颅脑损伤后综合征对男性勃起功能的影响

目的探讨颅脑损伤后综合征对男性勃起功能的影响。方法在颅脑损伤后6个月对126例男性颅脑损伤患者的颅脑损伤后综合征的发生情况及勃起功能障碍进行问卷式调查,并分析两者之间的关系。结果126例颅脑损伤患者中合并颅脑损伤后综合征45例,有勃起功能障碍者16例（35．56％）;没有合并颅脑损伤后综合征者81例,有勃起功能障碍者2例（2．47％）。两组患者勃起功能障碍发生率相差显著（P〈0．01）。结论颅脑损伤后,若遗留有颅脑损伤后综合征的男性患者,更易发生勃起功能障碍。     

颅脑损伤与性功能障碍的研究进展

在二十世纪八十年代晚期到九十年代初期,不少学者忽略了颅脑损伤后的性忧虑和性功能障碍问题,故此类病人资料相对非常缺乏。在很多颅脑损伤的文献中均忽略了性功能改变的描述,因此有必要开展这方面的研究,以增进我们对颅脑损伤后性功能障碍的病理生理及诊断和治疗方面的了解。1颅脑损伤后性功能障碍的病理生理1.1大脑的解剖生理基础由于性功能和大脑解剖生理关系的研究有限,使得颅脑损伤后的性功能异常很难预知。目前一般认为,边缘系统(除边缘叶的内、外环路外,还包括眶额后回、岛叶及颞极、杏仁体、透明隔、视前区等以及中脑被盖的边缘中脑…     

颅脑损伤后凝血功能障碍的机制及干预措施

正颅脑损伤伤后发生凝血功能障碍是神经外科急诊中的一种常见的并发症,发生率较高,在56%~70%[1]。颅脑损伤后的凝血功能障碍主要包括外伤后高凝状态和继发性纤溶系统亢进,使颅脑损伤后再出血和死亡的风险大大提高,严重影响病人预后。本文就颅脑损伤后凝血功能障碍的机制及干预措施进行综述。1发病机制在生理条件下,凝血功能主要通过内源性或外源性途径实现,并使凝血与纤溶系统之间保持一种平衡。颅脑损伤后出现凝血功能障碍,使正常的凝     

轻型闭合性颅脑损伤的记忆障碍

目的 了解轻型闭合性颅脑损伤即脑震荡患者在受伤后不同时间的记忆功能.方法 采用韦氏成人记忆量表对48例受伤后不同时间的患者进行评估,同时取32名健康成人为对照.结果 发现长时记忆有4项、短时记忆有3项、瞬时记忆有1项分测验平均成绩明显降低,记忆损害涉及瞬时记忆、短时记忆和长时记忆,患者组异常率为58.3%.受伤后不同时段的患者之间的比较,长时记忆中5项有3项两组之间有显著性统计学差异;短时记忆6项中有5项表现出显著的统计学差异;瞬时记忆和记忆商两组间也存在显著统计学差异.结论 脑震荡患者存在不同程度的记忆障碍,涉及记忆的各个环节,受伤后不同时间的病人记忆障碍的程度有一定差异,受伤早期记忆损害的程度较重,随时间的推移,记忆功能有一定程度的恢复.     

金刚烷胺对颅脑损伤患者意识障碍的临床疗效

目的 探讨金刚烷胺对颅脑损伤后意识障碍的疗效。方法 2012年7月至2014年7月收治颅脑损伤伴意识障碍52例,根据治疗方法分为观察组（25例）和对照组（27例）。对照组采取常规的对症支持及康复治疗;观察组在对照组治疗的基础上,每日给予金刚烷胺（100mg/次,2次/d）,连续4周。比较两组治疗前后残疾评定量表（DRS）评分及修订版昏迷恢复量表（CRS-R）评分。结果 两组患者治疗后DRS评分及CRS-R评分较治疗前均明显改善（P<0.05）,而且观察组改善更明显（P<0.05）。用药过程中,对照组有5例出现恶心呕吐等胃肠道反应,观察组有6例;对照组有2例出现癫痫发作,观察组有1例,经对症治疗后均能耐受药物。结论 金刚烷胺对颅脑损伤的意识障碍具有一定的促醒作用,有一定的临床疗效。     

