Traumatic Brain Injury Alters Word Memory Test Performance by Slowing Response Time and Increasing Cortical Activation: An fMRI Study of a Symptom Validity Test

The Word Memory Test (WMT) is an established symptom validity test that relies on verbal memory performance to make inferences about “effort.” Previous studies, using a functional MRI (fMRI) adaptation of the WMT with healthy controls, have shown that successful completion of the WMT relies on a widespread network of neural systems associated with high cognitive effort. Additional studies using the same fMRI paradigm with patients with severe traumatic brain injury (TBI) suggest that increased activation of cortical regions associated with cognitive load are recruited to meet the cognitive challenges that the WMT places on a compromised neural system. This study builds on previous findings as a result of highly uncommon circumstances in which fMRI data on the WMT task were made available from the very same individual both 1 year before and 1 year after sustaining a TBI. Interestingly, the effect of TBI did not appear to impair performance on the WMT in terms of standard accuracy measurements, though response times were notably slower. The main fMRI finding was a significantly stronger and more widespread pattern of activation post-injury, particularly in the frontal and parietal brain regions, suggesting that stronger engagement of these networks was necessary to sustain accurate WMT performance compared to pre-injury testing. This unique source of data, together with previous findings, suggests a more complex relationship between effort and performance levels on the WMT than what is commonly assumed.     

The Word Memory Test in medicolegal assessment: a measure of effort and malingering?

The Word Memory Test (WMT) is claimed to measure effort and to detect cognitive response bias. Archival data from n = 2526 cases referred in 2009–2016 for medicolegal assessment were analyzed. Each participant underwent a medical and a psychological examination including a cognitive test battery and several validity measures including the WMT. The WMT validity test scores do not approximately follow a normal distribution. Thus, parametric statistics for WMT validity scores may not be appropriate. WMT performance explains 0–20% of the variance in cognitive test performance. This is more than what substantial brain damage accounts for. The standard uniform cutoff indicating a ‘fail’ in all three WMT effort subtests (equal or less than 82.5% correct responses) seems not supported by the data. Taking into account the context of the testing, cutoffs may be chosen according to the desired sensitivity or specificity. ROC-statistics with modified Slick criteria as gold standard for malingering look alike for the three WMT effort subtests, with a AUC between 0.86 and 0.88. The WMT seems a good indicator of both effort and (Slick) malingering, however, little is gained by administering the entire test.     

Simulating amnesia and memories of a mock crime

Abstract

Defendants often feign (i.e. simulate) dissociative amnesia for their crimes. The Symptom Validity Test (SVT) may be used to detect such feigning. Some studies have shown that feigning amnesia for a mock crime has memory-undermining effects. In this study, we wanted to replicate the memory-undermining effects of simulated amnesia. We also examined whether such effects would occur when participants’ memories were evaluated with a SVT. Thirty participants committed a mock crime and then simulated amnesia for it. During a follow-up test, participants were instructed to perform as well as they could on a free recall test and a SVT. Their memory performance was compared with that of a control group (n=30). Although only a minority of simulating participants (7%) was detected by our SVT, the memory-undermining effect of simulating amnesia appeared to be a robust phenomenon. That is, ex-simulators displayed poorer free recall, more commission errors, and lower SVT scores relative to memory performance of honestly responding controls. However, at follow-up testing the poor memory of ex-simulators did not take the form of a real amnesia (i.e. random performance on SVT).     

脑外伤者血浆NSE含量与损伤程度的相关性

目的探讨血浆中神经元特异性烯醇化酶（NSE）含量与创伤性脑损伤程度的关系及法医学意义。方法选取25名健康体检者、34名颅脑损伤患者作为研究对象,根据入院时的GCS评分,将颅脑损伤患者分为轻中型组（GCS≥8分）和重型组（GCS〈8分）。用酶联免疫法对上述研究对象血浆中神经元特异性烯醇化酶含量进行检测。结果在脑外伤24h内,颅脑损伤组血浆中神经元特异性烯醇化酶含量较正常对照组升高,差异有统计学意义（P〈0.05）,重型组与轻中型组相比,差异有统计学意义（P〈0.05）,血清中血浆中神经元特异性烯醇化酶含量越高,患者颅脑损伤程度越严重。结论神经元特异性烯醇化酶可作为早期检测创伤性颅脑损伤的特异性指标,其含量越高,颅脑损伤程度越重。     

