and prevention of dementia.
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Project description:Blood-based biomarkers have been increasingly studied for diagnostic and prognostic purposes in patients with mild traumatic brain injury (MTBI). Biomarker levels in blood have been shown to vary throughout age groups. Our aim was to study four blood biomarkers, glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), neurofilament light (NF-L), and total tau (t-tau), in older adult patients with MTBI. The study sample was collected in the emergency department in Tampere University Hospital, Finland, between November 2015 and November 2016. All consecutive adult patients with head injury were eligible for inclusion. Serum samples were collected from the enrolled patients, which were frozen and later sent for biomarker analyses. Patients aged 60 years or older with MTBI, head computed tomography (CT) imaging, and available biomarker levels were eligible for this study. A total of 83 patients (mean age = 79.0, SD = 9.58, range = 60-100; 41.0% men) were included in the analysis. GFAP was the only biomarker to show statistically significant differentiation between patients with and without acute head CT abnormalities [U(83) = 280, p < 0.001, r = 0.44; area under the curve (AUC) = 0.79, 95% CI = 0.67-0.91]. The median UCH-L1 values were modestly greater in the abnormal head CT group vs. normal head CT group [U (83) = 492, p = 0.065, r = 0.20; AUC = 0.63, 95% CI = 0.49-0.77]. Older age was associated with biomarker levels in the normal head CT group, with the most prominent age associations being with NF-L (r = 0.56) and GFAP (r = 0.54). The results support the use of GFAP in detecting abnormal head CT findings in older adults with MTBIs. However, small sample sizes run the risk for producing non-replicable findings that may not generalize to the population and do not translate well to clinical use. Further studies should consider the potential effect of age on biomarker levels when establishing clinical cut-off values for detecting head CT abnormalities.
| S-EPMC9723459 | biostudies-literature
Project description:ObjectiveTo assess the relationship between posttraumatic brain injury statin use and (1) mortality and (2) the incidence of associated morbidities, including stroke, depression, and Alzheimer's disease and related dementias following injury.Setting and participantsNested cohort of all Medicare beneficiaries 65 years of age and older who survived a traumatic brain injury (TBI) hospitalization during 2006 through 2010. The final sample comprised 100 515 beneficiaries.DesignRetrospective cohort study of older Medicare beneficiaries. Relative risks (RR) and 95% confidence interval (CI) were obtained using discrete time analysis and generalized estimating equations.MeasuresThe exposure of interest included monthly atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin use. Outcomes of interest included mortality, stroke, depression, and Alzheimer's disease and related dementias.ResultsStatin use of any kind was associated with decreased mortality following TBI hospitalization discharge. Any statin use was also associated with a decrease in any stroke (RR, 0.86; 95% confidence intervals (CI), 0.81-0.91), depression (RR, 0.85; 95% CI, 0.79-0.90), and Alzheimer's disease and related dementias (RR, 0.77; 95% CI, 0.73-0.81).ConclusionThese findings provide valuable information for clinicians treating older adults with TBI as clinicians can consider, when appropriate, atorvastatin and simvastatin to older adults with TBI in order to decrease mortality and associated morbidities.
| S-EPMC6066463 | biostudies-literature
Project description:Traumatic brain injury (TBI) elicits an inflammatory response in the central nervous system (CNS) that involves both resident and peripheral immune cells. Neuroinflammation can persist for years following a single TBI and may contribute to neurodegeneration. However, administration of anti-inflammatory drugs shortly after injury was not effective in the treatment of TBI patients. Some components of the neuroinflammatory response seem to play a beneficial role in the acute phase of TBI. Indeed, following CNS injury, early inflammation can set the stage for proper tissue regeneration and recovery, which can, perhaps, explain why general immunosuppression in TBI patients is disadvantageous. Here, we discuss some positive attributes of neuroinflammation and propose that inflammation be therapeutically guided in TBI patients rather than globally suppressed.
| S-EPMC5260471 | biostudies-literature