急性缺氧条件下轻运动负荷脑电的变化及分布特征

本文实验研究了不同高度急性缺氧条件下运动状态脑电的变化,观察了低压舱内轻体力负荷对人体脑电的影响。结果表明,急性缺氧下轻体力负荷脑电的变化特点是:在以快波节律为主,α波普遍被阻抑的背景下,脑电图随缺氧高度的增加慢波(δ、θ)增加,α波出现并增加,而快波相对减少。经计算处理,δ、θ、α频段功量及分配指数随高度和时间的增加而增加。β频段功量相对稳定,但其分配指数呈降低趋势。这些变化在6000m缺氧高度具有统计学意义。     

临床很可能诊断的Creutzfeldt-Jakob病分析

目的 探讨Creutzfeldt-Jakob病（CJD）的临床和脑电图演变特征.方法 分析4例CJD临床、脑电图、MRI、CSF资料.结果 4例CJD患者的脑电图特点如下：弥漫性低波幅慢波背景上,间断出现或不对称或在某一局部突出的双相或三相性慢波,逐渐变为双侧广泛同步的周期性三相波,随着病情进展,逐渐变得明显而持续,最终成为持续的电静息.EEG早期异常不典型,需反复检测,方可见周期性三相复合波.结论 充分认识CJD的临床和脑电图演变特点,CJD的EEG演变过程与临床病情变化具有一致性.     

实验性颅内高压诱发家兔自发脑电非线性特征的变化

目的观察实验性高颅压条件下家兔自发脑电非线性特征的变化,探讨在重力变化引起颅内压改变,进而影响脑功能变化的研究中应用脑电复杂性指标的可能性。方法以家免为实验对象,以灌注法改变颅内压,应用关联维和李亚普诺夫指数等参数估计不同颅内压条件下脑电信号的复杂性特征。结果加压前正常颅内压条件下,动物的自发脑电信号均具有正的李亚普诺夫指数和分数关联维,提示这种信号具有混沌性质。实验性高颅压条件下,李亚普诺夫指数在每例动物都明显降低,提示脑电活动的复杂性降低。颅内压恢复正常值,李亚普诺夫指数的变化具有良好的可逆性,提示有限的高颅压引起的脑电活动的复杂度的变化是可逆的。结论自发脑电信号的李亚普诺夫指数作为监测颅内压变化时脑功能变化的指标,具有一定的应用价值。     

特定应激情况下军人症状自评量表、艾森克个性问卷与脑电图的相关性研究

目的探讨特定应激情况下军人的心理特点及人格特征与脑电图的相关性。为新兵及待退役士兵的心理健康及管理工作提供帮助。方法选取某部2008～2012年新入伍士兵及即将退役士兵251例,对其分别进行EEG检查及SCL-90、EPQ评估。结果（1）251例士兵EPQ各项中异常脑电组P分、N分高于正常组（P〈0．01）、L分高于正常组（P〈0．05）、E分低于正常组（P〈0．01）。慢波增多组中P分、N分高于正常脑电组（P〈0．01）、E分低于正常脑电组（P〈0．01）。痫性放电组E分低于正常脑电组（P〈0．01）、N分高于正常脑电组（P〈0．05）;②脑电图异常组士兵SCL-90各因子分值除躯体化及强迫外均高于脑电图正常组（P〈0．01,P〈0．05）。慢波增多组除恐怖及偏执外均高于正常脑电图组（P〈0．01）。痫性放电组在强迫、人际关系、敌对性、偏执、精神病性几方面高于正常脑电组（P〈0．01,P〈0．05）。结论脑电图异常改变与心理健康状况及人格特点可能存在一定的相关性,情绪不稳定及内向性格者心理问题更严重。脑电图的引入弥补了量表的主观性,二者结合可从客观和主观综合进行评价．使军队的思想管理工作更具针对性。     