颅脑损伤后血液中S100β含量与损伤程度的关系

目的探讨血清中S100β蛋白含量与创伤性脑损伤程度的关系及法医学意义。方法选取健康体检者、颅脑损伤患者和其他创伤患者各30名作为研究对象,再根据入院时的GCS评分,将颅脑损伤患者分为轻中型组（GCS≥8分）和重型组（GCS〈8分）。用ELISA法对上述研究对象血清中S100β蛋白含量进行检测。结果在脑外伤6h内,颅脑损伤组血清S100β蛋白含量较正常对照组和创伤对照组升高,差异有统计学意义（P〈0.05）;重型组与轻中型组相比,差异有统计学意义（P〈0.05）。血清中S100β蛋白含量越高,患者颅脑损伤程度越严重。结论S100β蛋白可作为早期检测创伤性颅脑损伤的指标之一,其含量越高,颅脑损伤程度越重。     

威斯康星卡片分类测验用于颅脑损伤者认知功能障碍鉴定

目的 探讨威斯康星卡片分类测验(Wisconsin Card Sorting Test,WCST)对颅脑损伤者认知功能障碍鉴定的应用价值.方法 对186例颅脑外伤要求鉴定的患者(实验组)和180例健康志愿者(对照组)分别进行WCST和中国修订版韦氏成人智力量表(Wechsler Adult Intelligence S...     

Homogenous Base Rates for Malingering in Neuropsychological Examination of Litigants

Base rates for malingering are often obtained and averaged across multiple clinicians who apply heterogeneous methods for detection (Mittenberg et al., J Clin Exp Neuropsychol 24: 1094?1102, 2002; Young, Psychol Inj Law 8: 200–218, 2015). Our aims of obtaining homogenous base rates included the following: (a) evaluation of all our legal cases in accordance with the guidelines set forth in the position papers by both the National Academy of Neuropsychology and the Association for Psychological Advancement in Psychological Injury and Law, (b) minimal variation between our comprehensive neuropsychological examinations, and (c) determination of base rates of failed effort in 150 consecutively examined legal cases in one medical setting. To assess the various levels of volitional exaggeration, we introduced four gradations of poor effort definitions, which relied on performance validity tests (PVTs). A comparison between two consecutive samples of 75 litigants indicated less frequent poor effort with increasingly more conservative criteria. In our analysis of a subset of litigants who sustained traumatic brain injuries (N?=?115), the four base rates for mild versus moderate-severe TBI groups were equivalent for the two more lenient malingering definitions but varied for the two more conservative definitions. Specifically, for the mild TBI cases investigated, the percentage of three PVT failures (or one PVT failure significantly below chance) arrived at 3.4 %. Our final aim was to compare the base rates of poor effort that were obtained with PVTs to the base rates of emotional and physical symptom endorsement, which were obtained with symptom validity tests (SVTs). No significant correlations emerged in this analysis. The discussion emphasizes the relatively lower base rates of poor effort found in the convenience sample studied in neuropsychological evaluations relative to the higher estimates in the literature (40 +/? 10 %, Larrabee et al., Clin Neuropsychol 23: 841–849, 2009) but not others based on comprehensive review (Young, Psychol Inj Law 8: 200–218, 2015).     

Traumatic brain injury in a forensic intellectual disability population

Traumatic brain injury (TBI) screening in forensic populations has been recommended, due to a high prevalence, links to specific offence profiles and poorer outcomes, such as higher rates of psychiatric disturbance, longer stays in prison, and reoffending. Research focusing on TBI among offenders with intellectual disability (ID) is lacking. This study therefore describes the implementation of TBI screening using the Brain Injury Screening Index (BISI©), TBI prevalence and correlates in a forensic ID service. TBI appeared under recorded in case notes, with considerably more patients self-reporting TBI. Reported causes of TBI differed somewhat to the general population, including childhood physical abuse, self-harming behaviour, and assault. Approximately one-third of injuries did not receive any treatment. Though further adaptations may be required on current screening measures for TBI in offenders with ID, screening can provide valuable information, contributing positively to individual patient therapeutic and risk formulations.     

