Cluster analysis of impairment measures to inform an evidence-based classification structure in RaceRunning, a new World Para Athletics event for athletes with hypertonia, ataxia or athetosis.

RaceRunning enables athletes with limited or no walking ability to propel themselves independently using a three-wheeled frame that has a saddle, handle bars and a chest plate. For RaceRunning to be included as a para athletics event, an evidence-based classification system is required. This study assessed the impact of trunk control and lower limb impairment measures on RaceRunning performance and evaluated whether cluster analysis of these impairment measures produces a valid classification structure for RaceRunning. The Trunk Control Measurement Scale (TCMS), Selective Control Assessment of the Lower Extremity (SCALE), the Australian Spasticity Assessment Scale (ASAS), and knee extension were recorded for 26 RaceRunning athletes. Thirteen male and 13 female athletes aged 24 (SD = 7) years participated. All impairment measures were significantly correlated with performance (rho = 0.55-0.74). Using ASAS, SCALE, TCMS and knee extension as cluster variables in a two-step cluster analysis resulted in two clusters of athletes. Race speed and the impairment measures were significantly different between the clusters (p < 0.001). The findings of this study provide evidence for the utility of the selected impairment measures in an evidence-based classification system for RaceRunning athletes.

Balance in chronic traumatic brain injury: correlations between clinical measures and a self-report measure.

OBJECTIVE: To assess associations among commonly used self-report and clinical measures of balance in chronic TBI. DESIGN: Cross-sectional analysis of balance in a convenience sample of individuals at least one year post TBI. MAIN OUTCOME MEASURES: Activities-Specific Balance Confidence Scale (ABC) (self-reported balance impairment), Community Balance and Mobility Scale (CB&M) (clinical measure validated in TBI), and Balance Evaluation Systems Test (BESTest) (clinical measure not validated in TBI). METHODS: Fifty-nine individuals (64% male, mean age 48.2 years) ambulating independently within the home participated in testing. Pearson correlation coefficients were used to quantify the direction and magnitude of the relationships among the three balance impairment measures. RESULTS: A significant positive correlation was noted between the ABC and CB&M (r = 0.42, p = 0.0008), between the ABC and BESTest (r = 0.46, p = 0.0002), and between the CB&M and BESTest (r = 0.86, p < 0.0001). CONCLUSIONS: This is the first study we are aware of in the chronic moderate to severe TBI population directly comparing patient's self-reported balance impairment with clinical measures. Positive correlations were found between the self-report measure and both clinical measures. Overall, individuals with chronic TBI tend to self-report less impaired balance than clinical measures indicate. These results provide preliminary evidence to support the need for validation of the BESTest in this population. ABBREVIATIONS: ABC: Activities-specific balance confidence scale; BESTest: balance evaluation systems test; BOS: base of support; COM: center of mass; CB&M: community balance and mobility scale; CI: confidence interval; IQR: interquartile range; PTs: physical therapists; SD: standard deviation; SE: standard error; TBI: traumatic brain injury.

A Clinical Framework for Functional Recovery in a Person With Chronic Traumatic Brain Injury: A Case Study.

BACKGROUND AND PURPOSE: This case study describes a task-specific training program for gait walking and functional recovery in a young man with severe chronic traumatic brain injury. CASE DESCRIPTION: The individual was a 26-year-old man 4 years post-traumatic brain injury with severe motor impairments who had not walked outside of therapy since his injury. He had received extensive gait training prior to initiation of services. His goal was to recover the ability to walk. INTERVENTION: The primary focus of the interventions was the restoration of walking. A variety of interventions were used, including locomotor treadmill training, electrical stimulation, orthoses, and specialized assistive devices. A total of 79 treatments were delivered over a period of 62 weeks. OUTCOMES: At the conclusion of therapy, the client was able to walk independently with a gait trainer for approximately 1km (over 3000 ft) and walked in the community with the assistance of his mother using a rocker bottom crutch for distances of 100m (330 ft). DISCUSSION: Specific interventions were intentionally selected in the development of the treatment plan. The program emphasized structured practice of the salient task, that is, walking, with adequate intensity and frequency. Given the chronicity of this individual's injury, the magnitude of his functional improvements was unexpected.Video Abstract available for additional insights from the Authors (see Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A175).

