RESUMO
In response to the need to better define the natural history of emerging consciousness after traumatic brain injury and to better describe the characteristics of the condition commonly labeled posttraumatic amnesia, a case definition and diagnostic criteria for the posttraumatic confusional state (PTCS) were developed. This project was completed by the Confusion Workgroup of the American Congress of Rehabilitation Medicine Brain Injury Interdisciplinary Special Interest group. The case definition was informed by an exhaustive literature review and expert opinion of workgroup members from multiple disciplines. The workgroup reviewed 2466 abstracts and extracted evidence from 44 articles. Consensus was reached through teleconferences, face-to-face meetings, and 3 rounds of modified Delphi voting. The case definition provides detailed description of PTCS (1) core neurobehavioral features, (2) associated neurobehavioral features, (3) functional implications, (4) exclusion criteria, (5) lower boundary, and (6) criteria for emergence. Core neurobehavioral features include disturbances of attention, orientation, and memory as well as excessive fluctuation. Associated neurobehavioral features include emotional and behavioral disturbances, sleep-wake cycle disturbance, delusions, perceptual disturbances, and confabulation. The lower boundary distinguishes PTCS from the minimally conscious state, while upper boundary is marked by significant improvement in the 4 core and 5 associated features. Key research goals are establishment of cutoffs on assessment instruments and determination of levels of behavioral function that distinguish persons in PTCS from those who have emerged to the period of continued recovery.
Assuntos
Lesões Encefálicas Traumáticas/psicologia , Confusão/diagnóstico , Transtornos da Consciência/diagnóstico , Testes de Estado Mental e Demência/normas , Confusão/psicologia , Transtornos da Consciência/psicologia , Consenso , Técnica Delphi , HumanosRESUMO
That learning and memory deficits persist many years following mild traumatic brain injury (mTBI) is controversial due to inconsistent objective evidence supporting subjective complaints. Our prior work demonstrated significant reductions in performance on the initial trial of a verbal learning task and overall slower rate of learning in well-motivated mTBI participants relative to demographically matched controls. In our previous work, we speculated that differences in strategy use could explain the differences in rate of learning. The current study serves to test this hypothesis by examining strategy use on the California Verbal Learning Test-Second Edition. Our present findings support the primary hypothesis that mTBI participants under-utilize semantic clustering strategies during list-learning relative to control participants. Despite achieving comparable total learning scores, we posit that the persisting learning and memory difficulties reported by some mTBI patients may be related to reduced usage of efficient internally driven strategies that facilitate learning. Given that strategy training has demonstrated improvements in learning and memory in educational and occupational settings, we offer that these findings have translational value in offering an additional approach in remediation of learning and memory complaints reported by some following mTBI.
Assuntos
Lesões Encefálicas/psicologia , Aprendizagem Verbal/fisiologia , Adulto , Algoritmos , Análise por Conglomerados , Feminino , Humanos , Masculino , Memória/fisiologia , Rememoração Mental/fisiologia , Testes NeuropsicológicosRESUMO
Following mild traumatic brain injury (TBI), a percentage of individuals report chronic memory and attention difficulties. Traditional neuropsychological assessments often fail to find evidence for such complaints. We hypothesized that mild TBI patients may, in fact, experience subtle cognitive deficits that reflect diminished initial acquisition that can be explained by changes in cerebral white matter microstructure. In the data presented here, a sample of nonlitigating and gainfully employed mild TBI patients demonstrated statistically significant differences from age and education matched control participants in performance on the first trial of a verbal learning task. Performance on this trial was associated with reduced fractional anisotropy in the uncinate fasciculus and the superior longitudinal fasciculus providing an anatomical correlate for the cognitive findings. Mild TBI patients were not impaired relative to control participants on total learning or memory composite variables. Performance on the first learning trial was not related to any psychological variables including mood. We concluded that patients with mild TBI demonstrate diminished verbal learning that is not often interpreted in standard neuropsychological assessment.
