Motor speech impairment in a case of childhood basilar artery stroke: Treatment directions derived from physiological and perceptual assessment

The perceptual and physiological characteristics of the speech of a nine year old child who suffered a basilar artery stroke at the age of five years were investigated using a battery of perceptual and physiological instrumental measures. Perceptual tests administered included the Frenchay Dysarthria Assessment, a perceptual analysis of a speech sample based on a reading of the Grandfather Passage and a phonetic intelligibility test. Instrumental procedures included: spirometric and kinematic analysis of speech breathing; electroglottographic evaluation of laryngeal function, nasometric assessment of velopharyngeal function and evaluation of lip and tongue function using pressure transducers. Physiological assessment indicated the most severe deficits to be in the respiratory and velopharyngeal sub-systems with significant deficits in the articulatory sub-system, all of which resulted in severely reduced intelligibility. These results were compared and contrasted with the subject's performance on the perceptual assessment battery. In a number of instances the physiological assessments were able to identify deficits in the functioning of components of the speech production apparatus either not evidenced by the perceptual assessments or where the findings of the various perceptual assessments were contradictory. The resulting comprehensive profile of the child's dysarthria demonstrated the value of using an assessment battery comprised of both physiological and perceptual methods. In particular, the need to include instrumental analysis of the functioning of the various subcomponents of the speech production apparatus in the assessment battery when defining the treatment priorities for children with acquired dysarthria is highlighted. Treatment priorities determined on the basis of both the perceptual and physiological assessments for the present CVA case are discussed.     

Different aspects of facial affect recognition impairment following traumatic brain injury: The role of perceptual and interpretative abilities

It is well established that many individuals with traumatic brain injury (TBI) are impaired at facial affect recognition, yet little is known about the mechanisms underlying such deficits. In particular, little work has examined whether the breakdown of facial affect recognition abilities occurs at the perceptual level (e.g., recognizing a smile) or at the verbal categorization stage (e.g., assigning the label “happy” to a smiling face). The aim of the current study was to investigate the integrity of these two distinct facial affect recognition subskills in a sample of 38 individuals with moderate-to-severe TBI and 24 demographically matched healthy individuals. Participants were administered an affect matching (perceptual skills) and an affect labeling (verbal categorization skills) task. Statistical analyses revealed that, while individuals with TBI showed significantly higher levels of impairment in the verbal categorization task than in the perceptual task, they performed less well than healthy comparison participants on both tasks. These findings indicate that facial affect recognition impairment can occur at different cognitive stages following TBI, suggesting the necessity of careful screening to offer targeted treatment. Moreover, they provide further neuropsychological evidence supporting the notion that distinct types of subskills are necessary to achieve successful recognition of facial affects.     

盐酸多奈哌齐治疗轻、中型脑外伤后认知障碍的临床研究

目的探讨盐酸多奈哌齐对轻、中型脑外伤患者伤后认知障碍及临床预后的影响。方法本组轻、中型脑外伤合并认知障碍患者78例,随机分成治疗组和对照组,治疗组应用盐酸多奈哌齐,对照组应用吡拉西坦,两组的治疗周期为12周。治疗前及治疗后分别应用简明精神状态检测量表（MMSE）、国人修订成人韦氏智力量表（WAIS-RC）和格拉斯哥预后评分（GOS）评价疗效。结果两组治疗后12周MMSE和WAIS-RC评分均较治疗前提高（P〈0.05）。治疗组MMSE和WAIS-RC评分提高较对照组明显（P〈0.05）,治疗组GOS预后优良率优于对照组（P〈0.05）。结论盐酸多奈哌齐对轻、中型脑外伤后认知障碍有积极治疗作用,并能改善临床预后。     

Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats**☆

BACKGROUND： In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor （BDNF） can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE： To explore changes in BDNF expression and cognitive function in rats after brain injury. DESIGN, TIME AND SETTING： The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University （China） from July 2007 to July 2008. MATERIALS： A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS： Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney＇s method （n = 24, each group）. A bone window was made in rats from the sham operation group （n = 24）, but no attack was conducted. MAIN OUTCOME MEASURES： At days 1, 2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry （streptavidin-biotin-peroxidase complex method）. Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS： Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups （P 〈 0.05）. CONCLUSION： BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats following i     

