亚低温对急性重型颅脑损伤患者颅内压及脑温影响的研究

目的研究亚低温对急性重型颅脑损伤患者颅内压及脑温的影响。方法选择52例急性重型颅脑损伤患者进行颅内压及脑温监测的同时,将患者随机分为亚低温组和对照组进行研究。结果亚低温组颅内压降低。伤后早期脑温比肛温高,但二者均高于正常值,在亚低温治疗过程中脑温和肛温均下降,但二者的差距逐渐增大,有显著性差异(P<0.05)。亚低温组病人死亡率低于对照组,而恢复良好率显著高于对照组(P<0.05)。结论亚低温能降低颅内压及脑温,改善预后。     

亚低温治疗重型颅脑损伤中脑组织氧分压的临床意义

目的观察亚低温治疗重型颅脑损伤过程中患者颅内压及脑组织氧分压的变化及临床意义。方法将80例急性重型颅脑损伤患者,随机分为亚低温治疗组(40例)和对照组(40例)。亚低温组入院后或术后立即给予亚低温治疗,保持肛温在32~34℃,持续24h~5d;对照组给予常规治疗。两组均观察颅内压(ICP)和脑组织氧分压(PbtO2)变化。结果亚低温组治疗后,ICP明显下降,PbtO2逐渐升高,与对照组相比有显著性差异。结论亚低温治疗能降低脑外伤后增高的ICP,提高PbtO2;伤后24h内持续PbtO2<5mmHg预示患者预后不良。     

重型颅脑损伤中脑温脑组织氧分压持续监测

目的研究重型颅脑损伤中脑温(BT)、脑组织氧分压(PbtO2)的持续变化及其意义.方法应用脑温、脑组织氧分压(PbtO2)探针脑白质温度、脑组织内物理性溶解的氧的压力.结果通过对10例重型闭合性颅脑损伤患者研究分析发现(1)在诱导低温后,直肠温度(RT)与BT的差异比正常体温时明显.(2)在重型颅脑伤后,PbtO2值降低,PbtO2＜10mmHg时,可认为是脑缺氧的阈值.(3)伤后24小时内PbtO2＜5mmHg预示病人预后不良.(4)脑组织氧分压测定技术可指导过度换气的应用.结论在低温状态下,RT与BT的差异加大,因此,在研究低温对脑外伤的影响时,最好能直接测量脑温.脑组织氧分压监测安全可靠,是脑组织氧合程度的一种灵敏的监测方法,它可以提示预后,并且对临床治疗具有重要的指导作用.     

亚低温治疗重型颅脑损伤的临床研究

目的 :探讨亚低温对重型颅脑损伤的临床治疗效果。方法 :亚低温治疗组 2 4例 ,均于伤后 2 4h内进行亚低温治疗 ,设定治疗温度为肛温 32～ 35℃。于降温前及亚低温治疗过程中监测体温 (T)、心率 (HR)、血压 (BP)、呼吸 (R)。对照组 2 7例 ,均于出院后评定预后。结果 :亚低温治疗组病人伤后早期较高的心率 (HR)降至正常范围 ;与对照组相比 ,亚低温治疗组未发生严重并发症 ,死亡率下降 ,预后得到显著改善。结论 :亚低温治疗重型颅脑损伤是一种有效的方法 ,无严重并发症 ,可降低死亡率 ,提高生存质量。     

亚低温治疗重型外伤性颅脑损伤的临床对照观察

目的 比较亚低温治疗和常温治疗重型外伤性颅脑损伤的治疗效果,方法 50例重型颅脑损伤患者随机分为常温组26例和亚低温组24例.入院后病人均持续监测颅内压7 d.对照组维持正常体温,亚低温组入院后在3～7 h内将肛温降至33℃左右,并维持3～7 d.比较2组GCS评分、颅内压、临床预后指标.结果 在伤后第7天,亚低温组和...     