Could NF-kappaB and caspase-3 be markers for estimation of post-interval of human traumatic brain injury?

BACKGROUND: Previous studies in a rat model showed expressions of caspase-3 (p20) and NF-kappaB (p65) in different time after TBI. We test the activation changes of caspase-3 and NF-kappaB of human specimen after traumatic brain injury (TBI) in this study to see whether they could be markers to estimate post-intervals of TBI for forensic practice. MATERIAL AND METHODS: Caspase-3 (p20) and NF-kappaB (p65) immunohistochemical staining were performed on 39 TBI specimens (dead from TBI) and eight controls (dead from none TBI reasons) grouped 0, 12, 24, 48, 72, 168, 264 and 480 h. Positive cells were counted and image analysis techniques were used to determine the morphological changes in each group. RESULTS: Immunohistochemical analysis showed a marked induction of caspase-3 (p20) in every injured group compared with normal controls; each positive group has it's morphological character with variant positive cell count. NF-kappaB (p65) did not showed markedly change compared with normal controls until 168 h after TBI and almost all nerve cells were stained by NF-kappaB (p65) in 264 and 480 h groups. CONCLUSION: NF-kappaB (p65) could contribute to estimate delayed death cases after TBI for forensic applications. Caspase-3 (p20) estimating post-TBI intervals are dubious but could suggest TBI exists.     

Chronic Traumatic Encephalopathy Pathology After Shotgun Injury to the Brain

Chronic traumatic encephalopathy (CTE) was initially conceptualized in boxers, but has extended to other athletes in recent years, albeit with limited clinical correlations. It is often asserted that CTE pathology represents the substrate for progressive neurodegenerative disease. We report the case of a shotgun injury to the brain with 42‐year survival and no neurological disease progression until shortly before death. The decedent had no other traumatic brain injury (TBI) exposure and did not play football or other high energy collision sport. Neuropathological examination confirmed tissue damage, but additionally demonstrated localized patterns of phosphorylated tau (p‐tau) meeting criteria for CTE pathology. P‐tau and TDP‐43 deposits within marginal tissue of damaged brain were also present focally. No amyloid‐β (Aβ) deposits were present. These findings indicate that CTE pathology may occur following a single, severe TBI.     

创伤性脑损伤与细胞凋亡

综述了创伤性脑损伤后神经细胞凋亡发生的证据、特点及其可能的分子机制。研究资料表明:创伤性脑损伤后存在有细胞凋亡,它与坏死的时序空间分布不同,创伤性脑损伤后的神经细胞凋亡可通过多种不同的途径发生,受多种基因的调控。同时,本文还探讨了创伤性脑损伤后神经细胞凋亡的研究在法医学方面的应用。     

Simulating Emotional Responses in Posttraumatic Stress Disorder: An fMRI Study

This study tested the extent to which coached participants can simulate the neural responses of participants with posttraumatic stress disorder (PTSD) when they are presented with signals of fear. Functional magnetic resonance imaging (fMRI) was used to study blood oxygenation level-dependent signal during the presentations of fearful and neutral faces under both conscious and nonconscious (masked) conditions. Participants comprised 12 patients with PTSD and 12 trauma-exposed controls who were instructed to simulate PTSD. During conscious fear processing, simulators showed greater activation in the left amygdala and medial prefrontal cortex (MPFC) than PTSD participants. By contrast, during nonconscious processing, PTSD participants had greater MPFC activation than simulators. These findings suggest that coached simulators produce a profile of ‘over-responding’ to fear when controlled conscious processing is possible, but are not able to simulate the exaggerated medial prefrontal responses observed in PTSD participants under conditions of nonconscious processing.     