载脂蛋白E基因对轻、中型创伤性脑损伤急性期脑电活动的影响

目的 探讨载脂蛋白E基因(APOE)对轻、中型创伤性脑损伤后急性期脑电活动的影响.方法 收集112例轻、中型创伤性脑损伤患者的临床资料,采用聚合酶链反应限制性片段长度多态性法(PCR-RFLP)检测APOE基因型;在伤后1周内对全部患者进行两次脑电图检测,采用定性及定量的方法判断脑电活动的变化;对APOE分型结果、脑电图及临床资料等应用SPSS 11.5统计学软件分别进行x2检验、方差分析和Logistic回归分析.结果 112例患者的APOE分型分布符合遗传学Hardy-Weinberg定律;在22例APOEε4携带者中有12例(55%)脑电图加重,其比率明显高于非ε4携带者(18%,P＜0.01);通过定量指标的分析发现,经过4～5 d的正规治疗,携带APOEε4的患者脑电图慢波增多(P＜0.01),而携带APOEε2、APOEε3的患者脑电图慢波减少(P＜0.05),APOEε2携带者前后两次脑电图慢波减少的程度较APOEε3携带者更明显(P＜0.05).单因素和多因素Logistic回归分析均提示,APOEε4是脑电图加重的危险因素.结论 APOEε4等位基因是轻、中型脑损伤患者急性期脑电图加重的危险因素,而APOEε2有利于脑电活动的恢复.     

脑电图在小鼠氧惊厥研究中的应用

目的 观察小鼠氧惊厥及惊厥后脑电图的改变。方法 小鼠头部预先埋置电极，进行舱内高压氧（HBO）暴露，动态观察记录氧惊厥小鼠脑电改变以及暴露后脑电恢复情况。结果 小鼠埋置电极3～5d后脑电改变恢复正常，舱内HBO暴露致氧惊厥时脑电图发生类似癫痫大发作时的痫波变化，并在氧暴露撤离后7d左右脑电图改变恢复正常。结论 脑电图记录在小鼠氧惊厥研究中是一种可行、客观和稳定的方法。     

急性脑血管病305例动态脑电图监测结果分析

目的：探讨动态脑电图监测在急性脑血管病中应用价值。方法：采用动态脑电图仪对305例急性脑血管病人进行24小时动态监测。结果：脑电图基本节律异常272例，病侧慢波优势194例，其异常程度与病变部位、痫变性质及病情轻重呈相关关系。结论：脑电病理波的出现及改变程度有助于急性脑血管的早期诊断，病情观察、病灶定位及预后判断。     

急性弥漫性脑肿胀发病机制的实验研究

目的探讨急性弥漫性脑肿胀的发病机制。方法电解毁损家兔下丘脑背内侧核、中脑网状结构和延髓网状结构，观察脑血流量和颅内压的变化。结果单独毁损引起短暂可逆性脑血流量增加和颅内压增高，联合毁损引起持续不可逆性颅内压增高，脑血流量超早期增加和早期减少，以及早期形成脑水肿。结论大脑血管紧张性调节中枢广泛存在于下丘脑、中脑和延髓，其结构或功能的破坏是急性弥漫性脑肿胀形成的根本基础     

用超选择阿米妥试验行脑动静脉畸形栓塞前的功能评价

作者分析了33例行栓塞治疗幕上脑动静脉畸形前的109次阿米妥试验。病人选择在栓塞过程中意识清楚者,以便能充分地估价注射阿米妥后出现的变化。女性22例,男性11例,年龄16～73岁。所有病人在栓塞前均获取一基线脑电图(EEG),记录于一连续的16道记录纸上,由计算机分析数据并以彩色脑地形图的方式来显示脑电活动的相对量。脑电波分成慢波(σ波<4 Hz),较慢波(Q波,4～8 Hz)正常快波(α波,8～13 Hz)和快波     

