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.     

Correlates of persistent sleep complaints after traumatic brain injury

The objective of the study was to examine factors associated with persistent sleep complaint (SC) after traumatic brain injury. The study design consisted of a retrospective chart review case series, with longitudinal follow-up data. Subjects were identified from Georgia Model Brain Injury System with sleep data post-injury. Twenty three (47.9%) had no sleep complaint at either 6 or 12 months post-injury or resolved sleep complaint at 12 months (Without Persistent SC group); 25 (52.1%) maintained a sleep complaint from 6 to 12 months or reported a sleep complaint at 12 months post-injury (With Persistent SC group). Demographic, premorbid and peri-injury characteristics and The Neurobehavioral Functioning Inventory (NFI) scores did not differentiate the two groups. The Without Persistent SC group had a slight improvement from 6 to 12 months post-injury in post-traumatic stress (PTS) symptoms and depression. Significant psychological patterns were identified in those with persistent SC at both 6 and 12 months post-injury, i.e., worse depression and worse PTS symptoms. This trend was apparent at 6 months and became significant at 12 months post-injury. However, subjects with newly emerging sleep complaints at 12 months had similar characteristics as the Without Persistent SC group. The observed psychological patterns associated with persistent sleep complaint in a specific time course after brain injury have important research and clinical implications that merit further study.     

An investigation of attention,executive, and psychomotor aspects of cognitive fatigability

Objective: Self-perceived mental fatigue is a common presenting symptom in many neurological diseases. Discriminating objective fatigability from self-perceived mental fatigue might facilitate neuropsychological diagnosis and treatment programs. However clinically valid neuropsychological instruments suitable for assessment of fatigability are still lacking. The prime aim of the study was to investigate aspects of cognitive fatigability and to identify properties of neuropsychological tests suitable to assess fatigability in patients with persistent cognitive complaints after mild brain injury. Another aim was to investigate whether cognitive fatigability captured by neuropsychological measures is influenced by depression or sleep disturbances. Method: Twenty-four patients with persistent cognitive symptoms after mild traumatic brain injury (mTBI), (aged 18–51 years) and 31 healthy controls (aged 20–49 years) underwent neuropsychological testing measuring three cognitive fatigability domains: Attention fatigability was assessed using the Ruff 2 & 7 Selective Attention Test, executive fatigability using the Color Word Test (Stroop), and psychomotor fatigability using the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale–Third Edition (WAIS–III). Subjective fatigue was measured using the Fatigue Severity Scale and a questionnaire of everyday consequences of fatigue. Depression was screened using the Hospital Anxiety and Depression Scale and sleep disturbances using the Pittsburgh Sleep Quality Index. Results: The patients reported significantly more mental fatigue and performed worse on tests of psychomotor and executive fatigability than the healthy controls. Furthermore, the cognitive fatigability measures were not influenced by depression or sleep disturbances, as was the case in self-reported fatigue. Conclusion: Tests demanding executive or simultaneous processing of several neuropsychological functions seem most sensitive in order to capture cognitive fatigability. Clinical tests that can capture fatigability enable a deeper understanding of how fatigability might contribute to cognitive complaints and problems in maintaining daily activities.     

Individuals with pain need more sleep in the early stage of mild traumatic brain injury