Assuntos
Lesões Encefálicas/complicações , Lesões Encefálicas/fisiopatologia , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Aprendizagem Verbal , Adulto , Lesões Encefálicas/diagnóstico , Doença Crônica , Imagem de Tensor de Difusão , Feminino , Humanos , Masculino , Testes Neuropsicológicos , Índice de Gravidade de DoençaRESUMO
OBJECTIVE: To characterize integrity of fronto-striatal circuitry in chronic traumatic brain injury (TBI). BACKGROUND: Due to both direct and indirect effects, TBI is hypothesized to affect frontal and striatal function. On the basis of elegant animal, lesion, and neuroimaging literatures, oculomotor testing can provide a useful tool for in vivo assessments of neurophysiologic function. The predictive saccade paradigm in oculomotor function is well established to provide assessment of this fronto-striatal circuit. METHODS: Sixty patients with a history of chronic TBI completed 2 specific tests of oculomotor function, including a test of reflexive visually guided saccades to assess basic oculomotor function and a predictive saccade test to assess procedural learning. RESULTS: TBI (mild and moderate/severe) was associated with a decrease in rates of procedural learning, with degree of impairment increasing with injury severity. This was observed as a decrease in the proportion of anticipatory saccades (primary measure of learning). CONCLUSIONS: This abnormal oculomotor performance supports the hypothesis that TBI results in chronic impairment of frontal-striatal functions proportionally to injury severity and demonstrate that oculomotor testing is sensitive to all severities of closed-head injury.
Assuntos
Lesões Encefálicas/psicologia , Lesão Encefálica Crônica/psicologia , Deficiências da Aprendizagem/psicologia , Movimentos Sacádicos/fisiologia , Adulto , Lesões Encefálicas/complicações , Lesão Encefálica Crônica/complicações , Movimentos Oculares/fisiologia , Feminino , Fixação Ocular/fisiologia , Humanos , Deficiências da Aprendizagem/etiologia , Masculino , Testes Neuropsicológicos , Valor Preditivo dos Testes , Desempenho Psicomotor/fisiologia , Fumar/psicologia , Fatores SocioeconômicosRESUMO
Traumatic brain injury (TBI) is a serious public health problem. Even injuries classified as mild, the most common, can result in persistent neurobehavioural impairment. Diffuse axonal injury is a common finding after TBI, and is presumed to contribute to outcomes, but may not always be apparent using standard neuroimaging. Diffusion tensor imaging (DTI) is a more recent method of assessing axonal integrity in vivo. The primary objective of the current investigation was to characterize white matter integrity utilizing DTI across the spectrum of chronic TBI of all severities. A secondary objective was to examine the relationship between white matter integrity and cognition. Twenty mild, 17 moderate to severe TBI and 18 controls underwent DTI and neuropsychological testing. Fractional anisotropy, axial diffusivity and radial diffusivity were calculated from the DTI data. Fractional anisotropy was the primary measure of white matter integrity. Region of interest analysis included anterior and posterior corona radiata, cortico-spinal tracts, cingulum fibre bundles, external capsule, forceps minor and major, genu, body and splenium of the corpus callosum, inferior fronto-occipital fasciculus, superior longitudinal fasciculus and sagittal stratum. Cognitive domain scores were calculated from executive, attention and memory testing. Decreased fractional anisotropy was found in all 13 regions of interest for the moderate to severe TBI group, but only in the cortico-spinal tract, sagittal stratum and superior longitudinal fasciculus for the mild TBI group. White Matter Load (a measure of the total number of regions with reduced FA) was negatively correlated with all cognitive domains. Analysis of radial and axial diffusivity values suggested that all severities of TBI can result in a degree of axonal damage, while irreversible myelin damage was only apparent for moderate to severe TBI. The present data emphasize that white matter changes exist on a spectrum, including mild TBI. An index of global white matter neuropathology (White Matter Load) was related to cognitive function, such that greater white matter pathology predicted greater cognitive deficits. Mechanistically, mild TBI white matter changes may be primarily due to axonal damage as opposed to myelin damage. The more severe injuries impact both. DTI provides an objective means for determining the relationship of cognitive deficits to TBI, even in cases where the injury was sustained years prior to the evaluation.
