Fatigue is a common symptom after traumatic brain injuries (TBI) and a crucial target of rehabilitation. The subjective and multifactorial nature of fatigue necessitates a biopsychosocial approach in understanding the mechanisms involved in its development. The aim of this study is to provide a comprehensive exploration of factors relevant to identification and rehabilitation of fatigue following TBI. Ninety-six patients with TBI and confirmed intracranial injuries were assessed on average 200 days post-injury with regard to injury-related factors, several patient-reported outcome measures (PROMS) of fatigue, neuropsychological measures, and PROMS of implicated biopsychosocial mechanisms. Factor analytic approaches yielded three underlying factors, termed Psychosocial Robustness, Somatic Vulnerability and Injury Severity. All three dimensions were significantly associated with fatigue in multiple regression analyses and explained 44.2% of variance in fatigue. Post hoc analyses examined univariate contributions of the associations between the factors and fatigue to illuminate the relative contributions of each biopsychosocial variable. Implications for clinical practice and future research are discussed.

Background Fatigue is one of the most commonly reported subjective symptoms following traumatic brain injury (TBI). The aims were to assess frequency of fatigue over the first 6 months after TBI, and examine whether fatigue changes could be predicted by demographic characteristics, injury severity and comorbidities. Methods Patients with acute TBI admitted to 65 trauma centers were enrolled in the study Collaborative European NeuroTrauma Effectiveness Research in TBI (CENTER-TBI). Subjective fatigue was measured by single item on the Rivermead Post-Concussion Symptoms Questionnaire (RPQ), administered at baseline, three and 6 months postinjury. Patients were categorized by clinical care pathway: admitted to an emergency room (ER), a ward (ADM) or an intensive care unit (ICU). Injury severity, preinjury somatic- and psychiatric conditions, depressive and sleep problems were registered at baseline. For prediction of fatigue changes, descriptive statistics and mixed effect logistic regression analysis are reported. Results Fatigue was experienced by 47% of patients at baseline, 48% at 3 months and 46% at 6 months. Patients admitted to ICU had a higher probability of experiencing fatigue than those in ER and ADM strata. Females and individuals with lower age, higher education, more severe intracranial injury, preinjury somatic and psychiatric conditions, sleep disturbance and feeling depressed postinjury had a higher probability of fatigue. Conclusion A high and stable frequency of fatigue was found during the first 6 months after TBI. Specific socio-demographic factors, comorbidities and injury severity characteristics were predictors of fatigue in this study.

Objective Fatigue is a common symptom in somatic and mental illness. Musculoskeletal pain and psychological distress have in turn frequently been shown to be associated with fatigue across clinical conditions and in the general population. The study aims to disentangle direct effects from those due to mere confounding from shared etiologies. Design The study used genetically informative longitudinal twin data, through a co-twin control design with an additional within-person dimension. Methods Data on fatigue, pain and distress from 2196 mono – and dizygotic twins from the Norwegian Twin Registry examined at two time points five years apart was analyzed using multilevel generalized linear regression modeling. Fatigue was regressed on pain and distress, with further controls added for confounding from genetic and stable non-shared environmental sources. Results Pain and distress had a significant impact on fatigue at genetic, stable non-shared environmental and time-varying levels, even when controlling for somatic comorbidity. Conclusion The findings indicate that a significant proportion of the association between fatigue, pain and distress is due to genetic and environmental confounding. Pain and distress exert significant, albeit smaller effects on fatigue even when controlling for genetic and stable environmental contributions, indicating direct effects. Potential etiological pathways and underlying mechanisms are discussed.

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