ObjectiveHypersomnia is frequently reported after mild traumatic brain injury (mTBI), but its cause(s) remain elusive. This study examined sleep/wake activity after mTBI and its association with pain, a comorbidity often associated with insomnia.MethodsActigraphy recording was performed for 7 ± 2 consecutive days in 56 individuals at one month post-mTBI (64% male; 38 ± 12 years), 24 individuals at one year post-mTBI (58% male; 44 ± 11years), and in 20 controls (50% male; 37 ± 12 years). Pain intensity and its effect on quality of life was assessed with a visual analogue scale and the Short Form Health Survey (SF-36) bodily pain subscale.ResultsOverall, few differences in sleep/wake patterns were found between mTBI patients and controls. However, higher percentages of mTBI individuals with moderate-to-severe pain were found to require more than eight hours of sleep per day (37% vs11%; p = 0.04) and to be frequent nappers (defined as those who took three or more naps per week) (42% vs 22%; p = 0.04) compared to those with mild or no pain at one month postinjury. Correcting for age and depression, The SF-36 score was found to be a significant predictor of sleep duration exceeding eight hours per day at one month (odds ratio = 0.95; 95% confidence interval = 0.92–0.99; p = 0.01), but not at one year post-mTBI. Pain and increased sleep need (in terms of hours per day or napping frequency) were found to co-exist in as much as 29% of mTBI patients at one month postinjury.ConclusionPain could be associated with more pronounced sleep need in about one-third of mTBI patients during early recovery. Unalleviated pain, found in more than 60% of mTBI patients, should therefore be looked for in all mTBI patients reporting new onset of sleep disorder, not only in those with insomnia.     

Neuropsychological support to relatives of patients with severe traumatic brain injury in the sub-acute phase

Many studies have reported emotional distress in relatives of patients with brain injury, but few studies have investigated neuropsychological interventions for relatives. The present study assessed the amount of neuropsychological support as well as the actual number of sessions with a neuropsychologist during rehabilitation in a sub-acute unit. The study also examined whether the amount of support was related to the condition of the patient or the relative at admission. The sample consisted of 26 patients and their closest relative, and measures included demographic variables as well as characteristics related to the patient: Glasgow Coma Scale, Injury Severity Score, Early Functional Abilities, Functional Independence Measure, Rancho Los Amigos; and to the relative: symptoms of anxiety and depression (SCL-90-R), quality of life (SF-36) and amount and number of sessions of neuropsychological support. On average, the relatives received about 18 units of 15 minutes and had six sessions with a neuropsychologist during hospitalisation. A total of 38% participated in group sessions. Relatives' symptoms of anxiety at admission were associated with the number of sessions as well as the amount of support, indicating that relatives with more symptoms of anxiety received more support during the hospitalisation.     

Screening for sleep dysfunction after traumatic brain injury

Numerous studies on the high prevalence of sleep disorders in individuals with traumatic brain injury (TBI) have been conducted in the past few decades. These disorders can accentuate other consequences of TBI, negatively impacting mood, exacerbating pain, heightening irritability, and diminishing cognitive abilities and the potential for recovery. Nevertheless, sleep is not routinely assessed in this population. In our review, we examined the selective screening criteria and the scientific evidence regarding screening for post-TBI sleep disorders to identify gaps in our knowledge that are in need of resolution. We retrieved papers written in the English-language literature before June 2012 pertinent to the discussion on sleep after TBI found through a PubMed search. Within our research, we found that sleep dysfunction is highly burdensome after TBI, treatment interventions for some sleep disorders result in favorable outcomes, sensitive and specific tests to detect sleep disorders are available, and the cost-effectiveness and sustainability of screening have been determined from other populations. The evidence we reviewed supports screening for post-TBI sleep dysfunction. This approach could improve the outcomes and reduce the risks for post-TBI adverse health and nonhealth effects (e.g., secondary injuries). A joint sleep and brain injury collaboration focusing on outcomes is needed to improve our knowledge.     

多奈哌齐治疗颅脑创伤后记忆和智能障碍的临床观察

目的 观察多奈哌齐治疗96 例颅脑创伤后记忆和智能障碍的疗效.方法 颅脑创伤后记忆和智能障碍患者96例,治疗组给予多奈哌齐片5mg,1次/d, 晚上睡前口服;对照组给予尼莫地平片常规治疗.治疗期为1个月.结果 治疗组患者记忆功能、认知功能改善较为明显, 与对照组比较有明显差异(P ＜ 0.05).结论 多奈哌齐对颅脑创伤后记忆和智能障碍患者早期治疗效果好, 安全性高, 不良反应少, 服用方便.     

