Assessing connectivity related injury burden in diffuse traumatic brain injury

Many of the clinical and behavioral manifestations of traumatic brain injury (TBI) are thought to arise from disruption to the structural network of the brain due to diffuse axonal injury (DAI). However, a principled way of summarizing diffuse connectivity alterations to quantify injury burden is lacking. In this study, we developed a connectome injury score, Disruption Index of the Structural Connectome (DISC), which summarizes the cumulative effects of TBI‐induced connectivity abnormalities across the entire brain. Forty patients with moderate‐to‐severe TBI examined at 3 months postinjury and 35 uninjured healthy controls underwent magnetic resonance imaging with diffusion tensor imaging, and completed behavioral assessment including global clinical outcome measures and neuropsychological tests. TBI patients were selected to maximize the likelihood of DAI in the absence of large focal brain lesions. We found that hub‐like regions, with high betweenness centrality, were most likely to be impaired as a result of diffuse TBI. Clustering of participants revealed a subgroup of TBI patients with similar connectivity abnormality profiles who exhibited relatively poor cognitive performance. Among TBI patients, DISC was significantly correlated with post‐traumatic amnesia, verbal learning, executive function, and processing speed. Our experiments jointly demonstrated that assessing structural connectivity alterations may be useful in development of patient‐oriented diagnostic and prognostic tools. Hum Brain Mapp 38:2913–2922, 2017. © 2017 Wiley Periodicals, Inc.     

Early metabolic crisis-related brain atrophy and cognition in traumatic brain injury

Traumatic brain injury often results in acute metabolic crisis. We recently demonstrated that this is associated with chronic brain atrophy, which is most prominent in the frontal and temporal lobes. Interestingly, the neuropsychological profile of traumatic brain injury is often characterized as ‘frontal-temporal’ in nature, suggesting a possible link between acute metabolic crisis-related brain atrophy and neurocognitive impairment in this population. While focal lesions and diffuse axonal injury have a well-established role in the neuropsychological deficits observed following traumatic brain injury, no studies to date have examined the possible contribution of acute metabolic crisis-related atrophy in the neuropsychological sequelae of traumatic brain injury. In the current study we employed positron emission tomography, magnetic resonance imaging, and neuropsychological assessments to ascertain the relationship between acute metabolic crisis-related brain atrophy and neurocognitive outcome in a sample of 14 right-handed traumatic brain injury survivors. We found that acute metabolic crisis‐related atrophy in the frontal and temporal lobes was associated with poorer attention, executive functioning, and psychomotor abilities at 12 months post-injury. Furthermore, participants with gross frontal and/or temporal lobe atrophy exhibited numerous clinically significant neuropsychological deficits in contrast to participants with other patterns of brain atrophy. Our findings suggest that interventions that reduce acute metabolic crisis may lead to improved functional outcomes for traumatic brain injury survivors.     

Graded model of diffuse axonal injury for studying head injury‐induced cognitive dysfunction in rats

Diffuse axonal injury (DAI) plays a major role in the development of cognitive dysfunction, emotional difficulties and behavioral disturbances in patients following closed head injury, even when they have no definite abnormalities on conventional MRI. This study aimed to develop a highly controlled and reproducible model for DAI that simulates post‐traumatic cognitive dysfunction in humans. Sprague‐Dawley (SD) rats were subjected to impact acceleration head injury, using a pneumatic impact targeted to a steel disc centered onto their skull. The severity of injury was graded as three levels by adjusting the driving pressure at 60, 70 or 80 pounds per square inch. In vivo MRI was obtained 2 days post‐injury. Cognitive function was evaluated using the Morris water maze at 1 and 2 weeks post‐injury. HE staining and immunohistochemistry were performed to assess neuronal and axonal damages after 2 weeks. MRI demonstrated that this model induced no gross structural modification in the brain. The degree and duration of cognitive dysfunction were dependent on the force of impact. Histological analysis revealed the force‐dependent damage of the neurons and microtubule‐associated protein 2‐positive axons in the neocortex. Hippocampal damage was much less pronounced and was not linked to cognitive dysfunction. This is the first report that precisely evaluates the threshold of impact energy to lead to neocortical damage and cognitive dysfunction in rodents. This model would be suitable for clarifying the complex mechanisms of post‐traumatic brain damage and testing novel therapeutic approaches against post‐traumatic cognitive dysfunction due to diffuse axonal damage.     