选择性脑降温防治重型颅脑损伤术中急性脑膨出

目的探讨选择性脑降温对重型颅脑损伤手术过程中急性脑膨出的防治作用。方法选择伤后6h内的急性弥漫性脑肿胀病人30例,术中在全身亚低温的基础上,开颅去骨瓣后用低温生理盐水冲洗暴露的脑膜表面,使脑温降至25℃～30℃进行手术。以未进行亚低温处理的同类患者30例作为对照。比较术中两组患者的急性脑膨出的发生率及死亡率。结果治疗组术中Ⅲ级脑膨出的发生率及死亡率分别为13.3%(4/30)和33.3%(10/30),对照组分别为36.7%(11/30)和63.3%(19/30),两组间均差异显著(P<0.05)。结论选择性脑降温对防治颅脑损伤术中急性脑膨出的发生是有效的。     

低温液体静脉灌注对兔局灶性脑缺血的保护作用

目的探讨低温液体(4℃)静脉灌注对家兔局灶性脑缺血的保护作用.方法30只家兔制成大脑中动脉梗死模型后,随机分成3组:对照组(I组)、体表降温组(Ⅱ组)和低温液体(4℃)静脉灌注组(Ⅲ组),脑温(Tc)降至(34.5±0.5)℃,维持24 h,并检测颅内压(ICP)、脑灌注压(CPP)和中心静脉压(CVP)等指标.结果两低温组脑温降至35℃用时分别为(48.0±7.1)min(Ⅱ组)和(52.3±8.9)min(Ⅲ组),两组间无显著性差异(P＞0.05);亚低温期,Ⅲ组ICP从(12.5±2.2)mmHg降至(11.0±2.2)mmHg(12 h)和(10.5±2.0)mmHg(24 h),CPP从(75.9±6.2)mmHg上升至(86.3±7.3)mmHg(2 h)、(81.9±3.9)mmHg(12 h)和(80.9±5.1)mmHg(24 h),与对照组比较,两低温组ICP降低,CPP升高(P＜0.05),同时Ⅲ组CPP显著高于Ⅱ组(P＜0.05).结论低温液体(4℃)静脉灌注能降低脑温和颅内压,并提高脑灌注压,对缺血性脑损伤有明显的保护作用,是一种安全有效的治疗方法.     

亚低温治疗急性重型颅脑损伤的体会

在重型颅脑损伤的治疗中,亚低温(肛温32～35℃)能显著减轻颅脑损伤后神经功能障碍和脑病理形态损害,保护血脑屏障功能,从而明显降低重型颅脑损伤患者的死亡率,改善预后。我院1996年8月至1999年8月收治80例重型颅脑伤病人,其中40例采用亚低温治疗,取得显著疗效。     

标准外伤大骨瓣开颅术联合局部亚低温对重型颅脑损伤患者术后脑功能恢复及并发症发生率的影响

目的探讨标准外伤大骨瓣开颅术联合局部亚低温对重型颅脑损伤患者术后脑功能恢复及并发症发生率的影响。方法选取我院2014-09—2016-09收治的69例重型颅脑损伤患者,依据建档顺序分组,对照组34例实施单一标准外伤大骨瓣开颅术治疗,观察组35例于对照组基础上加用局部亚低温治疗,观察比较2组脑功能障碍评分(DRS)及颅内压变化情况,并统计比较2组并发症发生情况。结果治疗后1个月观察组DRS评分低于对照组,差异具有统计学意义(P0.05);治疗后1周观察组颅内压低于对照组,差异具有统计学意义(P0.05);观察组并发症发生率为5.71%(2例),低于对照组的26.37%(9例),差异具有统计学意义(P0.05)。结论标准外伤大骨瓣开颅术加用局部亚低温治疗,可促进重型颅脑损伤患者脑功能恢复,改善颅内压,降低并发症发生率。     

血管内降温治疗重型颅脑损伤的临床研究

目的研究血管内降温治疗重型颅脑损伤的临床效果。方法将51例重型颅脑损伤病人随机分为对照组(n=20),传统亚低温组(n=20)和血管内降温组(n=11)。两个治疗组31病人均于伤后20 h内使直肠温度降至33~34℃,治疗持续4~7 d,当颅内压降至正常后24 h,停止亚低温治疗。同时床旁监测生命体征、颅内压等。根据GOS评估法判定疗效。结果三组病人的年龄及GCS评分等临床特征无明显统计学差异(P0.05);伤后第7天,两组亚低温治疗的病人颅内压明显低于对照组(P0.05),且基本降至正常。经6个月随访,两组亚低温治疗病人的病死率明显低于对照组,恢复良好率显著高于对照组(P0.05)。结论血管内降温治疗重型颅脑损伤与传统亚低温治疗效果相似,其可减少肌松药和镇静药的使用及机械通气所带来的并发症。该方法治疗重型颅脑损伤安全、有效。     

