急性脑梗死患者颈内静脉血氧饱和度的临床研究

目的探讨急性脑梗死后脑氧代谢变化的规律及其对预后的预测价值。方法将35例急性脑梗死患者分成重症组[22例,格拉斯哥昏迷评分(GCS)≤8分]和非重症组(13例,GCS>8分),通过颈内静脉置管采血测定两组患者颈内静脉血氧饱和度(SjvO2),计算动脉颈内静脉氧含量差(AVDO2)和脑氧摄取率(OEF),并分别以SjvO270%、AVDO24ml/dl、OEF25%为界将患者分组,比较其预后。结果重症组SjvO2高于非重症组(P<0.01),OEF则低于非重症组(P<0.01)。SjvO2≥70%组预后不良的发生率高于SjvO2<70%组(P<0.01);OEF≤25%组高于OEF>25%组(P<0.01);而AVDO2≤4ml/dl组与AVDO2>4ml/dl组预后差别无显著性(P>0.05)。结论SjvO2和OEF可以客观地反映急性脑梗死后全脑氧代谢和脑血流状况,对预测其预后具有参考价值。     

静吸复合麻醉对重症颅脑损伤患者脑氧代谢的影响

目的观察静吸复合麻醉对重症颅脑损伤患者脑氧代谢的影响。方法将80例重症颅脑损伤患者随机分为2组,对照组(n=40)靶控输注行丙泊酚+瑞芬太尼行静脉麻醉,观察组(n=40)靶控输注丙泊酚复合吸入七氟烷辅之以瑞芬太尼行静吸复合麻醉;比较2组患者不同时刻的血流动力学指标和脑氧代谢指标。结果观察组不同时刻的颈内静脉血氧饱和度(SjvO2)、桡动脉-颈内静脉血氧含量差(Da-jvO2)、脑氧摄取率(CERO2)与对照组比较差异具有统计学意义(P0.05)。结论静吸复合麻醉对重症颅脑损伤患者能够降低围术期的脑氧代谢率,发挥一定的脑保护作用。     

重型颅脑损伤患者脑灌注压与颈内静脉血氧饱和度的关系

目的评估颈内静脉血氧饱和度(SjvO2)作为重型颅脑损伤的预后指标可能性及其与脑灌注压(CPP)的相关性。方法重型颅脑损伤病人52例,每6h测定一次SjvO2,持续监测平均动脉压及颅内压,计算出CPP,分析SjvO2与预后的相关性。结果在监测期间有2次或2次以上SjvO2<50%或SjvO2>75%者预后良好率明显低于SjvO250%~75%者或仅有一次SjvO2<50%或SjvO2>75%者(P<0.01)。CPP≤60mmHg者,SjvO2与CPP显著正相关(r=0.679,P<0.01),而CPP>60mmHg者,SjvO2与CPP无明显相关(P>0.05)。结论 SjvO2和CPP联合监测能较可靠地预测重型颅脑损伤患者的预后。     

重型颅脑损伤后局部脑氧饱和度的监测及意义

目的探讨重型颅脑损伤后局部脑氧饱和度(rScO2)的变化规律及意义。方法选择29例重型颅脑损伤病人为研究对象,采用近红外线光谱仪(NIRS)持续监测rScO2,与脉搏血氧饱和度(SpO2)、动脉血氧饱和度(SaO2)、平均动脉压(MAP)、颅内压(ICP)和脑灌注压(CPP)等,并将监测结果进行分析比较。结果重型颅脑损伤后rScO2均明显降低。23例存活病人术后早期rScO2呈不同程度上升,此后随ICP变化呈普遍下降然后又逐步上升的趋势。另6例rScO2呈持续性降低者均死亡。SpO2、SaO2、MAP除在死亡病例临死前进行性降低外,整个监测过程中均正常。结论NIRS持续监测rScO2能准确反映重型颅脑损伤后脑氧代谢的变化规律,对临床治疗及预后评估也有重要价值。     