Executive functions after traumatic brain injury in children

There is growing recognition that executive function, the superordinate, managerial capacity for directing more modular abilities, is frequently impaired by traumatic brain injury in children and mediates the neurobehavioral sequelae exhibited by these patients. This review encompasses the definition of specific executive functions, age-related changes in executive functions in typically developing children, and the effects of traumatic brain injury on executive functions. The neural substrate for executive functions is described, including relevant functional brain imaging studies that have implicated mediation by prefrontal and parietal cortex and their circuitry. The vulnerability of the neural substrate for executive function to the pathophysiology of traumatic brain injury is discussed, including focal lesions and diffuse axonal injury. Domains of executive functions covered in this review include the basic processes of working memory and inhibition and more complex processes such as decision making. Other domains of executive function, including motivation, self-regulation, and social cognition are discussed in terms of research methodology, clinical assessment, and findings in children with traumatic brain injury. Proposed approaches to the rehabilitation of executive functions are presented.     

CNV evidence for the distinctiveness of frontal and posterior neural processes in a traumatic brain-injured population.

The association between certain behavioral tests of executive functions in humans and the integrity of the prefrontal lobes has rested primarily on studies comparing subjects with frontal versus other loci of damage. Another approach is to compare the within-group variation on a physiological index of frontal functioning with the behavioral tests of interest. In the present study, subjects with traumatic brain injury (TBI) were given four behavioural measures of executive function, two measures of posterior nonexecutive function, and a Contingent Negative Variation (CNV) task, a proposed electrophysiological index of frontal-lobe functioning. We found that three of the four executive function tests were significantly related to the CNV, accounting for 23-52% of the variance, while the CNV did not correlate at all with the posterior tasks.     

180例颅脑外伤后精神障碍的鉴定结果分析

目的探讨颅脑外伤后精神障碍的临床类型及相关因素。方法收集180例颅脑外伤后司法鉴定案例资料,并对精神障碍的临床类型及相关因素进行分析。结果精神障碍的鉴定诊断类型为:器质性遗忘综合征、器质性人格改变、器质性智能损害、器质性神经症样症状和器质性精神症状。以颞叶、额叶、弥漫性损伤多见,共163例,且CT显示多有颞叶、额叶软化灶等异常,共123例。影响智能损害的因素为颞叶或额叶损伤、外伤程度严重,CT及EEG异常。器质性神经症样症状多见于女性,外伤程度轻,多无弥漫性损伤,CT未见明显异常。结论颅脑外伤后精神障碍多见于颞叶、额叶、弥漫性损伤;智能损害者外伤程度严重,EEG异常率高;器质性神经症样症状与轻度脑损伤有关。     

Late MRI after head injury in children: relationship to clinical features and outcome

To characterize the brain pathology in relation to long-term outcome after pediatric head injury, 55 children were studied by magnetic resonance imaging (MRI) at least 3 months after sustaining moderate to severe closed head injury (CHI). Thirty-nine of the patients had abnormal signal intensity consistent with residual brain lesions, including 28 children with lesions involving the frontal lobes. The clinical features of children with frontal lesions, extrafrontal lesions, and diffuse injury were compared. The analysis disclosed that children with frontal lobe lesions were more frequently disabled than children who sustained diffuse injury. Our MRI findings indicate that residual brain lesions are more common after moderate to severe CHI in children than previously thought and that the frontal lobes are most frequently involved. Further investigation is indicated to elucidate whether distinctive cognitive and behavioral sequelae are associated with frontal lobe lesions in children.     