神经电刺激治疗颅脑损伤后意识障碍的研究进展

<正>意识障碍是中、重型颅脑损伤(traumatic braininjury,TBI)的严重并发症。近十年来,随着神经多模态监测技术、大骨瓣减压术等手术理念的推广以及神经危重症医学技术的进步,重型TBI的病死率明显下降,但伤后意识障碍的发生率也在持续增加^[1],临床治疗面临巨大的压力和挑战^[2]。     

复方醒脑液治疗颅脑损伤后综合征的临床观察

目的 观察复方醒脑液治疗颅脑损伤后综合征（PTBS）的疗效。方法 2011~2015年收治PTBS 80例,其中40例给予西医常规治疗（对照组）,40例在对照组基础上口服复方醒脑液（观察组;每次50 ml,每日2次）。采用临床疗效及90项症状清单（SCL-90）评分评估复方醒脑液治疗PTBS的效果。结果 观察组临床治愈2例,显效15例,好转10例,无效13例;对照组显效4例,好转10例,无效26例;观察组总有效率（67.5%,27/40）明显高于对照组（35.0%,14/40;P<0.05）。治疗后,观察组scl-90总分、躯体化评分、人际关系敏感评分较治疗前均明显降低（>P<0.05）;而且,明显低于对照组治疗后的评分（>P<0.05）。>结论 复方醒脑液具有减轻PTBS头痛、眩晕等症候群的作用;用药后躯体症状、人际关系敏感改善明显,对睡眠、饮食也有所改善。     

重型颅脑损伤病人创伤后应激障碍的风险因素分析

目的 探讨重型颅脑损伤病人并发创伤后应激障碍（PTSD）的危险因素。方法 回顾性分析2020年1月至2022年2月收治的110例重型颅脑损伤的临床资料。出院前采用PTSD自评量表（PTSD-SS）评估PTSD情况,总分≥50分表示存在PTSD。结果 110例PTSD-SS评分总分（49.64±7.29）分,其中≥50分52例（47.27%）。多因素logistic回归分析显示,女性、低龄、家庭人均月收入低、非亲属照顾、无经济赔偿、合并颅内感染为重型颅脑损伤并发PTSD的独立影响因素（P<0.05）。根据多因素logistic回归分析结果构建PTSD列线图显示一致性指数为0.886,预测PTSD具有较高的应用价值。结论 重症颅脑损伤病人并发PTSD的风险较高,女性、年轻病人、收入低、非亲属照顾、无经济赔偿、合并颅内感染等因素会增加PTSD发生风险,临床应密切关注,识别PTSD风险因素,并给予有效的防治措施降低PTSD发生率。     

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。     

颅脑损伤后中枢性低钠血症的临床分析

中枢性低钠血症是神经外科常见的并发症，约占其并发症的31．5％，对预后影响很大。中枢性低钠血症包括抗利尿激素分泌异常综合征（syndrome of inappropriate antidiuretic homone，SIADH）和脑性盐耗综合征（crebralsaltwasting syndrome，CSWS）。颅脑损伤并发中枢性低钠血症在临床表现上通常被颅脑损伤和低钠血症掩盖，容易漏诊，是致颅脑损伤患者病残和（或）死亡的主要因素之一。两者常规生化指标相同，临床表现相似，但治疗原则相悖，如不能正确区分，针对性治疗，常会加重病情，甚至造成严重脑水肿，危及生命。2005年1月～2007年3月我科收治颅脑损伤后中枢性低钠血症患者19例，现分析如下。     

Chronic cerebrovascular dysfunction after traumatic brain injury

Traumatic brain injuries (TBI) often involve vascular dysfunction that leads to long‐term alterations in physiological and cognitive functions of the brain. Indeed, all the cells that form blood vessels and that are involved in maintaining their proper function can be altered by TBI. This Review focuses on the different types of cerebrovascular dysfunction that occur after TBI, including cerebral blood flow alterations, autoregulation impairments, subarachnoid hemorrhage, vasospasms, blood–brain barrier disruption, and edema formation. We also discuss the mechanisms that mediate these dysfunctions, focusing on the cellular components of cerebral blood vessels (endothelial cells, smooth muscle cells, astrocytes, pericytes, perivascular nerves) and their known and potential roles in the secondary injury cascade. © 2016 Wiley Periodicals, Inc.     

Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis

Traumatic brain injury (TBI) represents a significant cause of death and disability in industrialized countries. Of particular importance to patients the chronic effect that TBI has on cognitive function. Therapeutic strategies have been difficult to evaluate because of the complexity of injuries and variety of patient presentations within a TBI population. However, pharmacotherapies targeting dopamine (DA) have consistently shown benefits in attention, behavioral outcome, executive function, and memory. Still it remains unclear what aspect of TBI pathology is targeted by DA therapies and what time-course of treatment is most beneficial for patient outcomes. Fortunately, ongoing research in animal models has begun to elucidate the pathophysiology of DA alterations after TBI. The purpose of this review is to discuss clinical and experimental research examining DAergic therapies after TBI, which will in turn elucidate the importance of DA for cognitive function/dysfunction after TBI as well as highlight the areas that require further study.     

Bipolar disorder after traumatic brain injury

Objective. We report the case of a 47-year-old man with no psychiatric antecedents who developed manic and depressive symptoms after traumatic brain injury (TBI). Methods and results. Findings on neurobehavioral examination, neuropsychological test battery, electrophysiological and imaging exams suggested the presence of a diffuse cerebral injury with a predominance of left fronto-temporal findings. Conclusions. This case demonstrates that TBI may cause vulnerability to psychiatric disorders, with long latency periods, and that its course may be independent of cognitive impairment and recovery.     

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.     

颅脑损伤后神经递质系统变化与认知障碍的研究进展

近年来,颅脑损伤(traumatic brain injury,TBI)的发生率、致残率逐渐增高,随着对脑外伤急性期治疗F段的不断提高,已能大大降低早期的死亡率.然而,它仍是慢性期致残的主要原因,其中认知功能障碍是最持久和最严重的症状之一[1].虽然大部分患者中这些功能在1年后恢复正常,但仍有10％～15％的轻型脑损伤患者存在功能障碍,在中、重型TBI患者中比例更高[2].TBI后认知障碍的确切机制至今仍不十分清楚,研究发现大脑内学习和记忆等认知活动与多种神经递质相关,包括乙酰胆碱(acetylcholine,Ach),去甲肾上腺素,多巴胺(DA),5-羟色胺(5-HT),γ-氨基丁酸,谷氨酸,神经营养因 子等[3].本文就TBI后主要神经递质系统的变化及其与认知障碍的研究进展进行简要综述.     

创伤性脑损伤后凝血功能障碍的发生机制和治疗进展

创伤性脑损伤与凝血系统的功能变化有密切的联系,然而对两者间相互影响的机制尚缺乏深入研究。颅脑创伤后的高凝状态、低凝状态可导致微血栓形成或加重颅内出血,从而引起一系列的继发损伤。为此,研究者们提出了多种假说,如组织因子的释放、弥散性血管内凝血、纤溶亢进和血小板功能障碍等。该文针对颅脑创伤后凝血功能异常的发生机制,以及临床诊治和预后进行综述。     