颅脑损伤程度对大鼠脑血流及氧代谢的影响

目的 对颅脑损伤影响脑血流及氧代谢进行前瞻性研究。方法 30只Wistar大白鼠分成3组：颅脑损伤1组（TBI1）、2组（TBI2）及3组（TBI3）各10只,分别为轻、中、重型颅脑损伤。用脑阻抗（REG）测定脑血流量,颈内静脉血氧饱和度（SjVO2)反映全脑氧代谢情况。结果 TBI、TBI2及TBI3组影响脑血流和氧代谢程度依次为TBI3＞TBI2＞TBI1,健侧脑组织含水量各组无明显差异,伤侧脑组织含水量TBI3组最多,其次为TBI2,明显高于TBI1组（P＜0．01）。结论 颅脑损伤后脑血流和氧代谢变化取决于损伤程度,脑血流和氧代谢各参数的监测对正确认识脑组织病理生理变化,指导临床治疗,判断预后有重要价值。     

脑糖氧代谢和急性出血性脑卒中老年患者生存状况的关系分析

目的考察脑糖氧代谢对急性出血性脑卒中老年患者生存状况的影响,并分析其与预后的关系。方法急性出血性脑卒中老年患者共62例,均行颈内静脉逆行置管,分别于颅脑体征发生的变化较大或每6~8h时进行采血送检,并于发病后24h采集患者血样送检,共监测3d。采集患者的桡动脉血与颈静脉血,计算动脉血氧饱和、颈内静脉氧饱和度脑动静脉氧差和血糖差、乳酸差、脑氧利用率、颈内静脉与动脉血二氧化碳分压差的绝对值等临床指标。记录患者的短期预后,存活的判定是体温、呼吸、心率、血压等基本稳定在正常范围内,而转出ICU的患者判定为存活,按照患者的短期预后存活与否,将患者分为存活组(45例)和死亡组(17例),比较2组在上述各临床指标上的差异,及其与预后间的关系。并从2013-08开始对所有患者进行6个月的前瞻性研究,分析患者的短期预后状况。结果(1)与死亡组比较,存活组CEO_2(29.42±12.25vs.48.56±18.67%)、Ca-jvO2(59.87±28.72vs.87.03±41.85mL/L)、A-VLac(0.24±0.15vs.1.42±0.34mmol/L)、A-VGlu(0.22±0.05vs.0.43±0.07mmol/L)显著降低(P0.05),Pa-jvCO_2(6.91±2.42vs.4.16±1.94mmHg)、SjvO_2(98.28±45.47vs.98.13±42.51%)明显升高(P0.05);(2)符合SjvO_252%,Ca-jvO283mL/L条件的,存活组5例,死亡组14例,2组的人口分布比例差异显著(χ2=29.465,P0.05)。根据患者发病3d内符合上述条件的患者为预死亡组(19例),不符的患者为预存活组(43例),患者发病1个月的预后,经Kaplan-Meier法分析,预存活组的中位存活时间(13.2±3.5)d长于预死亡组(6.9±1.8)d。结论入院时格拉斯哥昏迷评分(GCS)5~8分的急性出血性脑卒中老年患者的脑无氧代谢明显增加,SjvO_252%与Ca-jvO_283mL/L与该类老年患者的死亡相关。     

过度通气对62例重型颅脑损伤的临床观察

目的 研究过度通气对重型颅脑损伤（STBI）患者颅内压（ICP）,脑氧摄取,血清神经元特异性烯醇化酶（NSE）含量的影响.方法 62例重型颅脑损伤患者（GCS≤8分）,随机分成治疗组和对照组,治疗组采用过度通气使呼气末二氧化碳分压（PetPaCO,）维持在（4～4.67kPa）2h,同时监测颅内压,颈静脉氧饱和度（SjvO2）,动脉血氧饱和度（SaO2）.结果 重型颅脑损伤的患者行过度通气2h后,ICP有不同程度的下降,平均下降（0.53 kPa）,脑氧摄取与血清NSE含量没有统计学差异.结论 轻度过度通气有效地降低了颅内压,没有导致脑组织缺血缺氧及脑组织损伤,不能放弃这种简单有效的降低颅内压方法.     