Using magnetic resonance imaging to predict new learning outcome at 5 years after childhood traumatic brain injury

Memory and learning entail the recruitment of a number of neural areas, including the medial temporal lobes, temporal association areas, and prefrontal cortices. This study examined the effects of injury severity on long-term memory function in 55 children who sustained traumatic brain injury 5 years earlier and compared this with 17 healthy controls. It also investigated cortical damage and diffuse axonal injury and their association to memory and learning outcomes 5 years after traumatic brain injury. Children were administered memory tests of increasing complexity. Results indicated that injury severity affected aspects of complex memory, with no significant influence on working memory; that focal cortical damage was not predictive of working or complex memory, whereas diffuse axonal injury predicted outcome on complex memory tasks. Findings suggest that the implementation of diffuse axonal injury as an index of injury may assist in predicting memory outcome after childhood traumatic brain injury.     

Traumatic brain injury affects the frontomedian cortex—An event-related fMRI study on evaluative judgments

Traumatic brain injuries represent the leading cause of death and disability in young adults in industrialized countries. Recently, it has been suggested that dysfunctions of the frontomedian cortex, which enables social cognition, are responsible for clinical deficits in the long-term. To validate this hypothesis, we examined brain activation in seven young adults suffering from diffuse axonal injury during a cognitive task that specifically depends on frontomedian structures, namely evaluative judgments, contrasted with semantic memory retrieval. Brain activation in patients was compared with healthy age and gender matched control subjects using event-related functional magnetic resonance imaging. Evaluative judgments were related to a neural network discussed in the context of self-referential processing and theory of mind. More precisely, the neural network consisted of frontomedian regions, the temporal pole, and the posterior superior temporal gyrus and sulcus/angular gyrus. Patients showed higher activations in this network and the inferior frontal gyrus, whereas healthy control subjects activated more dopaminergic structures, namely the ventral tegmental area, during evaluative judgments. One possible interpretation of the data is that deficits in the ventral tegmental area, and consequently the mesocorticolimbic projection system, have to be compensated for by higher brain activations in the frontomedian and anterior cingulate cortex in patients with diffuse axonal injury. In conclusion, our study supports the hypothesis that traumatic brain injury is characterized by frontomedian dysfunctions, which may be responsible for clinical deficits in the long-term and which might be modified by rehabilitative strategies in the future.     

The usefulness of diffusion tensor imaging in detection of diffuse axonal injury in a patient with head trauma

Diffuse axonal injury is the predominant mechanism of injuries in patients with traumatic brain injury. Neither conventional brain computed tomography nor magnetic resonance imaging has shown sufficient sensitivity in the diagnosis of diffuse axonal injury. In the current study, we attempted to demonstrate the usefulness of diffusion tensor imaging in the detection of lesion sites of diffuse axonal injury in a patient with head trauma who had been misdiagnosed as having a stroke. A 44-year-old man fell from a height of about 2 m. Brain magnetic resonance imaging (32 months after onset) showed leukomalactic lesions in the isthmus of the corpus callosum and the left temporal lobe. He presented with mild quadriparesis, intentional tremor of both hands, and trunkal ataxia. From diffusion tensor imaging results of 33 months after traumatic brain injury onset, we found diffuse axonal injury in the right corticospinal tract (centrum semiovale, pons), both fornices (columns and crus), and both inferior cerebellar peduncles (cerebellar portions). We think that diffusion tensor imaging could be a useful tool in the detection of lesion sites of diffuse axonal injury in patients with head trauma.     

Functional magnetic resonance imaging of executive control in bipolar disorder

Bipolar disorder has been associated with dysfunction of executive control processes. Using functional magnetic resonance imaging, we examined brain activation during a counting Stroop task in 11 healthy adults and 11 patients with bipolar I disorder. Results revealed greater activation for the healthy than bipolar disorder group in distributed brain regions that included the right inferior and medial frontal gyri. With the exception of one area within the left posterior cingulate gyrus that was correlated with mania severity, regional activations where group differences were observed were not associated with mood symptoms in the patient group. These findings add to the growing body of evidence implicating neural circuitry subserving executive control in bipolar disorder.     