Sequelae following traumatic brain injury: The cerebrovascular perspective

Traumatic brain injury (TBI) initiates a huge repertoire of biochemical perturbations. On one hand, destructive events are set into motion while on the other hand, protective and recovery mechanisms are evoked, each with their own temporal and spatial characteristics. The brain exists as a finely tuned balance between vascular, neuronal and glial interactions and so a complex interplay between these factors will dictate the final evolution of pathogenesis. Although vascular damage is a key event, it remains a somewhat neglected component to the underlying degenerative processes that evolve following injury to the brain. The present review will act to integrate the current knowledge of the vascular events proceeding injury to the brain, with an emphasis on how this impacts the control of vascular function and thus cerebral blood flow.     

Consolidation deficits in traumatic brain injury: The core and residual verbal memory defect

While memory deficits are consistently found to be a salient problem in individuals with moderate to severe traumatic brain injury (TBI), the specific memory processes (i.e., encoding, consolidation, and retrieval) underlying the verbal memory deficit are disputed in the literature. The current study evaluated the recovery of these verbal memory processes over time. A TBI patient group evaluated acutely after the injury (baseline) and again at 6 months and 1 year post injury was compared to a demographically similar control group evaluated only once. The current results replicated previous findings in support of an impaired consolidation hypothesis as the primary deficit underlying memory impairment in TBI. These deficits are reflected in relatively more rapid forgetting through 1 year post injury and relatively less proactive interference up to 6 months post injury.     

Outcome measures for traumatic brain injury

Traumatic brain injury (TBI) is a major public health problem resulting in death and disabilities of young and productive people. Though the mortality of TBI has decreased substantially in recent years the disability due to TBI has not appreciably reduced. Various outcome scales have been proposed and used to assess disability after TBI. A few, commonly used are Glasgow Outcome Scale (GOS) with or without extended scores, Disability Rating Scale (DRS), Functional Independence Measure (FIM), Community Integration Questionnaire (CIQ), and the Functional Status Examination (FSE). These scales assess disability resulting from physical and cognitive impairments. For patients with good physical recovery a cognitive and neuropsychological outcome measure is required. Such measures include Neurobehavioural Function Inventory and specific neuropsychological tests like Rey Complex Figure for visuoconstruction and memory, Controlled Oral Word Association for verbal fluency, Symbol Digit Modalities (verbal) for sustained attention and Grooved Pegboard for fine motor dexterity. A more holistic and complete outcome measure is Quality of Life (QOL). Disease specific QOL measure for TBI, Quality of Life after Brain Injury (QOLIBRI) has also been recently proposed. The problems with outcome measures include poor operational definitions, lack of sensitivity or low ceiling effects, inability to evaluate patients who cannot report, lack of integration of morbidity and mortality categories, and limited domains of functioning assessed. GOSE-E satisfies most of the criteria of good outcome scale and in combination with neuropsychological tests is a near complete instrument for assessment of outcome after TBI.     

Self-regulation upon return to driving after traumatic brain injury

The aim of this study was to explore self-reported driving habits and the factors associated with these within the first three months of return to driving following traumatic brain injury (TBI). Participants included 24 individuals with moderate to severe TBI (post-traumatic amnesia duration M?=?33.26, SD?=?29.69 days) and 28 healthy age, education, and gender-matched controls who completed an on-road assessment. Driving frequency and avoidance questionnaires were administered to assess premorbid driving, anticipated driving upon resuming, and driving at three months post-assessment. There were no differences between groups for premorbid driving frequency or avoidance. Individuals with TBI anticipated greater reductions in driving frequency, t(29.57)?= ?3.95, p?<?.001, and increases in avoidance, U?=?171.00, z?=??2.69, p?<?.01. On follow up, significant reductions in frequency, t(48) =??3.03, p?<?.01, but not avoidance, U?=?239.00, z?=??1.35, p?=?.18, were observed. Females were more likely to reduce their driving frequency, rs?= ?.43, p?<?.05, while increased anxiety was associated with increased avoidance r?=?.63, p?<?.05, and reduced frequency r?=??.43, p?<?.05. It was concluded that individuals with TBI anticipated changes in their driving habits upon return to driving, indicating an expectation for post-injury changes to their driving lifestyle. On follow up, many of these intended changes to driving habits, particularly in relation to driving frequency, were reported by individuals with TBI, suggestive of some strategic self-regulation.     