交通伤所致重型颅脑损伤患者预后的临床影响因素分析

目的分析交通伤所致重型颅脑损伤患者预后的影响因素。方法回顾性分析2012-03-2014-04我院收治的108例交通伤所致重型颅脑损伤患者的临床资料,根据格拉斯哥预后评分(GOS)分为预后不佳组和预后良好组,对年龄、性别、收缩压、血氧饱和度、血糖、瞳孔评分、损伤严重度评分(ISS)、格拉斯哥昏迷评分(GCS)等可能的影响因素进行单因素分析,并对单因素分析结果中的危险因素进行多因素Logistic回归分析。结果单因素分析结果提示,血氧饱和度、收缩压、血糖、瞳孔评分、ISS评分、GCS评分与患者预后有关,P0.05;多因素Logistic回归分析提示,血糖、血氧饱和度、ISS评分、GCS评分为影响预后的独立危险因素,P0.05。结论交通伤所致重型颅脑损伤患者的预后与血糖、血氧饱和度、ISS评分、GCS评分具有密切关系,重点关注、针对性改善这些指标对改善此类患者的预后具有重要意义。     

重型颅脑损伤患者的预后因素分析

目的 探讨交通伤所致重型颅脑损伤患者预后的临床影响因素. 方法回顾性分析南方医科大学珠江医院神经外科自1998年2月至2008年2月收治的652例交通伤所致重型颅脑损伤患者的临床资料,伤后3个月根据患者格拉斯哥预后评分(GOS)分为预后良好组和预后不良组,比较患者性别、年龄、入院时间、瞳孔、血氧饱和度、收缩压、血糖、损伤严重度评分(ISS)、格拉斯哥昏迷评分(GCS)及脑损伤类型等10项指标在2组间的差异.结果 与预后良好组相比,预后不良组患者入院时间长、血糖和ISS评分较高,而瞳孔评分、血氧饱和度、收缩压、GCS分值较低,差异有统计学意义(P<0.05);脑挫裂伤、颅内多发血肿和颅内血肿患者预后较差;血糖、血氧、GCS评分和ISS评分为影响患者预后的独立因素.结论血糖、血氧、GCS评分和ISS评分可有效判断交通伤所致重型颅脑损伤患者的预后.     

急性高容量血液稀释联合控制性降压对颅内动脉瘤手术病人脑氧供需平衡及能量代谢的影响

目的观察急性高容量血液稀释(AHHD)联合应用控制性降压对颅内动脉瘤夹闭术病人脑氧供需平衡和能量代谢影响。方法15例择期颅内动脉瘤病人诱导后行AHHD(Hct>30%),暴露动脉瘤前用微量泵输注硝普钠,初始量1.5~2μg/(kg.min),平均动脉压维持在8.0~8.7kPa。分别在降压前(T0)、降压中(包括动脉瘤夹闭前T1、夹闭后T2)和升压后(T3)采集颈内静脉球部和桡动脉血进行血气分析。监测动脉血氧分压(PaO2)、动脉血氧饱和度(SaO2)、颈内静脉球部血氧分压(PjvO2)、二氧化碳分压(PjvCO2)、血氧饱和度(SjvO2)、血红蛋白(Hb)、动静脉血糖(GluA、GluV)、动静脉血乳酸(LacA、LacV)及差值。用Fick公式分别计算动脉血氧含量(CaO2)、颈内静脉球部血氧含量(CjvO2)及脑动-静脉血氧含量差(Ca-jvDO2)。结果与控制性降压前比较,降压中和升压后PaO2、PaCO2无明显变化(P>0.05),PjvO2、SjvO2和CjvO2在降压中显著升高(P<0.05),升压后亦有增高,但差异无统计学意义(P>0.05)。Ca-jvDO2在降压中显著降低(P<0.05),升压后亦有增高,但差异无统计学意义(P>0.05)。降压中和升压后Lac和Glu变化差异无统计学意义(P>0.05)。结论AHHD联合硝普钠控制性降压脑氧供需平衡,能量代谢良好,可以安全应用于颅内动脉瘤手术,但应把平均动脉压维持在8.0kPa以上,同时还要控制好通气,把PaCO2维持在正常水平。     

Anemic hypoxia in moderate intracerebral hemorrhage: the alterations of cerebral hemodynamics and brain metabolism.