皮层电图监测下切除继发性癫痫灶一例报告

患者,男性,37岁,以阵发性头晕、耳鸣、心悸5 年,加重2 年为主诉入院,每次发病持续几秒至数十秒不等,发病次数逐年增多,由2～3个月发病1次发展至1天10多次。查体无异常发现。两次脑血管造影(-),脑CT扫描:右颞叶占位性病变。术前两次检查脑电图均异常,表现为在弥散性慢波背景活动中,右颞额出现慢波病灶(以右颞为著)及右颞前棘波病灶。在右蝶骨电极出现持续性局限性1～7c/s慢波及阵发性6和14c/s阳性棘波,节律性棘波,三角定位于右颞前可见慢波位相倒置。脑超声示中线波左移0.3cm。术中见肿瘤主要位于右颞中后部,呈灰黄色,部分呈胶冻状及囊变,行…     

A Case of Habitual Neck Compression Induced Electroencephalogram Abnormalities: Differentiating from Epileptic Seizures Using a Tc-99m HMPAO SPECT

Self-induced hypoxia has been reported particularly in adolescents, and it can result in neurological injury. Here, we present a case of electroencephalogram (EEG) abnormalities induced by habitual neck compression differentiated from epileptic seizures by Tc-99m HMPAO SPECT. A 19-year-old male was admitted for evaluation of recurrent generalized tonic-clonic seizures. No interictal EEG abnormality was detected; however, abnormal slow delta waves were found immediately after habitual right neck compression. To differentiate EEG abnormalities due to a hemodynamic deficit induced by habitual neck compression from an epileptic seizure, Tc-99m HMPAO SPECT was performed immediately after right carotid artery compression. Abnormal delta waves were triggered, and cerebral hypoperfusion in the right internal carotid artery territory was detected on Tc-99m HMPAO SPECT. The slow delta wave detected on the EEG resulted from the cerebral hypoperfusion because of the habitual neck compression.     

The role of the central nervous system in heatstroke: reversible profound depression of cerebral activity in a primate model

BACKGROUND: The neurological manifestations of heatstroke victims vary. The exact sequence of the central nervous system (CNS) changes during lethal hyperthermia has only been partially explored, and the data covering the post-resuscitation CNS changes, which in most cases lead to secondary cardiac arrest, are insufficient. HYPOTHESIS: Following heating of the organism to cardiopulmonary arrest, successful resuscitation may be achieved by standard cardiopulmonary resuscitation (CPR), plus glucose and surface cooling. There is a characteristic sequence of neurological responses to hyperthermia preceding cardiopulmonary arrest, and questionable reversibility following successful resuscitation. METHODS: We exposed 12 pigtail monkeys under light anesthesia to total body hyperthermia (cerebral T = 42 degrees C) until cardiac arrest. We monitored EEG, mean arterial pressure (MAP), intracranial pressure (ICP), epidural temperatures, PaO2, PaCO2, serum sodium, osmolality, blood glucose, pupillary diameter, light response, corneal reflex, extremity movement, and seizures. RESULTS: During hyperthermia EEG frequency decreased and amplitude increased, followed by burst suppression pattern of the EEG. Then during severe hypoglycemia, EEG seizure activity and isoelectric EEG occurred when MAP and cerebral perfusion pressure (CPP) decreased while ICP was almost unchanged. Pupils were first responsive to light and became gradually unresponsive with maximal dilation, correlating with low CPP. After temporarily successful cardiopulmonary resuscitation (restoration of spontaneous circulation), normal EEG tracing and reversibility of the unresponsive pupils were observed. As shock led to secondary rearrest, deterioration with depression of all cerebral functions was documented. Some 147 min after restoration of spontaneous circulation, brains were macroscopically (and microscopically) normal in six of the eight monkeys. CONCLUSIONS: The acute cerebral derangements during and after lethal hyperthermia are reversible. The cause of death is probably not CNS damage, but systemic hemodynamic deterioration.     

