Brain Injury Functional Outcome Measure (BI-FOM): A Single Instrument Capturing the Range of Recovery in Moderate-Severe Traumatic Brain Injury.
Ontology highlight
ABSTRACT: Objective
To develop a measure of global functioning after moderate-severe TBI with similar measurement precision but a longer measurement range than the FIM.Design
Phase 1: retrospective analysis of 5 data sets containing FIM, Disability Rating Scale, and other assessment items to identify candidate items for extending the measurement range of the FIM; Phase 2: prospective administration of 49 candidate items from phase 1, with Rasch analysis to identify a unidimensional scale with an extended range.Setting
Six TBI Model System rehabilitation hospitals.Participants
Individuals (N=184) with moderate-severe injury recruited during inpatient rehabilitation or at 1-year telephone follow-up.Interventions
Participants were administered the 49 assessment items in person or via telephone.Main outcome measures
Item response theory parameters: item monotonicity, infit/outfit statistics, and Factor 1 variance.Results
After collapsing misordered rating categories and removing misfitting items, we derived the Brain Injury Functional Outcome Measure (BI-FOM), a 31-item assessment instrument with high reliability, greatly extended measurement range, and improved unidimensionality compared with the FIM.Conclusions
The BI-FOM improves global measurement of function after moderate-severe brain injury. Its high precision, relative lack of floor and ceiling effects, and feasibility for telephone follow-up, if replicated in an independent sample, are substantial advantages.
SUBMITTER: Whyte J
PROVIDER: S-EPMC9255898 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:OBJECTIVES:To characterize admission patterns, treatments, and outcomes among patients with moderate traumatic brain injury. DESIGN:Retrospective cohort study. SETTING:National Trauma Data Bank. PATIENTS:Adults (age > 18 yr) with moderate traumatic brain injury (International Classification of Diseases, Ninth revision codes and admission Glasgow Coma Scale score of 9-13) in the National Trauma Data Bank between 2007 and 2014. INTERVENTIONS:None. MEASUREMENT AND MAIN RESULTS:Demographics, mechanism of injury, hospital course, and facility characteristics were examined. Admission characteristics associated with discharge outcomes were analyzed using multivariable Poisson regression models. Of 114,066 patients, most were white (62%), male (69%), and had median admission Glasgow Coma Scale score of 12 (interquartile range, 10-13). Seventy-seven percent had isolated traumatic brain injury. Concussion, which accounted for 25% of moderate traumatic brain injury, was the most frequent traumatic brain injury diagnosis. Fourteen percent received mechanical ventilation, and 66% were admitted to ICU. Over 50% received care at a community hospital. Seven percent died, and 32% had a poor outcome, including those with Glasgow Coma Scale score of 13. Compared with patients 18-44 years, patients 45-64 years were twice as likely (adjusted relative risk, 1.97; 95% CI, 1.92-2.02) and patients over 80 years were five times as likely (adjusted relative risk, 4.66; 95% CI, 4.55-4.76) to have a poor outcome. Patients with a poor discharge outcome were more likely to have had hypotension at admission (adjusted relative risk, 1.10; 95% CI, 1.06-1.14), lower admission Glasgow Coma Scale (adjusted relative risk, 1.37; 95% CI, 1.34-1.40), higher Injury Severity Score (adjusted relative risk, 2.97; 95% CI, 2.86-3.09), and polytrauma (adjusted relative risk, 1.05; 95% CI, 1.02-1.07), compared with those without poor discharge outcomes. CONCLUSIONS:Many patients with moderate traumatic brain injury deteriorate, require neurocritical care, and experience poor outcomes. Optimization of care and outcomes for this vulnerable group of patients are urgently needed.