Correlation of brain-derived neurotrophic factor to cognitive impairment following traumatic brain injury in rats

BACKGROUND: In vitro and in vivo studies have confirmed that brain-derived neurotrophic factor (BDNF) can promote survival and differentiation of cholinergic, dopaminergic and motor neurons, and axonal regeneration. BDNF has neuroprotective effects on the nervous system. OBJECTIVE: To explore changes in BDNF expression and cognitive function in rats after brain injury DESIGN, TIME AND SETTING: The neuropathology experiment was performed at the Second Research Room, Department of Neurosurgery, Fujian Medical University (China) from July 2007 to July 2008. MATERIALS: A total of 72 healthy, male, Sprague Dawley, rats were selected for this study. METHODS: Rat models of mild and moderate traumatic brain injury were created by percussion, according to Feeney's method (n = 24, each group). A bone window was made in rats from the sham operation group (n = 24), but no attack was conducted. MAIN OUTCOME MEASURES: At days 1,2, 4 and 7 following injury, BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was examined by immunohistochemistry (streptavidin-biotin-peroxidase complex method). Changes in rat cognitive function were assessed by the walking test, balance-beam test and memory function detection. RESULTS: Cognitive impairment was aggravated at day 2, and recovered to normal at days 3 and 7 in rats from the mild and moderate traumatic brain injury groups. BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain was increased at 1 day, decreased at day 2, and then gradually increased in the mild and moderate traumatic brain injury groups. BDNF expression was greater in rats from the moderate traumatic brain injury group than in the sham operation and mild traumatic brain injury groups (P < 0.05). CONCLUSION: BDNF expression in the rat frontal lobe cortex, hippocampus and basal forebrain is correlated to cognitive impairment after traumatic brain injury. BDNF has a protective effect on cognitive function in rats following injury     

重型颅脑损伤256例临床分析

目的 探讨重型颅脑损伤治疗方法,提高重型颅脑损伤的治愈率和降低致残率、死亡率。方法 对我院2000-01～2005-12收治的256例重型颅脑损伤（GCS≤8分）的患者救治效果进行回顾性分析。结果 256例患者中,174例患者GCS评分6～8分,82例特重型颅脑损伤（GCS评3～5分）,恢复良好148例（57．8％）,中残57例（22．3％）,重残以及植物状态13例（5．1％）,死亡38例（14．9％）。结论 重型颅脑损伤应加强院前急救处理．早期明确诊断,手术中应充分减压以减轻对脑干的压迫,早期行气管切开、亚低温治疗和使用钙离子拮抗剂,昏迷时间较长者行高压氧治疗,密切监测生命体征和颅内压变化,积极防治并发症,是提高治俞率、改善预后和降低致残率、死亡率的有效措施.     

Dysphagia in childhood traumatic brain injury: A reflection on the evidence and its implications for practice

Background: Children with traumatic brain injury (TBI) may develop swallowing impairment or dysphagia with possible deleterious consequences of compromised nutritional intake or aspiration with subsequent respiratory complications.

Objective: To examine the evidence base for clinical management of dysphagia by reviewing empirical data on the epidemiology, assessment and diagnosis, and prognosis for dysphagia associated with childhood TBI.

Methods: A systematic review of the literature on dysphagia in children with TBI was conducted. Non-data driven studies or studies including data on individuals 18 years and over were excluded.

Results: Available data was sparse. Only nine studies met inclusion criterion. Current preliminary data revealed that acute dysphagia incidence is high (68–76%) for children with severe TBI. Children with severe injury (GCS ≤ 8) and a ventilation period of ≥1.5 days following motor vehicle accident are at increased risk for dysphagia. Resolution of dysphagia is typically achieved by 12 weeks in children with cortical injury.