Effect of acute hypoxia on specific and nonspecific brain systems in rabbits

At a simulated altitude of 8500-9000 m, an increase in the amplitude of the early positive and negative phase of the thalamic-cortical evoked potentials, and a slight prolongation of the latent period were seen. Changes in the reticulo-cortical and hypothalamo-cortical evoked potentials included a pronounced inhibition of their negative phase. In the EEG slow delat-waves increased gradually, becoming the major rhythm. The presence of EEG signs of the development of inhibitory processes in the cortex suggested that the changes in evoked potentials were also a result of inhibition of cortical neurons. Hypoxia-adapted rabbits tolerated acute hypoxia much better. They exhibited less pronounced changes in the electric manifestations of the function of specific and nonspecific projection systems of the brain.     

Isotope cisternography in patients with intracranial hypertension

Cerebrospinal fluid flow (CSF) was studied using isotope cisternography in 52 patients with increased intracranial pressure (ICP), all of whom showed acute transient rises of ICP, i.e., plateau waves, in their continuous ICP recordings. The patients were assigned to two groups. Group I was comprised of 23 patients without hydrocephalus and high ICP resulting from brain tumors, benign intracranial hypertension, and superior sagittal sinus thrombosis. Group II included 29 patients with either communicating hydrocephalus or high ICP resulting from rupture of intracranial aneurysm. Plateau waves were frequently observed in patients with baseline pressures ranging from 21 to 40 mmHg in both groups. The isotope cisternographic pattern in the Group I patients showed a large accumulation of radioactivity over the cerebral convexities, while that in the Group II patients revealed a complete obstruction of the subarachnoid space over both cerebral convexities. The isotope clearance from the intracranial CSF showed a marked delay in both groups of patients with one exception. The results suggest that, in the limited range of increased ICP caused by delayed CSF absorption, plateau waves are most evident regardless of the isotope cisternographic pattern.     

The headache of high altitude and microgravity--similarities with clinical syndromes of cerebral venous hypertension

Syndromes thought to have cerebral venous hypertension as their core, such as idiopathic intracranial hypertension and jugular foramen outlet obstruction, classically result in headaches. Do they provide an insight into the cause of the headache that commonly occurs at altitude? The classic theory of the pathogenesis of high altitude headache has been that it results from increased intracranial pressure (ICP) secondary to hypoxemia in people who have less compliant intracranial volumes (Roach and Hackett, 2001). However, there does not appear to be a correlation between the headache of acute mountain sickness (AMS) and the presence of cerebral edema (Bailey et al, 2006; Wilson et al, 2009). Research has concentrated on arterial perfusion to the brain in hypoxia, but there has been little study of venous drainage. Hypoxia results in markedly increased cerebral blood flow; however, if it has been considered at all, venous outflow has to date been assumed to be of little consequence. Retinal venous distension and the increased venous blood demonstrated by near infra-red spectroscopy and more recently by MRI imply that, in hypoxia, a relative venous insufficiency may exist. Similarly, there is increasing evidence that manifestations of the fluid shift during microgravity is of similar nature to idiopathic intracranial hypertension, which is thought to be primarily a venous insufficiency condition. The unique anthropomorphic adaptations of large brained biped humans with cerebral venous systems that have to cope with large changes in hydrostatic pressure may predispose us to conditions of inflow/outflow mismatch. In addition, slight increases in central venous pressures (e.g., from hypoxia-induced pulmonary vasoconstriction) may further compromise venous outflow at altitude. A better understanding of cerebral venous physiology may enlighten us with regards the pathogenesis of headaches currently considered idiopathic. It may also enable us to trigger headaches for study and hence enable us to develop new treatment strategies.     