To determine the influence of anemic hypoxia on cerebral hemodynamics and brain metabolism during pathological conditions of the brain, moderate-sized intracerebral hemorrhage (ICH) was created in canines with and without preoperatively inducing chronic anemia. The changes in cerebral perfusion pressure (CPP) and cerebral blood flow velocities (CBFv) were evaluated as well as the determinations for cerebral extraction fraction of oxygen (CEO2), arteriovenous oxygen content difference (AVDO2) and lactate (Lac) concentrations through the arterial and superior sagittal sinus (SSS) samples. Before ICH production, anemic animals (n = 8) showed a significant reduction in cerebral AVDO2 and arteriovenous Lac difference (AVDLac) but had higher CBFv as well as CEO2 than did nonanemic animals (n = 8). The CBFv began to decrease within 30 min after ICH in anemic but not in nonanemic animals, and the difference between the two groups was found to be significant at 2 h (P<0.05). Following ICH, anemic group also showed coupling reductions in CEO2 and AVDO2, indicating a decreased cerebral metabolic rate for oxygen (CMRO2) relative to the baseline data, compared with a constant CMRO2 in nonanemic group in which the CEO2, AVDO2, and CBFv remained relatively normal. Moreover, compared to the baseline data, a significant increase of the AVDLac was found in anemic but not in nonanemic group, although the former had lower Lac concentrations of the SSS than did the latter group throughout the whole observation period. We conclude that, in cases with chronically reduced Hct, cerebral hemodynamics and oxygenation remain in favorable conditions, thus decreasing Lac production of the brain. The findings suggest a lowered metabolic demand of the brain tissue due to reduced cerebral O2-carrying capacity. During the early phase of moderate ICH, the regulation capacity in cerebral hemodynamics and brain oxygenation tend to deteriorate in profound anemic hypoxia, which consequently leads to enhancing at least modest anaerobic glycolysis.     

高氧血颈动脉灌注治疗重型颅脑损伤

目的研究高氧血颈动脉灌注存重型颅脑损伤治疗中的作用。方法对22例重型颅脑损伤患者于伤后约3．5d行高氧血颈动脉灌注治疗，监测灌注前、中、后的PbtO2、PbtCO2、pHbt值变化以及伤后三月格拉斯哥预后评分(GOS)的变化。结果高氧血颈动脉灌注能改善重型颅脑损伤后早期继发性脑缺血缺氧状态和意识状态，进而改善患者预后。结论高氧血颈动脉灌注在重型颅脑损伤的早期治疗中起着积极和重要的作用。     

Jugular venous desaturation and outcome after head injury.

Early experience with continuous monitoring of jugular venous oxygen saturation (SjvO2) suggested that this technology might allow early identification of global cerebral ischaemia in patients with severe head injury. The purpose of the present study was to examine the relationship between episodes of jugular venous desaturation and neurological outcome. One hundred and sixteen severely head-injured patients had continuous monitoring of SjvO2 during days 1-5 after injury. Episodes of jugular venous desaturation (SjvO2 < 50% for more than 10 minutes) were prospectively identified, and the incidence of desaturation was correlated with neurological outcome: 77 episodes of desaturation occurred in 46 of the 116 patients; 27 had one episode and 19 had multiple episodes of desaturation. The causes of these episodes were systemic (n = 36), cerebral (n = 35), or both (n = 6). Most of the episodes were less than 1 hour in duration, and it is probable that many of them would not have been detected without continuous measurement of SjvO2. Episodes of desaturation were most common on day 1 after injury, and were twice as common in patients with a reduced cerebral blood flow as in patients with a normal or elevated cerebral blood flow. The occurrence of jugular venous desaturation was strongly associated with a poor neurological outcome. The percentage of patients with a poor neurological outcome was 90% with multiple episodes of desaturation and 74% in patients with one desaturation, compared to 55% in patients with no episodes of desaturation. When adjusted for all co-variates that were found to be significant, including age, Glasgow coma score, papillary reactivity, type of injury, lowest recorded cerebral perfusion pressure, and highest recorded temperature, the incidence of desaturation remained significantly associated with a poor outcome. Although a cause and effect relationship with outcome cannot be established in this study, the data suggest that monitoring SvO2 might allow early identification and therefore treatment of many types of secondary injury to the brain.     

