脑电图与经颅多普勒在脑梗死后癫(癎)患者中的应用价值

目的探讨脑电图与经颅多普勒在脑梗死后癫癎中的应用价值。方法对48例脑梗死后癫癎患者行脑电图及经颅多普勒检查。结果48例患者中,脑电图异常44例,异常率91.7%,主要表现为慢波增多,出现棘波、尖波及棘慢波、尖慢波等;经颅多普勒异常42例,异常率85.7%,主要表现为频谱形态异常及血流增快及减慢等。结论脑电图是脑细胞功能的最直接反映,对预测癫癎发作及病情变化有重要价值。经颅多普勒可反映脑血管功能情况,出现脑供血不足、脑组织缺血缺氧时可致癫癎发作。     

吗啡急性成瘾猫脑电图及神经病理特点

目的 建立吗啡急性成瘾猫模型,研究吗啡急性成瘾猫神经电生理及脑组织病理学变化,探讨其发病机制,为临床合理治疗提供病理学及电生理学依据. 方法 将12只家猫按照随机数字表法分成对照组(3只)、吗啡成瘾组(9只),用剂量递增法造模成功后,行大脑皮层及伏核、海马区域脑电图检测,并在光镜和电镜下观察各脑区皮质及垂体的形态学变化. 结果 吗啡急性成瘾猫模型成功建立,脑电图监测显示吗啡急性成瘾猫脑电图生理波减少,病理波频繁出现;病理学检查显示各脑区皮质的神经元变性、细胞器减少、线粒体肿胀、染色质边集、核固缩甚至坏死.结论长期使用吗啡可导致脑电图出现病理改变,脑功能损害,这种损害与脑内神经元超微结构改变有密切关系.

Abstract：

Objective To establish the cat models of acute morphine dependence, and explore the etiopathogenesis by investigating its electrophysiology and pathology changes of its brain tissue to provide pathological and electrophysiological evidences for clinical treatment. Methods Twelve cats were randomly divided into control group (n=3) and morphine dependent group (n=9); cats in the morphine dependent group were induced by injection of morphine hydrochloride in a daily increased manner, and at the same time, cats in the control group were injected physiological saline. After the success of model making, EEG was performed on the cortex, hippocampus and nucleus accumbens in cats of the 2 groups; the changes of every encephalic region and pituitary gland were observed under light microscope and electron microscope. Results Morphine dependent cat models were successfully established. EEG indicated that physiological waves decreased and pathological waves appeared frequently in cats of the morphine dependent group as compared with those in the normal ones.Physiological examinations showed that the neuronal degeneration, organelle reduction, mitochondria swelling, chromatin margination and karyopycnosis or even nuclear necrosis occurred in the cortex of every encephalic region. Conclusion Pathological changes and brain damages will appear under EEG after long-term use of morphine, which is intimately related to neuron ultramicrostructure changes.     

脑电图与经颅多普勒在脑梗死后癫痫患者中的应用价值

目的探讨脑电图与经颅多普勒在脑梗死后癫痫中的应用价值。方法对48例脑梗死后癫痫患者行脑电图及经颅多普勒检查。结果48例患者中，脑电图异常44例，异常率91．7％，主要表现为慢波增多，出现棘波、尖波及棘慢波、尖慢波等；经颅多普勒异常42例，异常率85．7％，主要表现为频谱形态异常及血流增快及减慢等。结论脑电图是脑细胞功能的最直接反映，对预测癫疴发作及病情变化有重要价值。经颅多普勒可反映脑血管功能情况，出现脑供血不足、脑组织缺血缺氧时可致癫痫发作。     

戊四氮点燃猫癫痫形成过程中行为和脑电的动态研究

目的:观察戊四氮点燃猫癫癎形成过程中行为和脑电特征。方法:用低于急性致惊厥剂量的戊四氮(PIZ,25 mg·kg~1)给成年雄性猫每日肌肉注射,观察脑电活动和行为特征。结果:1周后,猫出现发作性面部抽搐,脑电为不对称近额部的散发性棘波,基本节律存在;2周后出现节律性点头,脑电为双侧对称性广泛的散发性棘慢波;16 d后出现发作性四肢强直,脑电活动背景节律变慢,棘慢波呈现阵发性;20 d后出现持续半小时以上的全面性强直阵挛发作,脑电活动为较多不规则的θ和δ波,棘慢波持续时间明显延长。结论:PTZ点燃猫癫癎形成过程中,其行为和脑电阶段性变化明显,与人类癫癎的局灶性继发全面性发作癫癎表现相似。     