Function-structure connectivity in patients with severe brain injury as measured by MRI-DWI and FDG-PET.

A vast body of literature exists showing functional and structural dysfunction within the brains of patients with disorders of consciousness. However, the function (fluorodeoxyglucose FDG-PET metabolism)-structure (MRI-diffusion-weighted images; DWI) relationship and how it is affected in severely brain injured patients remains ill-defined. FDG-PET and MRI-DWI in 25 severely brain injured patients (19 Disorders of Consciousness of which 7 unresponsive wakefulness syndrome, 12 minimally conscious; 6 emergence from minimally conscious state) and 25 healthy control subjects were acquired here. Default mode network (DMN) function-structure connectivity was assessed by fractional anisotropy (FA) and metabolic standardized uptake value (SUV). As expected, a profound decline in regional metabolism and white matter integrity was found in patients as compared with healthy subjects. Furthermore, a function-structure relationship was present in brain-damaged patients between functional metabolism of inferior-parietal, precuneus, and frontal regions and structural integrity of the frontal-inferiorparietal, precuneus-inferiorparietal, thalamo-inferioparietal, and thalamofrontal tracts. When focusing on patients, a stronger relationship between structural integrity of thalamo-inferiorparietal tracts and thalamic metabolism in patients who have emerged from the minimally conscious state as compared with patients with disorders of consciousness was found. The latter finding was in line with the mesocircuit hypothesis for the emergence of consciousness. The findings showed a positive function-structure relationship within most regions of the DMN. Hum Brain Mapp 37:3707-3720, 2016. © 2016 Wiley Periodicals, Inc.

The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy.

Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. Like many other neurodegenerative conditions, at present, CTE can only be definitively diagnosed by post-mortem examination of brain tissue. As the first part of a series of consensus panels funded by the NINDS/NIBIB to define the neuropathological criteria for CTE, preliminary neuropathological criteria were used by 7 neuropathologists to blindly evaluate 25 cases of various tauopathies, including CTE, Alzheimer's disease, progressive supranuclear palsy, argyrophilic grain disease, corticobasal degeneration, primary age-related tauopathy, and parkinsonism dementia complex of Guam. The results demonstrated that there was good agreement among the neuropathologists who reviewed the cases (Cohen's kappa, 0.67) and even better agreement between reviewers and the diagnosis of CTE (Cohen's kappa, 0.78). Based on these results, the panel defined the pathognomonic lesion of CTE as an accumulation of abnormal hyperphosphorylated tau (p-tau) in neurons and astroglia distributed around small blood vessels at the depths of cortical sulci and in an irregular pattern. The group also defined supportive but non-specific p-tau-immunoreactive features of CTE as: pretangles and NFTs affecting superficial layers (layers II-III) of cerebral cortex; pretangles, NFTs or extracellular tangles in CA2 and pretangles and proximal dendritic swellings in CA4 of the hippocampus; neuronal and astrocytic aggregates in subcortical nuclei; thorn-shaped astrocytes at the glial limitans of the subpial and periventricular regions; and large grain-like and dot-like structures. Supportive non-p-tau pathologies include TDP-43 immunoreactive neuronal cytoplasmic inclusions and dot-like structures in the hippocampus, anteromedial temporal cortex and amygdala. The panel also recommended a minimum blocking and staining scheme for pathological evaluation and made recommendations for future study. This study provides the first step towards the development of validated neuropathological criteria for CTE and will pave the way towards future clinical and mechanistic studies.

Post-traumatic neurodegeneration and chronic traumatic encephalopathy.

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables-including age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities-all of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'.

Type and occurrence of serious complications in patients after mild traumatic brain injury.