Conclusion: There is a clear need for multi-centre prospective research studies in this field, however preliminary evidence can be used to inform aspects of clinical practice. First, routine swallowing screening may be implemented for children meeting criterion for being ‘at risk’ for dysphagia. Systematic referral of targeted patients is lacking in paediatric rehabilitative care, but early screening of these cases would optimize early dysphagia identification and management. Secondly, the positive prognosis for most cases with cortical injury suggests that long-term feeding options (i.e. gastrostomy) may not be indicated until at least 3 months have passed with minimal change in function.     

Working memory brain activation following severe traumatic brain injury

Functional magnetic resonance imaging (fMRI) has shown that brain activation during performance of working memory (WM) tasks under high memory loads is altered in adults with severe traumatic brain injury (TBI) relative to uninjured subjects (Perlstein et al., 2004; Scheibel et al., 2003). Our study attempted to equate TBI patients and orthopedically injured (OI) subjects on performance of an N-Back task that used faces as stimuli. To minimize confusion in TBI patients that was revealed in pilot work, we presented the memory conditions in two separate tasks, 0- versus 1-back and 0- versus 2-back. In the 0- versus 1-back task, OI subjects activated bilateral frontal areas more extensively than TBI patients, and TBI patients activated posterior regions more extensively than OI subjects. In the 0- versus 2-back task, there were no significant differences between the groups. Analysis of changes in activation over time on 1-back disclosed that OI subjects had decreases in bilateral anterior and posterior regions, while TBI patients showed activation increases in those and other areas over time. In the 2-back condition, both groups showed decreases over time in fusiform and parahippocampal gyri, although the OI group also showed increases over time in frontal, parietal, and temporal areas not seen in the TBI patients. The greatest group differences were found in the 1-back condition, which places low demand on WM. Although the extent of activation in the 2-back condition did not differ between the two groups, deactivation in the 2-back condition was seen in the OI patients only, and both groups' patterns of activation over time varied, suggesting a dissociation between the TBI and OI patients in recruitment of neural areas mediating WM.     

Mild traumatic brain injury

Traumatic brain injury (TBI) is one among the most frequent neurological disorders. Of all TBIs 90% are considered mild with an annual incidence of 100–300/100 000. Intracranial complications of mild traumatic brain injury (MTBI) are infrequent (10%), requiring neurosurgical intervention in a minority of cases (1%), but potentially life threatening (case fatality rate 0.1%). Hence, a true health management problem exists because of the need to exclude the small chance of a life‐threatening complication in a large number of individual patients. The 2002 EFNS guideline used the best evidence approach based on the literature until 2001 to guide initial management with respect to indications for computed tomography (CT), hospital admission, observation and follow‐up of MTBI patients. This updated EFNS guideline for initial management in MTBI proposes a more selective strategy for CT when major [dangerous mechanism, Glasgow Coma Scale (GCS) < 15, 2 points deterioration on the GCS, clinical signs of (basal) skull fracture, vomiting, anticoagulation therapy, post‐traumatic seizure] or minor (age, loss of consciousness, persistent anterograde amnesia, focal deficit, skull contusion, deterioration on the GCS) risk factors are present based on published decision rules with a high level of evidence. In addition, clinical decision rules for CT now exist for children as well. Since 2001, recommendations, although with a lower level of evidence, have been published for clinical observation in hospitals to prevent and treat other potential threats to the patient including behavioural disturbances (amnesia, confusion and agitation) and infection.     

创伤性脑损伤后脑红蛋白的表达变化

目的 观察创伤性脑损伤后伤灶周围皮质脑红蛋白（Ngb）的表达变化.方法 采用自由落体硬膜外撞击方法建立脑外伤模型,应用免疫组织化学和Western Blot技术,定量观察创伤性脑损伤后Ngb的表达变化.结果 各实验组之间阳性信号面积没有统计学差异（P＞0.05）;但外伤后,光密度或累积光密度均明显增高（P＜0.05或P＜0.01）.结论 脑外伤后伤灶周围皮质神经元Ngb的表达增高,提示Ngb可能参与了脑外伤后伤灶周围神经元的保护过程.     