Assuntos
Lesão Encefálica Crônica/patologia , Lesão Encefálica Crônica/psicologia , Encéfalo/patologia , Transtornos Cognitivos/etiologia , Adulto , Anisotropia , Mapeamento Encefálico/métodos , Transtornos Cognitivos/patologia , Imagem de Difusão por Ressonância Magnética/métodos , Feminino , Humanos , Processamento de Imagem Assistida por Computador/métodos , Masculino , Testes NeuropsicológicosRESUMO
A growing body of literature addresses the application of diffusion tensor imaging (DTI) to traumatic brain injury (TBI). Most TBIs are of mild severity, and their diagnosis and prognosis are often challenging. These challenges may be exacerbated in medicolegal contexts, where plaintiffs seek to present objective evidence that supports a clinical diagnosis of mild (m)TBI. Because DTI permits quantification of white matter integrity and because TBI frequently involves white matter injury, DTI represents a conceptually appealing method of demonstrating white matter pathology attributable to mTBI. However, alterations in white matter integrity are not specific to TBI, and their presence does not necessarily confirm a diagnosis of mTBI. Guided by rules of evidence shaped by Daubert v. Merrell Dow Pharmaceuticals, Inc., we reviewed and analyzed the literature describing DTI findings in mTBI and related neuropsychiatric disorders. Based on this review, we suggest that expert testimony regarding DTI findings will seldom be appropriate in legal proceedings focused on mTBI.
Assuntos
Lesões Encefálicas/diagnóstico , Imagem de Tensor de Difusão , Lesões Encefálicas/classificação , Lesões Encefálicas/fisiopatologia , Prova Pericial/normas , Medicina Legal , Humanos , Pesquisa , Índices de Gravidade do TraumaRESUMO
Hypoxic-ischemic brain injury (HI-BI) is a common cause of neurological morbidity in children and adults. Recent developments in neuroimaging techniques may permit in vivo identification of the structural and functional anatomy of HI-BI, and offer opportunities for the development of neuroimaging-guided prognosis. This article provides an update on the types and possible roles of currently-available neuroimaging techniques. The applications and limitations of these techniques to the study and clinical evaluation of persons with HI-BI are discussed, and the need of further research is highlighted.
Assuntos
Encéfalo , Diagnóstico por Imagem/métodos , Hipóxia-Isquemia Encefálica , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Diagnóstico por Imagem/classificação , Humanos , Hipóxia-Isquemia Encefálica/diagnóstico por imagem , Hipóxia-Isquemia Encefálica/patologia , Radiografia , CintilografiaRESUMO
OBJECTIVE: To characterize oculomotor function using visually guided saccade and antisaccade (AS) tasks in chronic traumatic brain injury (TBI) and assess the relationship to neuropsychologic testing. BACKGROUND: TBI causes dysfunction of prefrontal cortex, in part by disrupting cortical and subcortical pathways, resulting in specific cognitive impairments. Oculomotor function tests provide a method of assessing the integrity of these pathways. METHODS: Twenty mild TBI (MTBI), 17 moderate to severe TBI (M/STBI), and 19 healthy controls underwent oculomotor and neuropsychologic testing. RESULTS: On the visually guided saccade task, the M/STBI showed longer latencies and reduced accuracy. On the AS task, which is more dependent on prefrontal cortex function, both patient groups committed more prosaccade errors than controls. On neuropsychologic testing, only the M/STBI patients were significantly impaired. Correlations were found between AS and neuropsychologic performance. CONCLUSIONS: The M/STBI group was impaired on both oculomotor tasks and neuropsychologic testing, consistent with more global neuropathology. The MTBI group showed impaired performance primarily on the AS task, consistent with prefrontal system dysfunction. Hence, oculomotor testing is sensitive to the range of neuropathology in chronic TBI, and importantly, may be more sensitive to neuropathology in MTBI.
Assuntos
Lesões Encefálicas/complicações , Doenças do Nervo Oculomotor/diagnóstico , Doenças do Nervo Oculomotor/etiologia , Córtex Pré-Frontal/lesões , Adulto , Doença Crônica , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/etiologia , Feminino , Fixação Ocular/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Testes Neuropsicológicos , Movimentos Sacádicos/fisiologiaRESUMO
Catatonia is a common neuropsychiatric syndrome which may arise from GABA-A hypoactivity, dopamine (D2) hypoactivity,and possibly glutamate NMDA hyperactivity. Amantadine and memantine have been reported as effective treatments for catatonia in selected cases, and probably mediate the presence of catatonic signs and symptoms through complex pathways involving glutamate antagonism. The authors identified 25 cases of catatonia treated with either agent. This article provides indirect evidence that glutamate antagonists may improve catatonic signs in some patients who fail to respond to established treatment, including lorazepam or electroconvulsive therapy. Further study of glutamate antagonists in the treatment of catatonia is needed.