| S-EPMC5899009 | biostudies-literature
Project description:ObjectivesAfter traumatic brain injury, continuous electroencephalography is widely used to detect electrographic seizures. With the development of standardized continuous electroencephalography terminology, we aimed to describe the prevalence and burden of ictal-interictal patterns, including electrographic seizures after moderate-to-severe traumatic brain injury and to correlate continuous electroencephalography features with functional outcome.DesignPost hoc analysis of the prospective, randomized controlled phase 2 multicenter INTREPID study (ClinicalTrials.gov: NCT00805818). Continuous electroencephalography was initiated upon admission to the ICU. The primary outcome was the 3-month Glasgow Outcome Scale-Extended. Consensus electroencephalography reviews were performed by raters certified in standardized continuous electroencephalography terminology blinded to clinical data. Rhythmic, periodic, or ictal patterns were referred to as "ictal-interictal continuum"; severe ictal-interictal continuum was defined as greater than or equal to 1.5 Hz lateralized rhythmic delta activity or generalized periodic discharges and any lateralized periodic discharges or electrographic seizures.SettingTwenty U.S. level I trauma centers.PatientsPatients with nonpenetrating traumatic brain injury and postresuscitation Glasgow Coma Scale score of 4-12 were included.InterventionsNone.Measurements and main resultsAmong 152 patients with continuous electroencephalography (age 34 ± 14 yr; 88% male), 22 (14%) had severe ictal-interictal continuum including electrographic seizures in four (2.6%). Severe ictal-interictal continuum burden correlated with initial prognostic scores, including the International Mission for Prognosis and Analysis of Clinical Trials in Traumatic Brain Injury (r = 0.51; p = 0.01) and Injury Severity Score (r = 0.49; p = 0.01), but not with functional outcome. After controlling clinical covariates, unfavorable outcome was independently associated with absence of posterior dominant rhythm (common odds ratio, 3.38; 95% CI, 1.30-9.09), absence of N2 sleep transients (3.69; 1.69-8.20), predominant delta activity (2.82; 1.32-6.10), and discontinuous background (5.33; 2.28-12.96) within the first 72 hours of monitoring.ConclusionsSevere ictal-interictal continuum patterns, including electrographic seizures, were associated with clinical markers of injury severity but not functional outcome in this prospective cohort of patients with moderate-to-severe traumatic brain injury. Importantly, continuous electroencephalography background features were independently associated with functional outcome and improved the area under the curve of existing, validated predictive models.
| S-EPMC6639805 | biostudies-literature
Project description:Traumatic brain injury leads to significant loss of brain volume, which continues into the chronic stage. This can be sensitively measured using volumetric analysis of MRI. Here we: (i) investigated longitudinal patterns of brain atrophy; (ii) tested whether atrophy is greatest in sulcal cortical regions; and (iii) showed how atrophy could be used to power intervention trials aimed at slowing neurodegeneration. In 61 patients with moderate-severe traumatic brain injury (mean age = 41.55 years ± 12.77) and 32 healthy controls (mean age = 34.22 years ± 10.29), cross-sectional and longitudinal (1-year follow-up) brain structure was assessed using voxel-based morphometry on T1-weighted scans. Longitudinal brain volume changes were characterized using a novel neuroimaging analysis pipeline that generates a Jacobian determinant metric, reflecting spatial warping between baseline and follow-up scans. Jacobian determinant values were summarized regionally and compared with clinical and neuropsychological measures. Patients with traumatic brain injury showed lower grey and white matter volume in multiple brain regions compared to controls at baseline. Atrophy over 1 year was pronounced following traumatic brain injury. Patients with traumatic brain injury lost a mean (± standard deviation) of 1.55% ± 2.19 of grey matter volume per year, 1.49% ± 2.20 of white matter volume or 1.51% ± 1.60 of whole brain volume. Healthy controls lost 0.55% ± 1.13 of grey matter volume and gained 0.26% ± 1.11 of white matter volume; equating to a 0.22% ± 0.83 reduction in whole brain volume. Atrophy was greatest in white matter, where the majority (84%) of regions were affected. This effect was independent of and substantially greater than that of ageing. Increased atrophy was also seen in cortical sulci compared to gyri. There was no relationship between atrophy and time since injury or age at baseline. Atrophy rates were related to memory performance at the end of the follow-up period, as well as to changes in memory performance, prior to multiple comparison correction. In conclusion, traumatic brain injury results in progressive loss of brain tissue volume, which continues for many years post-injury. Atrophy is most prominent in the white matter, but is also more pronounced in cortical sulci compared to gyri. These findings suggest the Jacobian determinant provides a method of quantifying brain atrophy following a traumatic brain injury and is informative in determining the long-term neurodegenerative effects after injury. Power calculations indicate that Jacobian determinant images are an efficient surrogate marker in clinical trials of neuroprotective therapeutics.