大鼠脑损伤后NMDAR1表达及其认知障碍变化的关系

目的同步考量脑损伤后大鼠与认知功能较为密切的脑区N-甲基-D-天冬氨酸受体1（NMDAR1）表达与认知功能的变化。方法参照Feeney法建立大鼠创伤性脑损伤模型,伤后1d,2d,4d,7d1）．2免疫组化SABC法检测大鼠额叶皮质、海马区、基底前脑区NMDAR1表达,以行走实验、平衡实验及记忆功能测定评估大鼠认知障碍变化。结果轻、中型脑损伤组大鼠于伤后2d认知障碍最严重,分别于伤后3,7d基本恢复正常。轻型、中型脑损伤组脑额叶皮质、海马区、基底前脑区NMDAR1均于伤后1d升高,于2d降至较低水平后再呈缓慢增高趋势,与认知障碍变化趋势呈同步变化,且中型脑损伤组NMDAR1表达高于假手术组与轻型脑损伤组（P〈0．05）。结论大鼠经创伤性脑损伤后,额叶皮质、海马区、基底前脑区细胞中的NMDAR1含量和损伤后认知障碍的变化趋势有相似性;创伤性脑损伤后表达增加的NMDAR1对大鼠认知功能有加重损害作用。     

Cancelling planned actions following mild traumatic brain injury

Mild traumatic brain injury (mTBI) leads to a variety of attentional, cognitive, and sensorimotor deficits. An important aspect of behavior that intersects each of these functions is the ability to cancel a planned action. Thus, the purpose of this study was to determine the effects of mTBI on the ability to perform a countermanding saccade task. In this task, participants were asked to generate a saccade to a target appearing in peripheral vision, but to inhibit saccade execution if an auditory stop signal was presented. The delay between the appearance of the peripheral target and the presentation of the auditory stop signal was varied between 0 and 125ms. We found that the change in the probability of cancelling the saccade as a function of this delay was no different between participants with mTBI tested within 2 days of their injury and matched controls. However, saccadic reaction times and the stop signal reaction time were unexpectedly faster in the participants with mTBI and, furthermore, they inaccurately inhibited saccades during 15% of the trials with no stop signal. Taken together, this data suggests that the ability to cancel planned actions is subtly yet adversely affected by mTBI.     

重型颅脑外伤与肺部感染临床分析

目的研究重型颅脑外伤患者院内肺部感染原因及病原菌特点,探讨预防及控制感染措施。方法对260例重型颅脑外伤患者肺部感染危险因素及病原菌调查分析。结果根据入院后的调查研究,导致患者并发肺部感染的主要因素有年龄、住院时间、气管切开、休克、基础病变等;其中从260例肺部感染患者中分离了细菌190株,主要致病菌为革兰阴性菌,占71%,其次为革兰阳性菌,占15.8%,真菌占13.2%。治愈196例,因肺部感染死亡39例,放弃治疗25例。结论导致重型颅脑损伤并发肺部感染的主要因素有年龄、住院时间、气管切开、休克、基础病变等,其主要致病菌为革兰阴性菌、其次为革兰阳性菌、真菌,针对上述危险因素采取有效措施可降低感染率。     

黄体酮对创伤性脑损伤大鼠神经细胞凋亡的影响

目的 观察黄体酮对脑外伤后神经细胞凋亡的影响,探讨其对脑外伤(TBI)继发性脑损伤是否存在保护作用.方法 雄性Wistar 大鼠随机分为无脑损伤的假手术(sham)组、脑损伤(TBI)组、脑损伤后注射黄体酮治疗(P-TBI)组及注射二甲基亚砜(DMSO)溶剂(D-TBI)组,每大组24 只,再分1 d、3 d、5 d 和7 d 四个小组,每小组6 只.采用Freeney 法造成鼠脑挫裂伤模型,在伤后四个不同时相点用TUNEL 染色法分别检测四组大鼠脑组织中神经细胞凋亡情况.结果 创伤性脑损伤后凋亡细胞数量在TBI 第1 d 明显增加,TBI后第7 d 神经细胞凋亡达到高峰.伤后注射黄体酮治疗组神经细胞凋亡指数明显下降(P ＜0.05).结论 大鼠TBI 后周围脑组织神经细胞凋亡在伤后持续增加,注射黄体酮能抑制细胞凋亡,对脑组织有一定保护作用.     