七叶皂苷钠对大鼠弥漫性脑损伤合并二次损伤后脑组织ET和NO含量的影响

目的观察七叶皂苷钠对大鼠弥散性脑损伤合并二次脑损伤后内皮素(ET)和一氧化氮(NO)等指标的影响,进一步探讨其作用机制及对弥漫性脑损伤合并二次脑损伤的治疗作用。方法 105只SD大鼠分成3组,分别为假手术组、模型组、治疗组。治疗组在1h、24h和48h腹腔注射2.5mg/kg的七叶皂苷钠。模型组在相同时间腹腔注射等量的生理盐水。治疗组和模型组每天注射并饲养10d将各组大鼠断头处死,迅速剥离额叶皮质40mg,匀浆,离心取上清,采用放射免疫法测定ET,硝酸还原酶法测NO。结果与假手术组比较,模型组大鼠脑组织ET和NO水平显著升高(P<0.05);与模型组比较,七叶皂苷钠治疗组大鼠脑组织ET和NO水平显著下降(P<0.05)。结论七叶皂苷钠可通过清除氧自由基和稳定血管内皮细胞等机制,对弥漫性脑损伤合并二次脑损伤发挥保护神经组织的作用。     

The impact of erythropoietin on short-term changes in phosphorylation of brain protein kinases in a rat model of traumatic brain injury

We found that recombinant human erythropoietin (rhEPO) reduced significantly the development of brain edema in a rat model of diffuse traumatic brain injury (TBI) (impact-acceleration model). In this study, we investigated the molecular and intracellular changes potentially involved in these immediate effects. Brain tissue nitric oxide (NO) synthesis, phosphorylation level of two protein kinases (extracellular-regulated kinase (ERK)-1/-2 and Akt), and brain water content were measured 1 (H1) and 2 h (H2) after insult. Posttraumatic administration of rhEPO (5,000 IU/kg body weight, intravenously, 30 mins after injury) reduced TBI-induced upregulation of ERK phosphorylation, although it increased Akt phosphorylation at H1. These early molecular changes were associated with a reduction in brain NO synthesis at H1 and with an attenuation of brain edema at H2. Intraventricular administration of the ERK-1/-2 inhibitor, U0126, or the Akt inhibitor, {"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002, before injury showed that ERK was required for brain edema formation, and that rhEPO-induced reduction of edema could involve the ERK pathway. These results were obtained in the absence of any evidence of blood–brain barrier damage on contrast-enhanced magnetic resonance images. The findings of our study indicate that the anti edematous effect of rhEPO could be mediated through an early inhibition of ERK phosphorylation after diffuse TBI.     

Human brain atlas: For high-resolution functional and anatomical mapping

We present the new computerized Human Brain Atlas (HBA) for anatomical and functional mapping studies of the human brain. The HBA is based on many high-resolution magnetic resonance images of normal subjects and provides continuous updating of the mean shape and position of anatomical structures of the human brain. The structures are transformable by linear and nonlinear global and local transformations applied anywhere in 3-D pictures to fit the anatomical structures of individual brains, which, by reformatting, are transformed into a high-resolution standard anatomical format. The power of the HBA to reduce anatomical variations was evaluated on a randomized selection of anatomical landmarks in brains of 27 young normal male volunteers who were different from those on whom the standard brain was selected. The HBA, even when based only on standard brain surface and central structures, reduced interindividual anatomical variance to the level of the variance in structure position between the right and left hemisphere in individual brains. © 1994 Wiley-Liss, Inc.     

Traumatic brain injury history is associated with earlier age of onset of Alzheimer disease

Objective: This study examined whether a history of traumatic brain injury (TBI) is associated with earlier onset of Alzheimer disease (AD), independent of apolipoprotein ε4 status (Apoe4) and gender.Method: Participants with a clinical diagnosis of AD (n = 7625) were obtained from the National Alzheimer’s Coordinating Center Uniform Data Set, and categorized based on self-reported lifetime TBI with loss of consciousness (LOC) (TBI+ vs. TBI?) and presence of Apoe4. ANCOVAs, controlling for gender, race, and education were used to examine the association between history of TBI, presence of Apoe4, and an interaction of both risk factors on estimated age of AD onset.Results: Estimated AD onset differed by TBI history and Apoe4 independently (p’s < .001). The TBI+ group had a mean age of onset 2.5 years earlier than the TBI? group. Likewise, Apoe4 carriers had a mean age of onset 2.3 years earlier than non-carriers. While the interaction was non-significant (p = .34), participants having both a history of TBI and Apoe4 had the earliest mean age of onset compared to those with a TBI history or Apoe4 alone (M_Difference = 2.8 and 2.7 years, respectively). These results remained unchanged when stratified by gender.Conclusions: History of self-reported TBI can be associated with an earlier onset of AD-related cognitive decline, regardless of Apoe4 status and gender. TBI may be related to an underlying neurodegenerative process in AD, but the implications of age at time of injury, severity, and repetitive injuries remain unclear.     