亚低温对创伤性颅脑损伤后胃肠动力学影响的实验研究

目的 探讨亚低温对创伤性脑损伤(TBI)后胃肠动力的影响.方法 选取成年健康雄性SD大鼠75只,按照随机数字表法分为假手术组(Sham)、创伤组(TBI)、亚低温组(MIH).应用电子脑皮质撞击仪(eCCI)建立大鼠TBI模型,随即亚低温干预4h.分别检测各组大鼠胃动力、胃排空率、小肠推进率改变;动物处死后分别获取脑、胃、回盲部、距回盲部15 cm处小肠组织,HE染色观察其病理变化.结果 大鼠TBI后胃明显扩张,胃壁变薄,胃黏膜充血、水肿,部分黏膜上皮脱落,黏膜下层有出血,肠腔扩张胀气,肠黏膜出血坏死、绒毛脱落、中性粒细胞浸润,绒毛间隙增大,杯状细胞减少.胃黏膜充血血管计数和肠黏膜绒毛断裂数显示6 h TBI组与MIH组相比差异无统计学意义(P＞0.05),24 h、48 h和72 h MIH组与TBI组相比差异有统计学意义(P＜0.05).胃动力学检测显示各组胃运动频率相比差异无统计学意义(P＞0.05);胃运动波幅值TBI和MIT组均高于Sham组,差异有统计学意义(P＜0.05),24 h后MIT组低于TBI组,差异有统计学意义(P＜0.05).胃排空率,小肠推进率测定显示6 h TBI组和MIH组相比差异无统计学意义(P＞0.05),24 h、48 h和72 h MIH组与TBI组相比差异有统计学意义(P＜0.05).结论 TBI对大鼠胃肠黏膜和胃肠动力皆有影响,MIH干预后短期效应不显但长期疗效显著.     

Age-dependent synuclein pathology following traumatic brain injury in mice

Synucleins (Syn), a family of synaptic proteins, includes alpha-Syn, which plays a pivotal role in Parkinson's disease and related neurodegenerative diseases (synucleinopathies) by forming distinct brain pathologies (Lewy bodies and neurites). Since traumatic brain injury (TBI) is a poorly understood risk factor for Parkinson's disease, we examined the effects of TBI in the young and aged mouse brain on alpha-, beta-, and gamma-Syn. Immunohistochemical analysis showed that brains from sham-injured young and aged mice had normal alpha- and beta-Syn immunoreactivity (IR) in neuropil of cortex, striatum, and hippocampus with little or no gamma-Syn IR. At 1 week post TBI, the aged mouse brain showed a transient increase of alpha- and beta-Syn IR in the neuropil as well as an induction of gamma-Syn IR in subcortical axons. This was associated with strong labeling of striatal axon bundles by antibodies to altered or nitrated epitopes in alpha-Syn as well as by antibodies to inducible nitric oxide synthase. However, these TBI-induced changes disappeared by 16 weeks post TBI, and altered Syn IR was not seen in young mice subjected to TBI nor in alpha-Syn knockout mice while Western blots confirmed that TBI induced transient alterations of alpha-Syn in the mouse brains. This model of age-dependent TBI-induced transient alterations in alpha-Syn provides an opportunity to examine possible links between TBI and mechanisms of disease in synucleinopathies.     