Features of volume and pressure pulsations during changes in "reserve space" within the cranial cavity

Changes in the amplitude and phase characteristics of pulse variations of volumes and pressures in response to an increase in the intracranial pressure are discussed. The study of 60 neurosurgical patients has shown that as the intracranial (subdural) pressure grows the amplitude of pulse variations of subdural pressure increase to 30 mm Hg and then decreases, the phase characteristics of the pulse waves changing accordingly. The changes in the amplitudes of pulse variations produced by mechanical displacement of the walls of cerebral lateral ventricles measured with the aid of the noninvasive ultrasonic method suggest that an increase in the CSF pressure above 200 mm H2O makes the intracranial cavity too "tight", which depletes the reserve spaces of the cerebrospinal system. If the above changes develop consistently, then it can be assumed that each of the pressure ranges isolated can be characterized by amplitude-phase parameters of pulse waves that form a specific pattern. Taking into consideration the potentials of noninvasive measurements of amplitude-phase characteristics of the intracranial pulse wave by means of ultrasonic echolocation, it deems possible to develop noninvasive techniques for measuring compensatory abilities of the cerebrospinal system.     

短期进驻高原地区人体脑血流的变化

目的：观测短期进驻高原地区人体脑血流动力学的变化;方法：设立短期进驻高原组与对照组(平原组),观察其脑动脉的收缩峰值血流速度(Vp)及舒张末血流速度(Vd),进行分析对比;结果：短期进驻高原组脑动脉的收缩峰值血流速度(Vp)及舒张末血流速度(Vd)均增快。结论：缺氧可引起脑血流速度加快,脑血流量增加。     

Simultaneous use of rheoencephalography and electroencephalography for the monitoring of cerebral function.

Many of the changes in human performance under stress or in hazardous environments may be attributed, in part, to altered cerebral functions. These changes may take place in either the cerebral neurologic or cerebral circulatory systems. Investigation of the interaction between intracranial blood flow and neural activity during these exposures would provide a better understanding of the human response to these conditions. Experimental and analytical procedures are described whereby the combination of rheoencephalography (REG) and electroencephalography (EEG) may provide additional information during the study of cerebral function. Examples are given to demonstrate the simultaneous use of these techniques during mental arithmetic and antiorthostatic bed rest. Results of these tests in both the time and frequency domains show that REG and EEG can be used to provide graded quantitative measures of cerebral responses to externally applied stressors.     

持续性正加速度致意识丧失的机理及其监测

正在加速度引起的意识丧失（Ｇ－ＬＯＣ）是当胶威胁飞行安全的主要因素。综述了Ｇ＿ＬＯＣ的机理及其生理监测,慢增长率正加速度导致的意识丧失的机理主要大脑缺血／缺氧;快增长率正加速度导致物意识丧失可能与颅内高应力有关,但缺直接的实验证据。用于Ｇ－ＬＯＣ监测的生理指标中,眼水平动脉血压、脑氧饱和度等可能具有重要作用。     

A mathematical model of cerebral perfusion subjected to Gz acceleration

BACKGROUND: When the human body is exposed to a high gravitational load, the blood supply to the brain is reduced and loss of consciousness may occur. Our goal is to identify the principal mechanical causes of reduced blood supply to the brain during high +Gz. METHODS: We have developed a mathematical model to investigate the influence of Gz on the cerebral circulation. Blood flow is modeled using a one-dimensional flow approximation, in which the cross-sectional area of elastic vessels is determined as a non-linear function of the transmural (blood minus external) pressure. The intracranial vessels are subjected to cerebrospinal fluid pressure (PCSF) which is determined from the condition that the cranial volume is conserved. RESULTS: For a constant pressure difference of 100 mm Hg applied to the arterial and venous ends of the model, blood flow is diminished for +Gz. At approximately +5 G, the blood flow predicted by the model is insufficient to maintain normal functioning of the brain. PCSF is approximately equal to the blood pressure in the large intracranial veins for all values of Gz. Extracranial arteries and the intracranial vessels do not collapse, even when Gz is substantially higher than normal. However, the extracranial veins are collapsed even for moderate +Gz. CONCLUSIONS: Even if cardiac output is maintained at normal levels, cerebral perfusion will fall because of the increasing resistance of the cerebral flow circuit. This increase is largely due to the collapse of the extracranial veins, which begins at moderate Gz and becomes dominant at a Gz of approximately 4.5.