| S-EPMC5837530 | biostudies-literature
Project description:We report the clinical, neuroimaging, and neuropathologic characteristics of 2 patients who developed early onset dementia after a moderate-severe traumatic brain injury (TBI). Neuropathological evaluation revealed abundant ?-amyloid neuritic and cored plaques, diffuse ?-amyloid plaques, and frequent hyperphosphorylated-tau neurofibrillary tangles (NFT) involving much of the cortex, including insula and mammillary bodies in both cases. Case 1 additionally showed NFTs in both the superficial and deep cortical layers, occasional perivascular and depth-of-sulci NFTs, and parietal white matter rarefaction, which corresponded with decreased parietal fiber tracts observed on ex vivo MRI. Case 2 additionally showed NFT predominance in the superficial layers of the cortex, hypothalamus and brainstem, diffuse Lewy bodies in the cortex, amygdala and brainstem, and intraneuronal TDP-43 inclusions. The neuropathologic diagnoses were atypical Alzheimer disease (AD) with features of chronic traumatic encephalopathy and white matter loss (Case 1), and atypical AD, dementia with Lewy bodies and coexistent TDP-43 pathology (Case 2). These findings support an epidemiological association between TBI and dementia and further characterize the variety of misfolded proteins that may accumulate after TBI. Analyses with comprehensive clinical, imaging, genetic, and neuropathological data are required to characterize the full clinicopathological spectrum associated with dementias occurring after moderate-severe TBI.
| S-EPMC5939622 | biostudies-literature
Project description:(1) Background: White matter changes among individuals with mild-to-moderate traumatic brain injury (TBI) may be sensitive imaging markers reflecting functional impairment, particularly in the context of post-concussion syndrome. The objective of this study was to examine the altered white matter integrity in mild-to-moderate TBI patients compared with age-matched normal controls. (2) Methods: Diffusion tensor imaging data from 15 individuals with TBI and 15 control subjects were retrospectively obtained. We investigated and compared white matter integrity in both groups, with regard to fractional anisotropy (FA), radial diffusivity (RD), and axial diffusivity (AD) and examined the relationship with cognitive dysfunction and impaired balance in patients. (3) Results: In comparison with controls, the TBI patients had significantly decreased FA as well as increased RD, in the right corticospinal tract. Decreased RD was observed in the left cerebellar area near the middle cerebellar peduncle. Decreased AD was observed in the left inferior cerebellar peduncle, showing positive correlation with poor balance control. We observed decreased FA and increased AD in the left superior longitudinal fasciculus showing positive and negative correlation, respectively, with cognitive function in the TBI group. (4) Conclusions: Altered white matter integrity in mild-to-moderate TBI cases may be indicative of cognitive dysfunction and impaired balance.
| S-EPMC6780936 | biostudies-literature
Project description: Not available
| S-EPMC8478405 | biostudies-literature
Project description:Traumatic axonal injury (TAI), a signature injury of traumatic brain injury (TBI), is increasingly known to involve myelin damage. The objective of this study was to demonstrate the clinical relevance of myelin water imaging (MWI) by first quantifying changes in myelin water after TAI and then correlating those changes with measures of injury severity and neurocognitive performance. Scanning was performed at 3 months post-injury in 22 adults with moderate to severe diffuse TBI and 30 demographically matched healthy controls using direct visualization of short transverse component (ViSTa) MWI. Fractional anisotropy (FA) and radial diffusivity (RD) were also obtained using diffusion tensor imaging. Duration of post-traumatic amnesia (PTA) and cognitive processing speed measured by the Processing Speed Index (PSI) from Wechsler Adult Intelligence Scale-IV, were assessed. A between-group comparison using Tract-Based Spatial Statistics revealed that there was a widespread reduction of apparent myelin water fraction (aMWF) in TBI, consistent with neuropathology involving TAI. The group difference map of aMWF yielded topography that was different from FA and RD. Importantly, aMWF demonstrated significant associations with PTA (r = -0.564, p = .006) and PSI (r = 0.452, p = .035). In conclusion, reduced myelin water, quantified by ViSTa MWI, is prevalent in moderate-to-severe diffuse TBI and could serve as a potential biomarker for injury severity and prediction of clinical outcomes.