分析脑电图在头痛型癫痫诊断中的临床应用

目的分析脑电图在头痛型癫痫检查诊断中的临床应用。方法选取我院2011-01-2014-01收治的头痛型癫痫患者48例为研究对象,采用脑电仪对其进行扫描,对其脑电图的波形变化进行观察分析。结果所有患者中轻度异常18例(37.5%),异常30例(62.5%),其中11例脑电图表现为阵发高幅1~3c/s及4~7c/s慢波节律,且两侧对称同步出现,7例脑电图表现为局限在两额部或前头部的波幅;异常脑电图患者中8例为阵发高波幅慢节奏,且两侧对称性同步出现;15例为阵发尖波棘波、尖慢波或棘慢波综合波幅;5例为散发性棘波或棘2慢波;2例为局限性尖波或棘波。结论采用脑电图对头痛型癫痫进行临床诊断具有非常重要的应用价值。     

慢波睡眠期持续性棘慢波的癫痫综合征

慢波睡眠期持续性棘慢波 (CSWS)的癫痫综合征在儿童期发病 ,主要在夜间出现部分性或全面性发作 ,脑电图显示广泛的棘慢波放电 ,PET和SPECT发现局灶的脑功能异常 ,丙戊酸、乙琥胺、拉莫三嗪等治疗有效 ,预后良好。     

正常儿童癫痫样脑电图型的纵向研究

对正常儿童的脑电图研究,已有许多报告.由于检查人数、年龄和方法学的不一致,故关于正常儿童中癫癎样脑电图型的发生率,他们的结论不同.本文研究采用以前从未有过的人数,神经正常并无癫癎发作史的儿童3,726人,男性1,988人,女性1,738人,年龄6至13岁,并按年龄分组进行纵向追踪观察.在清醒安静和过度换气中描记脑电图.其中131人(3.54%)发现癫癎样脑电图型,包括每秒三次棘慢波放电(4例),多棘慢波综合(37例)中颞棘波(50例),中央区或顶叶棘波(27例),枕叶的棘波(2例)和多灶棘波(11例).男性异常发生率较高.这些异常的家族发生也有些迹象.脑电图异常的一半人有行为问题和/或轻度精神运动能力障碍.进行纵向追踪8-9年,这些脑电异常表现自发性消失,通常在学龄期,最迟到青春期.仅7例发生临床癫癎发作(1例失神发作、1例双侧肌阵挛发作,3例     

脑囊虫病人头痛发作的病因、临床表现及脑电图分析

目的探讨脑囊虫病人头痛发作的病因、临床特点及脑电图特征。方法对410例脑囊虫病人头痛发作的病因、临床表现、分型及脑电图资料进行统计分析。结果410例脑囊虫病人头痛发作的病因为颅内压增高和脑膜炎。以青壮年为主(72.20%),男性多于女性,农民发病率最高(73.66%)。脑室型头痛(9.51%)以发作性为特点,伴有Brun’s征;脑膜型头痛(9.02%)以持续性头痛为特点,伴有发热;脑实质型头痛(62.93%)以颅压高性或非颅压高性头痛为特点;混合型头痛以颅压高性为特点。脑电图检查正常87例(21.22%),异常323例(78.78%)。异常脑电图中207例(64.09%)主要表现为弥漫性慢波活动,116例(35.91%)为局限性慢波活动,27例在异常背景上有散在或阵发性棘、尖波或棘、尖慢综合波。结论头痛是脑囊虫病人常见症状,颅内压增高和脑膜炎是导致头痛的主要原因;脑电图表现以弥漫性或局限性慢波活动为主。     

多发性抽动症的视频脑电图观察

目的 探讨视频脑电图对多发性抽动症患儿的辅助诊断价值.方法 本文对100例多发性抽动症患儿进行视频脑电图描记,进行多导同步视频分析.结果 视频脑电图异常46例,异常率46%.其中轻度异常33例,大多表现为背景脑波频率变慢,出现高幅θ、δ波及活动,伴短程出现,中度异常11例,脑波表现为在高幅δ、θ波长程阵发,11例中度异常中4例背景上偶发尖波、棘波、棘慢波综合;重度异常2例.脑波表现为各导联出现较多的棘波或棘慢波综合.结论 视频脑电图检查即可长时间监测脑电情况,又可同步监测患儿临床特征,并且脑电图操作方便,无痛无创,易于被儿童接受,在多发性抽动症早期临床诊断中具有一定的应用价值.     