右美托咪啶在重型颅脑外伤手术中的脑保护作用

目的探讨右美托咪啶对重型颅脑外伤患者躁动镇静的临床效果及手术麻醉中的脑保护作用。方法选取2014-12-2016-12驻马店市第一人民医院收住的重型颅脑外伤患者50例为试验组,均采取手术治疗,在常规麻醉诱导前给予右美托咪啶1.0μg/kg静脉注射,之后以0.5μg/(kg·h)维持至手术结束。同期50例患者为对照组,在麻醉诱导前给予咪唑安定0.1mg/kg,静注,之后以30μg/(kg·h)维持至手术结束。采用Ramsay镇静评分评估术后24h内患者镇静状态,并分别于术前、术后24h采用酶联免疫吸附法(ELISA)检测血浆S-100蛋白及神经元特异性烯醇化酶(NSE)水平,并检测脑氧摄取率(CERO_2)、动脉-颈内静脉血氧含量差(Da-jvO_2)以及颈静脉血氧饱和度(SjvO2)。结果试验组术后12h、24hRamsay评分分别为(3.2±0.6)分、(2.5±0.6)分,对照组分别为(3.9±0.7)分、(3.1±0.6)分,试验组不同时间点镇静效果均优于对照组(P0.05)。术前2组患者S-100蛋白、NSE、CERO_2、Da-jvO_2及SjvO_2水平差异无统计学意义(P0.05)。术后24h2组S-100蛋白、NSE、CERO_2及SjvO_2水平升高(P0.05),但试验组S-100蛋白、NSE、CERO_2、Da-jvO_2低于对照组(P0.05),SjvO_2高于对照组(P0.05)。结论术中应用右美托咪啶可提高重型颅脑损伤患者镇静效果,并改善脑氧代谢,均具有一定的脑保护作用。     

Fracture of temporal bone with exsanguination: pathology and mechanism.

Eight cases of basal skull fracture with transverse fracture of the petrous temporal bone with medial extension to the internal carotid artery and lateral extension of the structures of the middle ear are described. Injuries in all cases were due to major blunt impact to the head usually occurring in a motor vehicle accident. General autopsy revealed major blood loss without any obvious external or internal site of hemorrhage suggesting that exsanguination was a complication of the head injury. The internal carotid arteries at the most medial extension of the fractures were lacerated or transected in all cases. In selected cases, the cervical internal carotid arteries were perfused and perfusate escaped rapidly from the ear(s) with the majority of fluid bypassing the cerebral venous system. Magnetic resonance image reconstruction of sequential sections of the fractured base of the skull confirmed the laceration of the internal carotid arteries and disruption of the middle ear. Based on this evidence, we propose that some displaced fractures of the base of the skull produce carotid-middle ear continuities which act as arterial shunts, resulting in rapid fatal exsanguination through the ear.     

大骨瓣减压对不同年龄重型颅脑创伤患者脑血流量及脑代谢的影响

目的 探讨大骨瓣减压对不同年龄重型颅脑创伤患者脑血流量及脑代谢的影响.方法 将71例重型颅脑创伤患者分为＜30岁组、30～50岁组和＞50岁组.每组又分为治疗组和对照组,大骨瓣减压手术前后行桡动脉和颈内静脉血气分析及血糖、血乳酸、血红蛋白监测,计算动脉-颈内静脉血糖差、颈内静脉-动脉乳酸差以及脑氧摄取率,TCD测定脑血流量.结果 术后第1天开始,≤50岁治疗组患者的脑血流量和脑氧摄取率均明显大于对照组;＞50岁治疗组患者的脑血流量明显高于对照组,脑氧摄取率明显低于对照组(P＜0.05).术后第3天开始,≤50岁治疗组患者的动脉-颈内静脉血糖差明显高于对照组,颈内静脉-动脉乳酸差明显低于对照组;＞50岁治疗组患者的动脉-颈内静脉血糖差明显低于对照组(P＜0.05),颈内静脉-动脉乳酸差明显高于对照组(P＜0.05).结论 大骨瓣减压能增加50岁以下重型颅脑创伤患者的脑血流量和脑氧代谢,能增加50岁以上患者的脑血流量并降低脑氧代谢.