Traumatic brain injury (TBI) remains a major public health and socio-economic problem, and 70-90% of all TBIs are classified as mild. Mild TBIs and concussions are mostly considered to be non-serious conditions with symptoms subsiding within a few days or weeks. However in 10-15% of patients, the symptoms persist one year after concussion and mostly include headache, fatigue, irritability, and cognitive problems (e.g. memory, concentration). These persisting symptoms negatively influence patient daily activities as postconcussion syndrome (PCS). Second-impact syndrome (SIS) is a very rare but usually fatal condition and occurs when repeated brain injuries lead to a catastrophic diffuse brain swelling. There is no scientific evidence on the incidence and risk of SIS. Chronic traumatic encephalopathy (CTE) is a progressive degenerative disease of the brain found in patients with a history of repetitive brain trauma. CTE presents with behavioural, cognitive, and motor symptoms. The literature to date lacks prospective epidemiological studies of the incidence of CTE. In recent medical literature, there is a description of 110 athletes with postmortem diagnosis of CTE (Tab. 1, Ref. 37).

Right frontal pole cortical thickness and social competence in children with chronic traumatic brain injury: cognitive proficiency as a mediator.

OBJECTIVE: To examine the association between right frontal pole cortical thickness, social competence, and cognitive proficiency in children participants with a history of chronic traumatic brain injury (TBI). PARTICIPANTS: Twenty-three children (65% male; M age = 12.8 years, SD = 2.3 years) at least 1 year post-injury (M = 3.3 years, SD = 1.7 years) were evaluated with the Cognitive Proficiency Index (CPI) from the Wechsler Intelligence Scale for Children, 4th Edition, and their caregiver completed the Child Behavior Checklist. Social competence was evaluated with the Social Competence and Social Problems subscales from the Child Behavior Checklist. Right frontal pole cortical thickness was calculated via FreeSurfer from high-resolution 3-dimensional T1 magnetic resonance imaging scans. RESULTS: Direct effect of right frontal pole cortical thickness on social competence was significant (ß = 14.09, SE = 4.6, P < .01). Right frontal pole cortical thickness significantly predicted CPI (ß = 18.44, SE = 4.9, P < .05), and CPI significantly predicted social competence (ß = 0.503, SE = 0.17, P < .01). Findings were consistent with the hypothesized mediation model. CONCLUSIONS: The association between right frontal lobe cortical integrity and social competence in pediatric participants with chronic TBI may be mediated through cognitive proficiency.

Exposure to sub-concussive head injury in boxing and other sports.

BACKGROUND: Current characterizations of chronic traumatic brain injury (CTBI) in boxing, football and other sports are reviewed in the context of the history of research on sub-concussive brain trauma in athletes. METHODS: The utility of exposure models for understanding CTBI in boxers is examined and concerns regarding the paucity of findings supportive of an exposure model for CTBI in football players are discussed. RESULTS AND CONCLUSIONS: Recommendations for development of exposure models for sport-specific phenotypic characterizations of CTBI are presented.

Chronic traumatic encephalopathy in professional sports: retrospective and prospective views.

PRIMARY OBJECTIVE: The purposes of this paper are to review: (1) the history of chronic traumatic encephalopathy (CTE) in sports, (2) the similarities and differences between historic and current definitions of CTE, (3) recent epidemiology and cohort studies of CTE and (4) controversies regarding the current CTE positions. RESEARCH DESIGN: Not applicable. METHODS AND PROCEDURES: Selective review of published articles relevant to CTE. MAIN OUTCOME AND RESULTS: The current definitions of CTE have evolved from its original definition and now rely heavily on the post-mortem detection of hyperphosphorylated tau for diagnosis. As of 2013, there is a blended cohort of 110 professional athletes diagnosed with CTE. It is being assumed that concussions and/or sub-concussive impacts in contact sports are the sole cause of CTE. CONCLUSIONS: There are multiple causes of abnormal tau protein deposition in the human brain and the pathogenesis of CTE may not be related solely to concussion and/or sub-concussive injury. In all likelihood, the causes of CTE are a multivariate, as opposed to a univariate, phenomenon.