Tremor induced by thalamic deep brain stimulation in patients with complex regional facial pain.

We report on two patients who developed a new postural and action tremor after chronic stimulation of the contralateral thalamus (VPM nucleus) during treatment of a complex regional facial pain syndrome. The tremor was only present during deep brain stimulation (DBS) and was suppressed with adjustment of the stimulation parameters. Tremor was seen only with low frequency stimulation (50 Hz or lower) and disappeared with higher stimulation frequencies. In addition to being an unusual side effect of thalamic DBS, we believe that this phenomenon affords insight into one possible mechanism underlying essential tremor (ET). A central oscillatory mechanism involving the olivocerebellar complex and the thalamus, which is a part of the cerebro-cerebello-cerebral circuit, is thought to play an important role in the genesis of ET. Induction of a tremor resembling ET in our patients indicates an active role for low frequency stimulation. A plausible explanation for this is that low frequency stimulation in the thalamic area enhances the output of the tremor-producing network. This leads credence to the concept of central oscillations in a "tremor circuit," of which the thalamus is a part, as being important in ET.     

Regional changes in phenylethanolamine-N-Methyltransferase of rat brain during development

The changes of phenylethanolamine-N-methyltransferase (PNMT, EC 2.1.1.28), the enzyme that catalyzes the final step in the biosynthesis of adrenaline, were studied during the development of several regions of rat brain. PNMT is present in medulla oblongata-pons, hypothalamus, cerebellum, and midbrain five days before birth, and a progressive increase in the enzyme activity is observed during development. The adult levels are attained between 15 and 20 days, depending on the region. The increases in PNMT activity in the rostral regions are higher than in the caudal regions. PNMT attains adult levels earlier than tyrosine hydroxylase and dopamine-β-hydroxylase. The apparatus for adrenaline synthesis seems to be mature at three weeks after birth in the medulla oblongata-pons, which contains the cell bodies of adrenaline-containing neurons. In the other regions the adult levels of enzyme activity are attained at 15 days after birth.     

Association of late effects of single,severe traumatic brain injury with Alzheimer’s disease using amyloid PET

Traumatic brain injury (TBI) is suggested to be a risk factor for the onset of Alzheimer’s disease (AD); however, the data remain controversial. This is the first report on cognitive decline in patients with TBI over 30 years post-injury. The medical significance/key learning points of this report are that (1) Functional Independence Measure (FIM) is useful in clinical settings, such as for higher brain dysfunction and dementia; (2) amyloid PET findings represent an essential biomarker for follow-up after TBI; and (3) cognitive decline can occur in patients with TBI more than 30 years post-injury.     

Increased serum-GFAP in patients with severe traumatic brain injury is related to outcome

OBJECTIVES: Several studies have established the relevance of S-100 in blood as a marker of brain damage after traumatic brain injury. However, a more specific marker is required and glial fibrillary acidic protein (GFAP) is considered to be a good candidate. METHODS: In order to assess the increase of GFAP in serum (s-GFAP) after a severe traumatic brain injury (TBI) we collected daily serum samples from 59 patients with severe TBI starting on the day of the trauma. S-GFAP was measured using a sandwich ELISA. The Glasgow outcome scale (GOS) assessed outcome after 1 year. RESULTS: All but one patient had maximal s-GFAP values above the laboratory reference value (median increased 10-fold). The highest detected levels were seen during the first days after TBI and then decreased gradually. Patients with unfavourable outcome had significantly (p<0.001) higher maximal s-GFAP values in the acute phase compared with patients with favourable outcome. All patients (n=5) with s-GFAP>15.04 microg /L died (reference level<0.15 microg/L). We found no significant difference in the maximal s-GFAP levels of patients with isolated brain injury in comparison with patients with multiple traumas. CONCLUSION: Serum-GFAP is increased during the first days after a severe traumatic brain injury and related to clinical outcome.     

Transcranial magnetic stimulation induces alterations in brain monoamines

Summary Transcranial magnetic stimulation has been suggested as a possible therapeutic tool in depression. In behavioral models of depression, magnetic stimulation induced similar effects to those of electroconvulsive shock. This study demonstrates the effect of a single session of rapid TMS on tissue monoamines in rat brain. Alterations in monoamines were selective and specific in relation to brain areas and type of monoamine. The results imply on a biochemical basis to the suggested ECT-like treatment potential of TMS.