Assuntos
Catatonia/tratamento farmacológico , Antagonistas de Aminoácidos Excitatórios/uso terapêutico , Catatonia/psicologia , Ensaios Clínicos como Assunto , Eletroconvulsoterapia , Moduladores GABAérgicos/uso terapêutico , Humanos , Lorazepam/uso terapêutico , Escalas de Graduação Psiquiátrica , Esquizofrenia Catatônica/tratamento farmacológico , Esquizofrenia Catatônica/psicologiaRESUMO
OBJECTIVE: Apolipoprotein E isoform (E4) has been posited to affect outcomes after central nervous system injury. This project sought to determine the relationship between the apoE4 allele and the recovery of amino acid neurotransmitters (aspartate, glutamate, and lactate/pyruvate ratio [L/P]) following a traumatic brain injury (TBI) after controlling for patient characteristics. DESIGN: This prospective clinical study examined neurotransmitters and L/P within the cerebrospinal fluid and compared the trends by apoE genotypes. SETTING: Adults with TBI were recruited from a neurotrauma intensive care unit within a trauma I university medical center. PATIENTS: Ninety-one patients were enrolled into the study after a severe TBI (Glasgow Coma Scale [GCS] score, =8). Cerebrospinal fluid was serially sampled from a ventriculostomy every 4 hrs for the first 24 hrs and every 6 hrs for 25-120 hrs after injury. MEASUREMENTS AND MAIN RESULTS: Hierarchical linear modeling analyses were used to compare the change of glutamate, aspartate, and L/P over time by the presence or absence of the apoE4 allele, with GCS score, sex, race, and therapeutic hypothermias included as covariates. There was a significant apoE4 allele group effect on both the linear and quadratic slopes in aspartate. In glutamate, the rate of change in glutamate was statistically related to GCS score. There was no significant difference in the glutamate response over time by the presence of the apoE4 allele. There was a significant difference in the change in L/P across time, with faster recovery when the apoE4 allele was absent. CONCLUSIONS: Recovery of aspartate and L/P differed depending on the presence of the apoE4 allele. Patients with the allele had significant increased and sustained levels of aspartate and L/P after TBI. Changes in glutamate were related to severity of illness and were independent of the presence of the apoE4 allele.
Assuntos
Apolipoproteínas E/genética , Lesões Encefálicas/líquido cefalorraquidiano , Lesões Encefálicas/diagnóstico , Aminoácidos Excitatórios/líquido cefalorraquidiano , Adolescente , Adulto , Idoso , Alelos , Apolipoproteínas E/análise , Biomarcadores/análise , Cromatografia Líquida de Alta Pressão , Aminoácidos Excitatórios/análise , Feminino , Marcadores Genéticos/genética , Genótipo , Escala de Coma de Glasgow , Humanos , Escala de Gravidade do Ferimento , Unidades de Terapia Intensiva , Masculino , Pessoa de Meia-Idade , Probabilidade , Prognóstico , Estudos Prospectivos , Estudos de Amostragem , Sensibilidade e EspecificidadeRESUMO
Amantadine, a dopamine agonist, is reported to have beneficial effects on the neurobehavioral sequelae of clinical brain injury. However, there are currently no published laboratory reports on its use in the assessment of functional or histopathological outcome following experimental traumatic brain injury (TBI). To this end, we examined the effects of daily amantadine treatment on functional recovery (motor and Morris water maze performance) and hippocampal neuronal survival following controlled cortical impact (CCI) injury (4 meters/sec, 2.7 mm tissue deformation). Male Sprague-Dawley rats were pretrained on motor performance tasks (beam balance and beam walking) one day prior to injury and tested on post-operative days 1-5. Additionally, all subjects were trained on the Morris water maze on post-operative days 14-18. Beginning one day after CCI injury or sham surgery, animals were injected once daily for 18 days with either amantadine (10 mg/kg, i.p.) or saline. The amantadine treatment regimen was ineffective in promoting motor recovery and increasing survival of hippocampal neurons in both the CA1 and CA3 regions following TBI, but did show improved swim latencies during the five days of water maze testing (Day 14 vs. Day 18, p < 0.01) when compared to saline controls. Mean (+/- SE) swim latencies on Day 18 were 15.12 +/- 2.8, 13.25 +/- 4.18, 70.83 +/- 11.1, and 38.5 +/- 3.55 sec for the sham/saline, sham/amantadine, injured/saline, and injured/amantadine treatment groups, respectively. Thus, while the daily administration of amantadine exhibited a neutral effect on motor behavior, it produced a modest attenuation of water maze performance deficits. This latter finding is consistent with published clinical data suggesting a beneficial effect on functional outcome with amantadine therapy.