Anatomical integration of newly generated dentate granule neurons following traumatic brain injury in adult rats and its association to cognitive recovery

The hippocampus is particularly vulnerable to traumatic brain injury (TBI), the consequences of which are manifested as learning and memory deficits. Following injury, substantive spontaneous cognitive recovery occurs, suggesting that innate repair mechanisms exist in the brain. However, the underlying mechanism contributing to this is largely unknown. The existence of neural stem cells in the adult hippocampal dentate gyrus (DG) and their proliferative response following injury led us to speculate that neurogenesis may contribute to cognitive recovery following TBI. To test this, we first examined the time course of cognitive recovery following lateral fluid percussion injury in rats. Cognitive deficits were tested at 11-15, 26-30 or 56-60 days post-injury using Morris Water Maze. At 11-15 and 26-30 days post-injury, animals displayed significant cognitive deficits, which were no longer apparent at 56-60 days post-TBI, suggesting an innate cognitive recovery at 56-60 days. We next examined the proliferative response, maturational fate and integration of newly generated cells in the DG following injury. Specifically, rats received BrdU at 2-5 days post-injury followed by Fluorogold (FG) injection into the CA3 region at 56 days post-TBI. We found the majority of BrdU+ cells which survived for 10 weeks became dentate granule neurons, as assessed by NeuN and calbindin labeling, approximately 30% being labeled with FG, demonstrating their integration into the hippocampus. Additionally, some BrdU+ cells were synaptophysin-positive, suggesting they received synaptic input. Collectively, our data demonstrate the extensive anatomical integration of new born dentate granule neurons at the time when innate cognitive recovery is observed.     

Role of valued living and associations with functional outcome following traumatic brain injury

Valued living (VL) is associated with improved enjoyment and engagement with daily activities despite negative emotional state or ongoing pain. However, the role of VL in recovery following traumatic brain injury (TBI) has yet to be investigated. This study aimed to examine changes in VL over the course of recovery and variables associated with VL. Participants with moderate-to-severe TBI were recruited from a rehabilitation hospital in three cohorts: “Early” (n?=?25), “Mid” (n?=?9) and “Late” (n?=?36) post-TBI. All participants were assessed at time of recruitment and 12 months later. The main measure was the Valued Living Questionnaire. Compared to pre-injury estimates, VL was significantly reduced at 12 months post-injury. Levels of VL remained reduced between 2 and 3 years and increased between 3 and 6 years post-injury. VL was strongly associated with improved functional and psychosocial outcomes. Changes in VL occur over at least 3–5 years post-injury, with 12 months post-TBI a suitable time for intervention given VL remains low over the next 24 to 36 months post injury. Targeted intervention to modify values and/or valued activities to be consistent with post-injury capacity could improve rates of return to pre-injury levels of VL.     

Randomized treatment trial in mild traumatic brain injury

OBJECTIVE: To determine whether multidisciplinary treatment of mild traumatic brain injury (MTBI) improves neurobehavioral outcome at 6 months postinjury. METHODS: Subjects with MTBI were randomly assigned to treatment (n=97) or nontreatment (control, n=94) groups. Treated patients were assessed within 1 week of injury and thereafter managed by a multidisciplinary team according to clinical need for a further 6 months. Control subjects were not offered treatment. Six-month outcome measures included: severity of postconcussive symptoms (Rivermead Post-Concussion Disorder Questionnaire), psychosocial functioning (Rivermead Follow-up Questionnaire), psychological distress (General Health Questionnaire), and cognition (neurocognitive battery). RESULTS: Treatment and control subjects were well-matched for demographic and MTBI severity data. In addition, the two groups did not differ on any outcome measure. However, in individuals with preinjury psychiatric difficulties (22.9% of the entire sample), subjects in the treatment group had significantly fewer depressive symptoms 6 months postinjury compared with untreated controls (P=.01). CONCLUSIONS: These findings suggest that routine treatment of all MTBI patients offers little benefit; rather, targeting individuals with preinjury psychiatric problems may prove a more rational and cost-effective approach.     