Chronic traumatic encephalopathy: contributions from the Boston University Center for the Study of Traumatic Encephalopathy.

OBJECTIVE: Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease associated with repetitive brain trauma (RBT). Initially described in boxers, CTE has now been found in other contact sport athletes with a history of RBT. In recent years, there has been tremendous media attention regarding CTE, primarily because of the deaths of high profile American football players who were found to have CTE upon neuropathological examination. However, the study of CTE remains in its infancy. This review focuses on research from the Centre for the Study of Traumatic Encephalopathy (CSTE) at Boston University. METHODS: This study reviews the formation of the CSTE, major CSTE publications and current ongoing research projects at the CSTE. RESULTS: The neuropathology of CTE has been well-described. Current research focuses on: methods of diagnosing the disease during life (including the development of biomarkers), examination of CTE risk factors (including genetic susceptibility and head impact exposure variables); description of the clinical presentation of CTE; development of research diagnostic criteria for Traumatic Encephalopathy Syndrome; and assessment of mechanism and pathogenesis. CONCLUSIONS: Current research at the BU CSTE is aimed at increasing understanding of the long-term consequences of repetitive head impacts and attempting to begin to answer several of the unanswered questions regarding CTE.

Chapter 3 animal models of traumatic brain injury: is there an optimal model that parallels human brain injury?

Traumatic brain injury (TBI) is the leading cause of mortality and morbidity in the younger population worldwide. Survivors of TBI often experience long-term disability in the form of cognitive, sensorimotor, and affective impairments. Despite the high prevalence in, and cost of TBI to, both individuals and society, some of its underlying pathophysiology is not completely understood. Animal models have been developed over the past few decades to closely replicate the different facets of TBI in humans to better understand the underlying pathophysiology and behavioral impairments and assess potential therapies that can promote neuroprotection. However, no effective treatment for TBI has been established to date in the clinical setting, despite promising results generated in preclinical studies in the use of neuroprotective strategies. The failure to translate results from preclinical studies to the clinical setting underscores a compelling need to revisit the current state of knowledge in the use of animal models in TBI.

Negative neuroplasticity in chronic traumatic brain injury and implications for neurorehabilitation.

Based on growing findings of brain volume loss and deleterious white matter alterations during the chronic stages of injury, researchers posit that moderate-severe traumatic brain injury (TBI) may act to "age" the brain by reducing reserve capacity and inducing neurodegeneration. Evidence that these changes correlate with poorer cognitive and functional outcomes corroborates this progressive characterization of chronic TBI. Borrowing from a framework developed to explain cognitive aging (Mahncke et al., Progress in Brain Research, 157, 81-109, 2006a; Mahncke et al., Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12523-12528, 2006b), we suggest here that environmental factors (specifically environmental impoverishment and cognitive disuse) contribute to a downward spiral of negative neuroplastic change that may modulate the brain changes described above. In this context, we review new literature supporting the original aging framework, and its extrapolation to chronic TBI. We conclude that negative neuroplasticity may be one of the mechanisms underlying cognitive and neural decline in chronic TBI, but that there are a number of points of intervention that would permit mitigation of this decline and better long-term clinical outcomes.

High-level mobility in chronic traumatic brain injury and its relationship with clinical variables and magnetic resonance imaging findings in the acute phase.