轻度颅脑损伤患者的执行功能研究

背景 颅脑损伤常遗留神经精神的损害,包括认知功能损害、精神病性障碍和行为问题等.认知功能损害是颅脑损伤后常见的后遗问题,其中执行功能是一个十分重要的维度.轻度颅脑损伤一直被认为是脑遭受外力打击后出现的暂时的脑功能障碍,无肉眼可见的器质性损害.近年来这一传统的观点受到质疑,目前国内外一些学者认为轻度颅脑损伤是一种弥漫性的脑损伤.关于轻度颅脑损伤患者的神经心理学研究是众多研究者争论的焦点,观点不一致.本研究对恢复期的颅脑损伤患者进行执行功能评定,目的是探讨轻度颅脑损伤患者的执行功能状况.方法 对159例因交通事故造成颅脑外伤的幸存者于损伤后3～6个月医疗终结后进行执行功能评定,并与68例正常人对照.病例组的入组标准为①年龄16～65岁;②文化程度小学及以上文化,能理解执行功能测验的内容;③右利手;④有明确的脑损伤史;⑤检查前4周内未使用抗精神病药物或其他影响中枢神经系统功能的药物;⑥资料齐全;⑦自愿参加本研究.正常对照组的入组标准为①年龄16～65岁;②文化程度小学及以上文化,能理解认知功能测验的内容;③右利手;④自愿参加本研究.排除标准为①以往有脑损伤史、脑部疾患史、精神疾病史者;②精神发育迟滞者;③严重的躯体疾患者;④有药物、酒精或其他影响中枢神经系统功能的物质滥用史者;⑤色盲、色弱者;⑥对测验不合作或不能有效完成测验者.病例组分组根据颅脑损伤伤情评定的国际标准格拉斯哥昏迷计分法将病例组分成三组轻度脑损伤组78例(49.1%)GCS评分15～13分,伤后昏迷时间＜20 min;中度脑损伤组52例(32.7%)GCS评分12～9分,伤后昏迷时间20 min至6 h;重度脑损伤组29例(18.2%)GCS评分8～6分,伤后昏迷时间＞6 h.测验包括韦氏智力测验中的木块拼图测验、STROOP测验、威斯康辛卡片分类测验-改良版(M-WCST)和词汇的流畅性测验,比较轻度颅脑损伤与中、重度颅脑损伤患者的测验成绩,以及CT/MRI有无阳性发现患者的测验成绩,分析与执行功能有关的因素.结果 轻度颅脑损伤患者所有的测验成绩均低于正常对照组,其差异达到显著性水平(P＜0.01).而与中度损伤组的成绩比较则没有显著性差异(P＞0.05).在轻度组与重度组的比较中,除STROOP测验和WCST的分类个数外,其余测验成绩均存在显著性差异(P＜0.05).CT/MRI结果为阳性的病例中,不同脑损伤程度组间的执行功能检测成绩除木块拼图测验外均不具有显著性差异;CT/MRI结果为阴性的病例中,结果显示不同脑损伤程度组间的执行功能测验成绩没有显著性差异(P＞0.05).相关分析显示木块拼图和词汇流畅性两个测验成绩与脑损伤程度呈负相关(P＜0.05).年龄和执行功能呈负相关,受教育程度与执行功能呈正相关.结论 轻度颅脑损伤患者在医疗终结时仍然存在执行功能损害.我们在伤残评定中应对轻度颅脑损伤患者予以重视,同时要注意综合多方面的检测结果考虑.     