| S-EPMC6444291 | biostudies-literature
Project description:Symptoms are commonly more severe in pediatric traumatic brain injury (TBI) patients than in young adult TBI patients. To understand the mechanism, juvenile mice received a controlled cortical impact (CCI) injury at moderate level. Tissue lesion and cell death were measured and compared to our previous reports on brain injury in the young adult mice that received same level of impact using same injury device. Tissue lesion and cell death in the cortex was much less in the juvenile mouse brain in the first few hours after injury. However, once the injury occurred, it developed more rapidly, lasted much longer, and eventually led to exaggerated cell death and a 32.7% larger tissue lesion cavity in the cortex of juvenile mouse brain than of young adult mouse brain. Moreover, we found significant cell death in the thalamus of juvenile brains at 72 h, which was not commonly seen in the young adult mice. In summary, cell death in juvenile mice was delayed, lasted longer, and finally resulted in more severe brain injury than in the young adult mice. The results suggest that pediatric TBI patients may have a longer therapeutic window, but they also need longer intensive clinical care after injury.
| S-EPMC5943589 | biostudies-literature
Project description:IntroductionFew studies account for prehospital deaths when estimating incidence and mortality rates of moderate and severe traumatic brain injury (msTBI). In a population-based study, covering both urban and rural areas, including also prehospital deaths, the aim was to estimate incidence and mortality rates of msTBI. Further, we studied the 30-day and 6-month case-fatality proportion of severe TBI in relation to age.MethodsAll patients aged ≥17 years who sustained an msTBI in Central Norway were identified by three sources: (1) the regional trauma center, (2) the general hospitals, and (3) the Norwegian Cause of Death Registry. Incidence and mortality rates were standardized according to the World Health Organization's world standard population. Case-fatality proportions were calculated by the number of deaths from severe TBI at 30 days and 6 months, divided by all patients with severe TBI.ResultsThe overall incidence rates of moderate and severe TBI were 4.9 and 6.7 per 100,000 person-years, respectively, increasing from age 70 years. The overall mortality rate was 3.4 per 100,000 person-years, also increasing from age 70 years. Incidence and mortality rates were highest in men. The case-fatality proportion in people with severe TBI was 49% in people aged 60-69 years and 81% in people aged 70-79 years.ConclusionThe overall incidence and mortality rates for msTBI in Central Norway were low but increased from age 70 years, and among those ≥80 years of age with severe TBI, nearly all died. Overall estimates are strongly influenced by high incidence and mortality rates in the elderly, and studies should therefore report age-specific estimates, for better comparison of incidence and mortality rates.
| S-EPMC10866178 | biostudies-literature
Project description:Traumatic brain injury is a major source of global disability and mortality. Preclinical TBI models are a crucial component of therapeutic investigation. We report a tunable, monitored model of murine non-surgical, diffuse closed-head injury-modCHIMERA-characterized by impact as well as linear and rotational acceleration. modCHIMERA is based on the Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA) platform. We tested this model at 2 energy levels: 1.7 and 2.1 Joules-substantially higher than previously reported for this system. Kinematic analysis demonstrated linear acceleration exceeding injury thresholds in humans, although outcome metrics tracked impact energy more closely than kinematic parameters. Acute severity metrics were consistent with a complicated-mild or moderate TBI, a clinical population characterized by high morbidity but potentially reversible pathology. Axonal injury was multifocal and bilateral, neuronal death was detected in the hippocampus, and microglial neuroinflammation was prominent. Acute functional analysis revealed prolonged post-injury unconsciousness, and decreased spontaneous behavior and stimulated neurological scores. Neurobehavioral deficits were demonstrated in spatial learning/memory and socialization at 1-month. The overall injury profile of modCHIMERA corresponds with the range responsible for a substantial portion of TBI-related disability in humans. modCHIMERA should provide a reliable platform for efficient analysis of TBI pathophysiology and testing of treatment modalities.
| S-EPMC5955903 | biostudies-literature