OBJECTIVES: To compare high-level mobility in individuals with chronic moderate-to-severe traumatic brain injury (TBI) with matched healthy controls, and to investigate whether clinical variables and magnetic resonance imaging (MRI) findings in the acute phase can predict high-level motor performance in the chronic phase. DESIGN: A longitudinal follow-up study. SETTING: A level 1 trauma center. PARTICIPANTS: Individuals (N=136) with chronic TBI (n=65) and healthy matched peers (n=71). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: High-Level Mobility Assessment Tool (HiMAT) and the revised version of the HiMAT performed at a mean of 2.8 years (range, 1.5-5.4y) after injury. RESULTS: Participants with chronic TBI had a mean HiMAT score of 42.7 (95% confidence interval [CI], 40.2-45.2) compared with 47.7 (95% CI, 46.1-49.2) in the control group (P<.01). Group differences were also evident using the revised HiMAT (P<.01). Acute-phase clinical variables and MRI findings explained 58.8% of the variance in the HiMAT score (P<.001) and 59.9% in the revised HiMAT score (P<.001). Lower HiMAT scores were associated with female sex (P=.031), higher age at injury (P<.001), motor vehicle collisions (P=.030), and posttraumatic amnesia >7 days (P=.048). There was a tendency toward an association between lower scores and diffuse axonal injury in the brainstem (P=.075). CONCLUSIONS: High-level mobility was reduced in participants with chronic, either moderate or severe TBI compared with matched peers. Clinical variables in the acute phase were significantly associated with high-level mobility performance in participants with TBI, but the role of early MRI findings needs to be further investigated. The findings of this study suggest that the clinical variables in the acute phase may be useful in predicting high-level mobility outcome in the chronic phase.

Relation between cognition and neural connection from injured cingulum to brainstem cholinergic nuclei in chronic patients with traumatic brain injury.

BACKGROUND: This study investigated the relation between cognition and the neural connection from injured cingulum to brainstem cholinergic nuclei in patients with traumatic brain injury (TBI), using diffusion tensor tractography (DTT). METHODS: Among 353 patients with TBI, 20 chronic patients who showed discontinuation of both anterior cingulums from the basal forebrain on DTT were recruited for this study. The Wechsler Intelligence Scale and the Memory Assessment Scale (MAS; short-term, verbal, visual and total memory) were used for assessment of cognition. Patients were divided into two groups according to the presence of a neural connection between injured cingulum and brainstem cholinergic nuclei. RESULTS: Eight patients who had a neural connection between injured cingulum and brainstem cholinergic nuclei showed better short-term memory on MAS than 12 patients who did not (p < 0.05). However, other results of neuropsychological testing showed no significant difference (p > 0.05). CONCLUSIONS: Better short-term memory in patients who had the neural connection between injured cingulum and brainstem cholinergic nuclei appears to have been attributed to the presence of cholinergic innervation to the cerebral cortex through the neural connection instead of the injured anterior cingulum. The neural connection appears to compensate for the injured anterior cingulum in obtaining cholinergic innervation.

Military traumatic brain injury: a review.

Military mild traumatic brain injury (mTBI) differs from civilian injury in important ways. Although mTBI sustained in both military and civilian settings are likely to be underreported, the combat theater presents additional obstacles to reporting and accessing care. The impact of blast forces on the nervous system may differ from nonblast mechanisms, mTBI although studies comparing the neurologic and cognitive sequelae in mTBI survivors have not provided such evidence. However, emotional distress appears to figure prominently in symptoms following military mTBI. This review evaluates the extant literature with an eye towards future research directions.

Professional fighters brain health study: rationale and methods.

Repetitive head trauma is a risk factor for Alzheimer's disease and is the primary cause of chronic traumatic encephalopathy. However, little is known about the natural history of, and risk factors for, chronic traumatic encephalopathy or about means of early detection and intervention. The Professional Fighters Brain Health Study is a longitudinal study of active professional fighters (boxers and mixed martial artists), retired professional fighters, and controls matched for age and level of education. The main objective of the Professional Fighters Brain Health Study is to determine the relationships between measures of head trauma exposure and other potential modifiers and changes in brain imaging and neurological and behavioral function over time. The study is designed to extend over 5 years, and we anticipate enrollment of more than 400 boxers and mixed martial artists. Participants will undergo annual evaluations that include 3-tesla magnetic resonance imaging scanning, computerized cognitive assessments, speech analysis, surveys of mood and impulsivity, and blood sampling for genotyping and exploratory biomarker studies. Statistical models will be developed and validated to predict early and progressive changes in brain structure and function. A composite fight exposure index, developed as a summary measure of cumulative traumatic exposure, shows promise as a predictor of brain volumes and cognitive function.