Long-term neurological and neuropsychological outcome in patients with severe traumatic brain injury

Background

Severe traumatic brain injury (TBI) remains a major cause of death and disability worldwide. The aim of the study was to evaluate predictors for neurological and neuropsychological long-term outcome in patients with severe TBI treated according to an intracranial pressure (ICP-) targeted therapy.

Methods

From 08/2005 to 12/2008, 46 patients with severe TBI and more than 12 h of intensive care treatment were included in this study. Neurological outcome was assessed with the Glasgow Outcome Scale (GOS). Neuropsychological performance assessing 9 different domains was evaluated at long-term follow-up (median 20.5 months; range 10–46). Logistic regression was used to identify favourable outcomes according to the GOS and Fisher's exact tests were used to identify predictors of severe neuropsychological impairments at follow-up.

Results

Twenty-nine patients were available for neuropsychological assessment at long-term follow-up. Only 2 out of 29 patients presented normal or average neuropsychological findings throughout all 9 neuropsychological domains at long-term follow-up. The percentage of a favourable outcome (GOS 4-5) increased from 13.8% at hospital discharge to 75.8% at rehabilitation discharge to 79.3% at long-term follow-up, respectively. Age ≤40 was found to be a strong predictor of favourable outcome at follow-up (OR 5.95, 95% CI 1.41 25.00, p = 0.015). The GOS at hospital discharge was not a predictor for severe impairments in any of the 9 different neuropsychological domains (all p-values were p > 0.268). In contrast, the GOS at rehabilitation discharge was found to be a predictor of severe impairments at follow-up in all but one domain assessed (all p-values less than p < 0.038).

Conclusions

The GOS at rehabilitation discharge should be regarded as a better predictor for neuropsychological impairments at long-term follow-up than the GOS at hospital discharge. Even in patients with favourable GOS after finishing a course of rehabilitation, three quarters of these patients may have at least one severe neuropsychological deficit. Therefore, it remains of paramount importance to provide long-term neuropsychological support to further improve outcome after TBI.     

Brain lesion correlates of fatigue in individuals with traumatic brain injury

ABSTRACT

The purpose of this study was to investigate the neurological correlates of both subjective fatigue as well as objective fatigability in individuals with traumatic brain injury (TBI). The study has a cross-sectional design. Participants (N?=?53) with TBI (77% male, mean age at injury 38 years, mean time since injury 1.8 years) underwent a structural magnetic resonance imaging (MRI) scan and completed the Fatigue Severity Scale (FSS), while a subsample (N?=?36) was also tested with a vigilance task. While subjective fatigue (FSS) was not related to measures of brain lesions, multilevel analyses showed that a change in the participants’ decision time was significantly predicted by grey matter (GM) lesions in the right frontal lobe. The time-dependent development of the participants’ error rate was predicted by total brain white matter (WM) lesion volumes, as well as right temporal GM and WM lesion volumes. These findings could be explained by decreased functional connectivity of attentional networks, which results in accelerated exhaustion during cognitive task performance. The disparate nature of objectively measurable fatigability on the one hand and the subjective experience of fatigue on the other needs further investigation.     

Malingering detection with the Wisconsin Card Sorting Test in mild traumatic brain injury

This study evaluates the ability of several Wisconsin Card Sorting Test (WCST; Psychological Assessment Resources, 1990) variables to detect malingering in mild traumatic brain injury (TBI). The sample consisted of 373 TBI patients and 766 general clinical patients. Classification accuracy for seven indicators is reported across a range of injury severity and scores levels. Overall, most WCST scores were ineffective in discriminating malingering from non-malingering mild TBI patients. Failure-to-Maintain-Set, the Suhr & Boyer formula, and the King et al. formula detected about 30% of malingerers at cutoffs associated with a false positive error rate of ≤11%. The clinical interpretation and use of these indicators are discussed.