Midline brain injury in the immature rat induces sustained cognitive deficits, bihemispheric axonal injury and neurodegeneration

Infants and children less than 4 years old suffer chronic cognitive deficits following mild, moderate or severe diffuse traumatic brain injury (TBI). It has been suggested that the underlying neuropathologic basis for behavioral deficits following severe TBI is acute brain swelling, subarachnoid hemorrhage and axonal injury. To better understand mechanisms of cognitive dysfunction in mild-moderate TBI, a closed head injury model of midline TBI in the immature rat was developed. Following an impact over the midline suture of the intact skull, 17-day-old rats exhibited short apnea times (3–15 s), did not require ventilatory support and suffered no mortality, suggestive of mild TBI. Compared to un-injured rats, brain-injured rats exhibited significant learning deficits over the first week post-injury (p < 0.0005), and, significant learning (p < 0.005) and memory deficits (p < 0.05) in the third post-injury week. Between 6 and 72 h, blood–brain barrier breakdown, extensive traumatic axonal injury in the subcortical white matter and thalamus, and focal areas of neurodegeneration in the cortex and hippocampus were observed in both hemispheres of the injured brain. At 8 to 18 days post-injury, reactive astrocytosis in the cortex, axonal degeneration in the subcortical white matter tracts, and degeneration of neuronal cell bodies and processes in the thalamus of both hemispheres were observed; however, cortical volumes were not different between un-injured and injured rat brains. These data suggest that diffuse TBI in the immature rat can lead to ongoing degeneration of both cell soma and axonal compartments of neurons, which may contribute, in part, to the observed sustained cognitive deficits.     

Risk factors for corticosteroid insufficiency during the sub-acute phase of acute traumatic brain injury

Hypothalamic-pituitary-adrenal axis dysfunction may lead to the occurrence of critical illness-related corticosteroid insufficiency.Critical illness-related corticosteroid insufficiency can easily occur after traumatic brain injury,but few studies have examined this occurrence.A multicenter,prospective,cohort study was performed to evaluate the function of the hypothalamic-pituitary-adrenal axis and the incidence of critical illness-related corticosteroid insufficiency during the sub-acute phase of traumatic brain injury.One hundred and forty patients with acute traumatic brain injury were enrolled from the neurosurgical departments of three tertiary-level hospitals in China,and the critical illness-related corticosteroid insufficiency incidence,critical-illness-related corticosteroid insufficiency-related risk factors,complications,and 28-day mortality among these patients was recorded.Critical illness-related corticosteroid insufficiency was diagnosed in patients with plasma total cortisol levels less than 10μg/dL(275.9 nM)on post-injury day 4 or when serum cortisol was insufficiently suppressed(less than 50%)during a dexamethasone suppression test on post-injury day 5.The results demonstrated that critical illness-related corticosteroid insufficiency occurred during the sub-acute phase of traumatic brain injury in 5.6%of patients with mild injury,22.5%of patients with moderate injury,and 52.2%of patients with severe injury.Traumatic brain injury-induced critical illness-related corticosteroid insufficiency was strongly correlated to injury severity during the sub-acute stage of traumatic brain injury.Traumatic brain injury patients with critical illness-related corticosteroid insufficiency frequently presented with hemorrhagic cerebral contusions,diffuse axonal injury,brain herniation,and hypotension.Differences in the incidence of hospital-acquired pneumonia,gastrointestinal bleeding,and 28-day mortality were observed between patients with and without critical illness-related corticosteroid insufficiency during the sub-acute phase of traumatic brain injury.Hypotension,brain-injury severity,and the types of traumatic brain injury were independent risk factors for traumatic brain injury-induced critical illness-related corticosteroid insufficiency.These findings indicate that critical illness-related corticosteroid insufficiency is common during the sub-acute phase of traumatic brain injury and is strongly associated with poor prognosis.The dexamethasone suppression test is a practical assay for the evaluation of hypothalamic-pituitary-adrenal axis function and for the diagnosis of critical illness-related corticosteroid insufficiency in patients with traumatic brain injury,especially those with hypotension,hemorrhagic cerebral contusions,diffuse axonal injury,and brain herniation.Sub-acute infection of acute traumatic brain injury may be an important factor associated with the occurrence and development of critical illness-related corticosteroid insufficiency.This study protocol was approved by the Ethics Committee of General Hospital of Tianjin Medical University,China in December 2011(approval No.201189).     