Heart rate variability biofeedback, executive functioning and chronic brain injury.

PRIMARY OBJECTIVE: To determine if individuals with brain injury can modify heart rate variability (HRV) through biofeedback and, if so, enhance its pattern to improve emotional regulation and problem-solving ability. DESIGN: A quasi-experimental design with repeated measures was employed. Thirteen individuals aged 23-63 years with severe brain injury (13-40 years post-onset) participating in a community-based programme were enrolled. MAIN OUTCOMES: Response-to-treatment was measured with HRV indices, Behavior Rating Inventory of Executive Function (BRIEF-A-Informant) and attention/problem-solving tests. RESULTS: At post-treatment, HRV indices (Low Frequency/High Frequency [LF/HF] and coherence ratio) increased significantly. Increased LF/HF values during the second-half of a 10-minute session were associated with higher attention scores. Participants who scored better (by scoring lower) in informant ratings at pre-treatment had highest HRV scores at post-treatment. Accordingly, at post-treatment, families' ratings of participants' emotional control correlated with HRV indices; staffs' ratings of participants' working memory correlated with participants' HRV indices. Self-ratings of the BRIEF-A Task Monitoring scale at post-treatment correlated with family ratings at pre-treatment and post-treatment. CONCLUSIONS: Results demonstrate an association between regulation of emotions/cognition and HRV training. Individuals with severe, chronic brain injury can modify HRV through biofeedback. Future research should evaluate the efficacy of this approach for modifying behavioural problems.

The current role of decompressive craniectomy in the management of neurological emergencies.

Decompressive craniectomy has been used as a lifesaving procedure for many neurological emergencies, including traumatic brain injury, ischaemic stroke, subarachnoid haemorrhage, cerebrovenous thrombosis, severe intracranial infection, inflammatory demyelination and encephalopathy. The evidence to support using decompressive craniectomy in these situations is, however, limited. Decompressive craniectomy has only been evaluated by randomized controlled trials in traumatic brain injury and ischaemic stroke and, even so, its benefits and risks in these situations remain elusive. If one considers a modified Rankin Scale of 4 or 5 or dependency in daily activity as an unfavourable outcome, decompressive craniectomy is associated with an increased risk of survivors with unfavourable outcome (relative risk [RR] = 2.9, 95% confidence interval [CI] = 1.5-5.8, p = 0.002, I(2 )= 0%; number needed to operate to increase an unfavourable outcome = 3.5, 95% CI = 2.4-7.4), but not the number of survivors with a favourable outcome (RR = 1.5, 95% CI = 0.9-2.6, p = 0.13, I(2 )= 0%).

A comparison of insufficient effort rates, neuropsychological functioning, and neuropsychiatric symptom reporting in military veterans and civilians with chronic traumatic brain injury.

Neuropsychological evaluation of persons with chronic traumatic brain injury (TBI) symptoms is complicated by multiple factors. The authors explored the impact of mechanism of injury, effort testing performance, and neuropsychiatric status in a sample of military veterans (V-TBI) and civilians (C-TBI) with chronic TBI. V-TBI (n = 74), C-TBI (n = 67), and healthy civilian control (C-HC) participants (n = 66), completed a battery of neuropsychological, effort, and self-report neuropsychiatric measures. Results indicated that C-HC and C-TBI participants exhibited comparably low failure rates on effort tests (6% and 3%, respectively). V-TBI participants exhibited significantly higher rates of failure (18%). Subgroups (n = 20) of effort-screened participants matched for demographics and disability level were compared regarding neuropsychological performance and neuropsychiatric self-report. Both TBI groups exhibited limited neuropsychological impairment, relative to the C-HC participants. The V-TBI group exhibited pronounced neuropsychiatric symptomology compared with the other participant groups. The implications of these findings are discussed for evaluation in the context of disability and litigation.