实验性脑挫伤后caspase-3表达的免疫组织化学研究

目的 观察大鼠在不同程度及不同时间脑挫伤后caspase-3表达的变化。方法 对48例实验性脑挫伤大鼠的脑组织进行检验,同时以10例非脑挫伤的脑组织做对照。结果 伤后1h,caspase-3即有表达;24～48h达高峰,2周时仍有阳性细胞存在。阳性细胞多集中于挫伤区及周围带皮质和脑实质内海马区;不同程度脑挫伤组之间于伤后1h,12h,24h,72h,1周和2周caspase-3表达有差异。结论 不同程度脑损伤后caspase-3表达量不同;在脑损伤后caspase-3的表达有时间变化规律,对探讨脑挫伤后二次损害原因和研究脑挫伤程度有一定意义。     

Trials and tribulations of using beta-amyloid precursor protein immunohistochemistry to evaluate traumatic brain injury in adults

Axonal pathology is increasingly identified by beta-amyloid precursor protein (betaAPP) immunohistochemistry in the brains of patients who may or may not have a history of trauma. The presence of betaAPP-IR(+) has been variously interpreted as either that diffuse traumatic axonal injury (TAI) is indeed a universal finding in cases of fatal traumatic brain injury (TBI) or there are other causes of betaAPP-IR(+) axons which under certain circumstances may be sufficient to mimic TBI and therefore make the medico-legal interpretation of certain cases very difficult. To address some of the uncertainties we have undertaken a detailed analysis of the amount and distribution of betaAPP immunohistochemistry in 63 cases of fatal TBI, 17 cases of patients dying after cardiac arrest, 12 cases dying in association with status epilepticus, 3 cases of carbon monoxide (CO) poisoning, 13 cases of hypoglycaemia and in 60 controls. Three patterns of betaAPP-IR(+) were identified. First, diffuse multi-focal, second, corresponding to the outline of an infarct or haematoma, and thirdly a mixture of the two. The first pattern was seen in cases of the lesser grades of TAI, CO poisoning, and hypoglycaemia, the second pattern in cases in which there was evidence of raised intracranial pressure and the third in cases of severe TAI. It is concluded that the proper interpretation of cases requires the examination of a sufficient number of blocks ( [Formula: see text] ), processing using standardised protocols including betaAPP immunohistochemistry and in some cases the mapping of any IR(+) on anatomical line diagrams. betaAPP carried out on a small number of randomly taken blocks is likely to lead to misinterpretation of the clinico-pathological correlations and possibly to a miscarriage of justice.     

大鼠脑外伤后溶酶体酶Cathepsin—B和D的表达

目的研究大鼠脑外伤后溶酶体酶cathepsin-B和-D是否被激活及其不同时段表达变化,阐述其与凋亡执行因子caspase-3表达的关系,并探讨对脑外伤诊断及形成时间的意义。方法采用自由落体打击法建立脑外伤动物模型,并对模型及对照样本进行免疫荧光、双标和激光共聚焦检测,结果用SPSS10.0软件处理。结果脑外伤后1hcathepsin-B表达即增加,4～8d达高峰,脑外伤后32d仍处于高表达水平;cathepsin-D的表达于脑外伤后12h增加,4～8d达高峰,32d的表达仍然高于12h的表达水平。脑外伤初期,cathepsin-B和-D阳性细胞与caspase-3阳性细胞重叠较少,脑外伤后6h开始增加,32d仍然有很多阳性细胞重叠。结论脑外伤后cathepsin-B和-D被激活,其激活在脑外伤早期可能抑制细胞凋亡执行因子caspase-3的激活,之后(6h后)则与caspase-3起协同作用,共同促进细胞死亡;cathepsin-B和-D表达的时程变化对于脑外伤的法医学诊断和中晚期的时间推断有参考意义。     