Reliability and validity of questionnaire for neurobehavioral disability following traumatic brain injury

The neurobehavioral disability recognized in traumatic brain injury (TBI) is a severe sequela, but there is no appropriate classification due to its various manifestations. In the present study a questionnaire for a simple investigation of this disability was prepared, and its reliability and validity verified. The survey was conducted on 72 patients with TBI by the caregiver of each patient. As a result, good reliability was indicated by the split-half method (coefficient of reliability: 0.95, obtained using Spearman-Brown correction formula). The total score of the questionnaire had a significant correlation with the total score of the simultaneously conducted Japanese version of Neuropsychiatry Inventory at the 0.01 level (Spearman's rank correlation, 0.47). It also had a significant correlation with the total score of the simultaneously conducted Japanese version of the Dysexecutive Questionnaire at the 0.05 level (Spearman's rank correlation, 0.36). Six factors constituting this neurobehavioral disability were extracted from a factor analysis of the questionnaire survey. These factors are angry outburst, avolition, deficits of sympathy, depressed mood, discourse deficits, and degradation of appearance. Each factor indicated good internal consistency (Cronbach alpha, 0.86-0.94). The present results indicate that this questionnaire has good reliability and validity, therefore it can be a significant indicator in TBI neurobehavioral disability study.     

Epidemiology of traumatic brain injury: a population based study in western Sweden

Background – This study on traumatic brain injury (TBI) is based on prospective and retrospective population based data from a head injury register in Borås. Methods – Data was collected from the hospital emergency unit, the discharge register, the regional neurosurgical clinic and the coroner's records during 1 year. This district is mixed urban and rural with a population of 138 000. Results – The 753 cases identified represent an incidence of 546 per 100 000 which includes deaths (0.7%), hospital admissions (67%) and attendance at the emergency department in patients not admitted (32%). Males (644 per 100 000), had 1.46 higher overall rate than females (442 per 100 000). The external causes were dominated by fall from same level (31%) and fall from different level (27%) followed by traffic accidents (16%) and persons hit by objects (15%). Conclusions – The incidence of TBI found in this study is high but well in accordance with earlier published Swedish studies.     

儿童重型颅脑损伤

目的探讨儿童重型颅脑损伤的发病机理、临床特点及治疗方法。方法回顾性分析儿童重型颅脑损伤131例。结果临床结果根据GOS标准判断：Ⅴ级(良好)91例，Ⅳ级(中残)10例，Ⅲ级(重残)6例，Ⅱ级(植物生存)0例，Ⅰ级(死亡)24例。结论儿童在颅脑解剖、中枢神经系统生理及病理生理方面有其固有的特性，颅脑损伤后耐受性差，病情常突变，而小儿巾枢神经系统修复能力相对较强，如及时解除脑受压，神经功能恢复快，疗效好。早期诊断、正确选择治疗方法及手术方式能明显改善患儿的预后．     

Review: The long‐term consequences of microglial activation following acute traumatic brain injury

The brain is vulnerable to a number of acute insults, with traumatic brain injury being among the commonest. Neuroinflammation is a common response to acute injury and microglial activation is a key component of the inflammatory response. In the acute and subacute phase it is likely that this response is protective and forms an important part of the normal tissue reaction. However, there is considerable literature demonstrating an association between acute traumatic brain injury to the brain and subsequent cognitive decline. This article will review the epidemiological literature relating to both single and repetitive head injury. It will focus on the neuropathological features associated with long‐term complications of a single blunt force head injury, repetitive head injury and blast head injury, with particular reference to chronic traumatic encephalopathy, including dementia pugilistica. Neuroinflammation has been postulated as a key mechanism linking acute traumatic brain injury with subsequent neurodegenerative disease, and this review will consider the response to injury in the acute phase and how this may be detrimental in the longer term, and discuss potential genetic factors which may influence this cellular response. Finally, this article will consider future directions for research and potential future therapies.