Cognitive rehabilitation interventions for executive function: moving from bench to bedside in patients with traumatic brain injury

Executive function mediated by prefrontally driven distributed networks is frequently impaired by traumatic brain injury (TBI) as a result of diffuse axonal injury and focal lesions. In addition to executive cognitive functions such as planning and working memory, the effects of TBI impact social cognition and motivation processes. To encourage application of cognitive neuroscience methods to studying recovery from TBI, associated reorganization of function, and development of interventions, this article reviews the pathophysiology of TBI, critiques currently employed methods of assessing executive function, and evaluates promising interventions that reflect advances in cognitive neuroscience. Brain imaging to identify neural mechanisms mediating executive dysfunction and response to interventions following TBI is also discussed.     

Robust detection of traumatic axonal injury in individual mild traumatic brain injury patients: Intersubject variation, change over time and bidirectional changes in anisotropy

To identify and characterize otherwise occult inter-individual spatial variation of white matter abnormalities across mild traumatic brain injury (mTBI) patients. After informed consent and in compliance with Health Insurance Portability and Accountability Act (HIPAA), Diffusion tensor imaging (DTI) was performed on a 3.0 T MR scanner in 34 mTBI patients (19 women; 19-64 years old) and 30 healthy control subjects. The patients were imaged within 2 weeks of injury, 3 months after injury, and 6 months after injury. Fractional anisotropy (FA) images were analyzed in each patient. To examine white matter diffusion abnormalities across the entire brain of individual patients, we applied Enhanced Z-score Microstructural Assessment for Pathology (EZ-MAP), a voxelwise analysis optimized for the assessment of individual subjects. Our analysis revealed areas of abnormally low or high FA (voxel-wise P-value < 0.05, cluster-wise P-value < 0.01(corrected for multiple comparisons)). The spatial pattern of white matter FA abnormalities varied among patients. Areas of low FA were consistent with known patterns of traumatic axonal injury. Areas of high FA were most frequently detected in the deep and subcortical white matter of the frontal, parietal, and temporal lobes, and in the anterior portions of the corpus callosum. The number of both abnormally low and high FA voxels changed during follow up. Individual subject assessments reveal unique spatial patterns of white matter abnormalities in each patient, attributable to inter-individual differences in anatomy, vulnerability to injury and mechanism of injury. Implications of high FA remain unclear, but may evidence a compensatory mechanism or plasticity in response to injury, rather than a direct manifestation of brain injury.     

轻中型颅脑损伤后认知功能障碍的DTI研究

目的应用弥散张量成像(diffusion tensor imaging,DTI)技术探讨轻中型颅脑损伤病人不同部位脑白质微结构改变与其认知功能障碍的相关性。方法分析127例轻中型颅脑损伤病人的临床资料,伤后10 d采用蒙特利尔认知评估量表(Mo CA)评定有无认知功能障碍,并常规行头颅MRI检查,采集DTI数据,测量两侧额叶、颞叶内侧、顶叶,胼胝体膝部和压部,中脑部位的感兴趣区各向异性分数(FA值)、表观弥散系数(ADC值),并与Mo CA评估结果进行相关性分析。结果以Mo CA量表为标准评定,无认知功能障碍41例(32.28%,无认知障碍组),存在认知功能障碍86例(67.72%,认知障碍组),主要表现为视空间与执行功能、注意力和计算力、语言、抽象能力、延迟记忆的障碍。与无认知障碍的病人相比,认知障碍的病人两侧额叶、颞叶内侧、胼胝体膝部FA值降低,ADC值增加,差异具有统计学意义(P0.01)。结论轻中型颅脑损伤病人早期存在显著认知功能障碍,以视空间与执行功能、注意力和计算力、语言、抽象能力、延迟记忆障碍为主。颅脑损伤后早期认知功能障碍与病人额叶、颞叶、胼胝体白质受损密切相关。     