实验性脑挫伤后caspase—1表达的研究

目的阐明不同程度及不同时间脑挫伤后caspase-1表达的变化。方法应用免疫组织化学染色、Western-blotting和RT-PCR方法对48例实验性脑挫伤大鼠的脑组织进行了检验,同时以3例非脑挫伤和3例假手术的脑组织做对照。结果脑挫伤后1h caspase-1即有表达,24-48h达高峰,挫伤后两周caspase-1阳性细胞仍维持较高水平。阳性细胞多集中于挫伤区及周围带皮质和脑实质内海马区,不同程度脑挫伤各组之间阳性细胞面积存在差异;损伤组caspase-1酶原裂解增加;损伤组caspase-1mRNA表达量明显高于对照组;不同程度脑挫伤组之间于各个时间段caspase-1mRNA表达未见差异。 结论 Caspase-1表达增加,可辅助诊断1h-14d的脑挫伤,并可根据caspase-1阳性细胞面积的变化来确定脑挫伤程度,同时对判断挫伤时间方面也有一定的价值。caspase-1参与脑挫伤后的神经细胞凋亡。     

颅脑损伤后动态姿势平衡评估

目的探讨颅脑损伤后平衡功能障碍的特点和原因。方法对95例交通事故致颅脑损伤的患者进行动态姿势图检查,将其测试结果与正常值比较;并按照原发颅脑损伤程度和是否伴有听力障碍对患者进行分组,将测试结果进行组间比较。结果颅脑损伤患者平衡总分较正常值低,对视觉和前庭觉等信息的利用能力下降,以前庭觉下降明显;原发颅脑损伤的严重程度以及是否伴听力下降对姿势稳定性无明显影响。结论不伴有肢体功能障碍的颅脑损伤患者的姿势稳定性差,对环境的反应与适应能力下降,可能与外周前庭器官及平衡中枢的损伤有关。     

Review of the Evidence Supporting the Medical and Legal Use of NeuroQuant® in Patients with Traumatic Brain Injury

Decades of research have shown that the brain atrophies after traumatic brain injury (TBI). However, multiple practical issues made it difficult to detect brain atrophy in individual patients with mild to moderate TBI. This situation improved by 2007 with the FDA approval of NeuroQuant®, a commercially available, computer-automated software program for measuring MRI brain volume in human subjects. Several peer-reviewed scientific studies have supported the reliability and validity of NeuroQuant®. This review addresses whether NeuroQuant® meets the Daubert standard for admissibility in court cases involving persons with TBI. The review finds that NeuroQuant® is an objective, reliable, and practical means of measuring brain volume and therefore can be an important tool for measuring the effects of TBI on brain volume in clinical or medicolegal settings.     

大鼠不同程度脑挫伤后caspase-3表达的研究

目的阐明不同程度及不同时间脑挫伤后caspase-3表达的变化。方法应用免疫组织化学染色、Westernblot和RT-PCR方法对48例实验性脑挫伤大鼠的脑组织进行了检验,同时以3例非脑挫伤和3例假手术的脑组织做对照。结果伤后1hcaspase-3即有表达,24～48h达高峰,挫伤后14dcaspase-3仍维持较高水平。阳性细胞多集中于挫伤区及周围带皮质和脑实质内海马区,不同程度脑挫伤各组之间阳性细胞面积和灰度存在差异;损伤组caspase-3酶原裂解增加,不同程度脑挫伤各组之间存在一定的差异;损伤组cas鄄pase-3表达量明显高于对照组;不同程度脑挫伤组之间于各个时间段caspase-3mRNA表达未见差异。结论Caspase-3表达增加,可辅助诊断1h～14d的脑挫伤,caspase-3阳性细胞面积和灰度的变化及酶原裂解程度与脑挫伤程度有关。     

MMP-2和MMP-9与脑损伤及其法医学意义

基质金属蛋白酶2和9（MMP-2、MMP-9）是基质金属蛋白酶（matrix metalloproteinases，MMPs）家族中的两个成员，可降解Ⅳ型胶原、层粘连蛋白等基质成分，从而使血脑屏障结构破坏，通透性增加，导致血管源性脑水肿，在脑血管疾病和脑损伤形成过程中起着重要的作用。在损伤后不同时段，MMP-2和MMPO含量及分布均呈现一定的波动性，探讨这些问题对脑损伤的治疗及在法医学中推断脑损伤时间有十分重要的意义。本文就这些问题的相关研究作一概述。