脑损伤后发作性自主神经功能障碍的临床特点

目的探讨脑损伤后发作性自主神经功能障碍的临床特点。方法回顾性分析22例脑损伤后发作性自主神经功能障碍患者的临床资料。结果22例患者均处于植物状态,其原发损伤为重型颅脑外伤14例,脑或小脑出血血肿清除术后2例,海洛因中毒性脑病1例,重度一氧化碳中毒2例,电击伤心肺复苏术后1例,冠状动脉造影支架植入术心脏骤停复苏后1例,麻醉意外致心脏骤停心肺复苏后1例。全组患者均出现发作性躁动、发热、多汗、呼吸急促、心动过速、血压升高、肌张力障碍、抽搐等症状中的多项表现。发作时脑电图未见癫疒间放电;听觉诱发电位或体感诱发电位显示各波潜伏期延长、波幅下降甚至未引出。神经影像学检查提示大脑皮质、皮质下、脑干等部位有不同程度的损害。治疗上应用多巴胺受体激动剂或阻滞剂、苯二氮艹卓类及肌松剂等药物对症处理;22例中10例在起病后1~13个月脱离植物状态。结论脑损伤后发作性自主神经功能障碍临床主要表现为发作性自主神经功能紊乱伴肌张力障碍,重症者多处于植物状态;药物治疗仅限于对症处理。     

创伤性脑损伤后大鼠海马区糖皮质激素受体mRNA的表达

目的研究创伤性脑损伤(TBI)后大鼠海马区糖皮质激素受体(GR)mRNA表达的变化及其对大鼠认知功能的影响。方法建立大鼠头颅侧向旋转加速脑创伤模型,应用逆转录酶-聚合酶链式反应(RT-PCR)和Morris水迷宫检测伤后大鼠海马区GR mRNA的表达与学习记忆功能的关系。结果伤后4～7 d大鼠海马区GR持续低表达;Morris水迷宫检测伤后大鼠出现认知功能障碍。结论 TBI大鼠海马区GR mRNA的降低影响大鼠认知功能。     

The relationship between olfactory dysfunction and executive function in children with traumatic brain injury

Introduction: Olfactory dysfunction (OD) has been suggested as a possible marker of executive function (EF) deficits after traumatic brain injury (TBI) in adults. Little is known about the relationship between EF and OD in pediatric TBI (pTBI). This study aimed to investigate EF, explore the relationship between OD and EF, and determine the utility of olfactory performance as a marker of later EF in pTBI. It was hypothesized that (i) children with TBI would perform more poorly on EF measures relative to normative expectation; (ii) children with OD would perform more poorly on tests of EF than those with normal olfaction after TBI; and (iii) acute olfactory function would predict later EF for children with TBI.

Method: This was a prospective longitudinal study. Twenty seven children aged 8–16 with TBI completed olfactory assessment using the University of Pennsylvania Smell Identification Test at 0–3, 8 and 18 months post injury. Assessment of EF occurred at 8 and 18 month follow-up.

Results: At 8 month follow-up the pTBI cohort did not demonstrate a consistent pattern of impairment in EF, contrary to our first hypothesis. Children with OD showed significantly poorer performance on a single EF measure of Fluency when compared to those with normal olfaction at 8 months post injury, partially supporting our second hypothesis. Acute olfactory function did not significantly predict EF outcomes at either 8 or 18 months post injury.

Conclusions: Overall our findings provide little support for a significant relationship between EF and OD in pTBI. In particular, there was no strong evidence that acute olfactory function is an accurate predictor of later EF in pTBI. Given the dearth of pediatric research, the limitations of our study and the potential significance of acute olfactory performance as an early marker of later EF deficits in children, further investigation is warranted.     

脑外伤患者恢复期的注意障碍

目的探索脑外伤恢复期患者注意的改变及其特征.方法对42例大型医院神经外科住院治疗的脑外伤恢复期患者和42名正常人进行"2,7"划消测验和Strop测验.结果脑外伤患者在标准情况、不相关分心情况和相关分心情况下的划消速度明显低于正常对照组,而精确率无明显差异.进一步比较相关分心情况下划消速度的下降率显示脑外伤患者显著大于正常对照组.Stroop测验显示脑外伤患者读单色字时间、读色块时间和读彩色字颜色时间较正常对照组显著延长,但两组之间错误数无显著性差异.比较两组读彩色字颜色时间的延长率和读彩色字文字时间的延长率,脑外伤患者均显著大于对照组.结论脑外伤后患者的注意力下降.注意的分配受损,抗干扰能力下降,而选择注意相对完整.