Executive dysfunction following traumatic brain injury: neural substrates and treatment strategies

Executive dysfunction is among the most common and disabling aspects of cognitive impairment following traumatic brain injury (TBI), and may include deficits in reasoning, planning, concept formation, mental flexibility, aspects of attention and awareness, and purposeful behavior. These impairments are generally attributed to frontal systems dysfunction, due either to direct insult to the frontal lobes or to disruption of their connections to other brain regions. Evaluation of executive deficits typically includes neuropsychological assessment, though adjunctive interviews can be critical in detecting subtle dysexecutive symptoms that may not be apparent on standardized testing. Rehabilitation programs emphasizing cognitive-behavioral approaches to the retraining of planning and problem-solving skills can be effective in ameliorating identified executive deficits. In addition, pharmacological approaches may be useful in addressing aspects of executive dysfunction. This review summarizes the nature of executive deficits following TBI, their neuroanatomical substrates, selected assessment and treatment strategies, and recent research findings and trends.     

Neurobehavioral disability following traumatic brain injury: 7 cases that exhibited neuropsychological impairments and neuropsychiatric syndromes]

The term "higher brain dysfunction" is used to describe neurobehavioral disability or neuropsychological impairment in Japan. Patients with sphenoidal injury and diffuse axonal injury after traumatic brain injury manifest clinical and neuropsychological symptoms. Following closed head injury, patients exhibit a variety of symptoms. In this paper, the author describes neuropsychological dysfunctions/courses and neuropsychiatric syndromes in 7 representative cases who were characterized by : (1) attention deficit, (2) memory dysfunction, (3-a) perseveration, (3-b) dysexecutive syndrome, (4) disorders of drive and motivation, (5) emotional deficits, and (6) lack of ability to recognize the effects of his/her behavior. There are wide varieties of difficulties in assessment, treatment, and rehabilitation for cognitive impairment and behavioral disability after traumatic brain injury. Neuropsychiatrists are expected to participate in this field in Japan.     

An analysis of communication in conversation after severe traumatic brain injury

Background and objective: Communication disorders have been reported following severe traumatic brain injury. However, we have little information about patient behaviour during dyadic interaction. Here, we analyzed conversation at the rehabilitation and chronic phase post traumatic brain injury (TBI), to define the main mechanisms of verbal and non‐verbal communication disorders and relationship with other cognitive difficulties. Methods: Sixteen patients were evaluated at the rehabilitation phase (2–12 months) and 18 at the chronic phase (after 2 years) following severe TBI. They were compared with equivalent groups of matching (gender, age, education level) control subjects. We used the Lille Communication Test, which comprises three parts: participation to communication (greeting, attention, engagement), verbal communication (verbal comprehension, speech outflow, intelligibility, word production, syntax, verbal pragmatics, verbal feedback) and non‐verbal communication (understanding gestures, affective expressivity, producing gestures, pragmatics, non‐verbal feedback). We also investigated executive functions (Stroop test, trail‐making test, categorical evocation), language (Montreal‐Toulouse protocol) and behaviour (Neurobehavioural Rating Scale). Verbal communication disorders were relatively equivalent at the rehabilitation and chronic phases. Results: Patients were impaired (P ≤ 0.01) in their participation to communication, especially in greeting behaviour. Verbal communication was mostly affected by difficulties in producing fluent and intelligible language and using pragmatics (responding to open questions, presenting new information and introducing new themes, organizing discourse and adapting to interlocutor knowledge). Non‐verbal communication was impaired by difficulties in using pragmatics (mostly adapted prosody). Participation and verbal communication correlated with the executive functions, language and behavioural assessment. Conclusions: Disorders of social communication justify systematic assessment in patients with TBI.