Abstract：

Objective To explore the effects of decompressive craniectomy on cerebral blood flow volume and brain metabolism in different aged patients with severe traumatic brain injury.Method 71 cases were divided into three groups according age:group A( ＜30 years) ,group B(30 ～50 years) ,group C ( ＞ 50 years).Each group was divided into decompressive craniectomy ( DC ) treatment group and control group.Monitor dynamically blood gas analysis, glucose, lactic acid, hemoglobin in radial artery and internal jugular venous bulb, accounting the cerebral oxygen extraction ( CEO2 ) and the D - values of glucose and lactic acid respectively between radial artery and internal jugular venous bulb.Color doppler ultrasonography was used to determine the cerebral blood flow volume(CBFV).Results From the 1 st to 7th day, the CBFV and CEO2 of DC group were significantly greater than control group in group A and group B.The CBFV was significantly greater than control group while the CEO2 was lower than control group in group C ( P ＜ 0.05 ).From third day, the D - values of glucose of DC group was significantly higher than control group while the D - values of lactic acid was lower than control group in group A and group B, the D - values of glucose of DC group was significantly lower than control group while the D - values of lactic acid was higher than control group in group C( P ＜ 0.05 ).Conclusions Decompression craniectomy can increase the CBFV and brain oxygen metabolism in STBI patients before age 50 and increase the CBFV in patients after age 50 whereas decrease the brain oxygeon metabolism.     

Cerebral energy failure after subarachnoid hemorrhage: the role of relative hyperglycolysis.

After subarachnoid hemorrhage (SAH) cerebral metabolism is significantly impaired. Hyperglycolysis describes the reduction of oxidative metabolism followed by a relative increase of anaerobic glycolysis to maintain energy supply. This phenomenon is known in head injury but has not as yet been shown after SAH. This study was conducted to test the hypothesis that hyperglycolysis is present in SAH patients and is associated with vasospasm. A total of 105 measurements were conducted on 21 SAH patients (age 49+/-15 years, median World Federation of Neurosurgical Societies Grade 4) over the first 5 days following admission. Arteriovenous differences were calculated for oxygen (avDO2) and glucose (avDGlc). Relative hyperglycolysis was defined as metabolic ratio (MR=avDO2[mmol/L]/avDGlc[mmol/L])<3.44. Jugular-venous saturation for oxygen (SjvO2), mean arterial blood pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP) were monitored. Relative hyperglycolyis was recorded in 34% of studies after SAH. In hyperglycolytic studies both jugular-venous lactate and SjvO2 were significantly elevated (jugular-venous lactate 14.9+/-9.9 vs. 11.8+/-5.5 mg/dL, p=0.04; SjvO2: 70.0+/-18% vs. 81.7+/-9%, p=0.002). Relative hyperglycolysis is associated with outcome after SAH. In patients who died after SAH almost 50% of studies showed hyperglycolysis, whereas patients who survived without neurological deficit had no hyperglycolytic events. Relative hyperglycolysis is a common event after SAH. It may be associated with relative hyperemia but most importantly with outcome.     

Treatment of the traumatic cerebral vasospasm with the calciumchannel blocker nimodipine: a preliminary report

Five patients with severe head injury, rating between 3 and 5 on the Glasgow Coma Scale, were treated with the calciumchannel blocker nimodipine continuously for up to 12 days (2 mg/h) because of severe spasm of cerebral arteries. All cases involved the intracranial carotid artery and the first segments of the medial and anterior cerebral arteries. Control angiograms performed in 4 cases showed improved or normalized vessel calibre after the treatment. Intracranial pressure as well as blood pressure were not altered during nimodipine treatment. EEG improved within 7 days after treatment in all cases. Repeated CT scans showed reduction of cerebral edema. Hypothalamic disorders observed in 3 cases were stabilized. Based on these preliminary results, calciumchannel blocker reverses traumatic vasospasm and ameliorates physiologic function of the brain structures after severe head injury.     

Treatment of the traumatic cerebral vasospasm with the calciumchannel blocker nimodipine: A Preliminary Report

Five patients with severe head injury, rating between 3 and 5 on the Glasgow Coma Scale, were treated with the calciumchannel blocker nimodipine continuously for up to 12 days (2 mg/h) because of severe spasm of cerebral arteries. All cases involved the intracranial carotid artery and the first segments of the medial and anterior cerebral arteries. Control angiograms performed in 4 cases showed improved or normalized vessel calibre after the treatment. Intracranial pressure as well as blood pressure were not altered during nimodipine treatment.

EEG improved within 7 days after treatment in all cases. Repeated CT scans showed reduction of cerebral edema. Hypothalamic disorders observed in 3 cases were stabilized.

Based on these preliminary results, calciumchannel blocker reverses traumatic vasospasm and ameliorates physiologic function of the brain structures after severe head injury.