成人患者显示棘慢波综合的统计学意义

本文分析了20300次脑电图记录,其中20岁以上显示棘慢波综合或棘慢波者259名共878份脑电图记录(以下称SPW组),并以20岁以上显示散发性棘波者169名共689份脑电图记录作为对照。发现SPW组有如下特征:     

急性吗啡成瘾猫脑组织超微结构变化的研究

目的观察吗啡成瘾后猫脑组织形态学的变化,探讨吗啡成瘾猫中枢神经系统毒理病理损伤机制。方法成年雄性家猫12只,分成实验组(n=9)和正常对照组(n=3),于背部皮下分别注射盐酸吗啡、生理盐水,按逐日递增原则,连续5d给药,第6天实验组注射纳洛酮诱发戒断症状。急性吗啡成瘾猫模型制造成功3周后行脑组织取材,利用光镜和电镜技术观察猫脑组织形态学变化。结果实验组:光镜观察到猫皮质神经元胞体变性、坏死,核质疏松,甚至核固缩、碎裂;电镜下观察到神经元凋亡或者变性、坏死,胞突变性、脱髓鞘,部分皮质突触密集,腺垂体细胞结构紊乱,胞质内神经内分泌颗粒异常。正常对照组的猫脑组织未见上述改变。结论吗啡成瘾可导致脑组织慢性、持续性的损害,神经细胞和神经纤维超微结构皆发生不同程度改变。     

Effect of the ganglioside GM1 on neurologic function, electroencephalogram amplitude, and histology in chronic middle cerebral artery occlusion in cats

The effect of the ganglioside GM1 on amplitude of the electroencephalogram, neurologic function, and histology has been studied in chronic middle cerebral artery occlusion in cats. Ischemia was produced by a 2-hour occlusion of the left middle cerebral artery and was followed by a 7-day observation period. GM1 was intravenously administered 30 minutes after occlusion and daily during the observation period. Using the reduction in the electroencephalogram amplitude to measure stroke severity, three cats with mild, three cats with moderate, and three cats with severe stroke were treated with 5 mg/kg GM1. Nine cats, three in each group, were treated with 30 mg/kg GM1, while nine cats, three in each group, received middle cerebral artery occlusion but no treatment. In all cats there was a precipitous fall in mean electroencephalogram amplitude during occlusion, followed by a secondary fall during the observation period. Treated cats showed better recovery of electroencephalogram amplitude during the first 4 hours of reperfusion and a smaller secondary fall than untreated cats. Treated cats, especially those treated with 5 mg/kg GM1, showed significant recovery of neurologic deficits compared with untreated cats. Histologic damage was less in treated cats than in untreated cats. Some cats treated with 30 mg/kg GM1 exhibited convulsions, whereas no untreated cat showed any seizure activity. Our findings suggest that gangliosides may improve the recovery of both neurologic deficits and morphologic damage in the central nervous system. These positive effects might be tentatively explained by stimulation of enzymatic activities such as Na+, K+-ATPase and adenyl cyclase.     

吗啡成瘾大鼠脑内核团毁损后的行为学研究及形态学变化

目的研究脑内核团毁损对吗啡成瘾大鼠戒断症状及行为学方面的影响．以及毁损前后的脑形态学变化。方法将120只雄性SD大鼠随机分成对组、吗啡成瘾组、伏核毁损组、海马毁损组及伏核、海马假毁损组，通过旷场实验和隔离残杀实验观察大鼠目的性探究行为和攻击行为的变化．并在光镜和电镜下观察脑内伏核、海马的形态学变化。结果成瘾组和毁损组在自然戒断症状、旷场实验、隔离残杀实验方面经统计学分析，组间差异有统计学意义（P〈0．05）；成瘾大鼠伏核、海马的神经元细胞器减少、线粒体肿胀、染色质边集、核固缩甚至坏死。结论长期使用吗啡可导致脑内神经元超微结构损害：毁损伏核、海马后可改善成瘾大鼠的戒断症状．使其探索行为和攻击性行为发生变化。     

左旋多巴诱发异动症大鼠模型黑质网状部电活动的研究

目的:研究左旋多巴诱发异动症(LID)大鼠模型基底节输出核黑质网状部(SNr)电活动的改变。方法:将记录电极立体定位插入大鼠损毁侧SNr,使用脑电图仪分别记录正常组、非LID组、LID组和MK801+LID组注射左旋多巴前后SNr电活动。结果:用药前,与正常组比较其余三组SNr脑电图波频均明显降低(P<0.05)。用药后,与用药前比较正常组波频无明显降低(P>0.05),非LID组和LID组波频无明显变化(P>0.05)。MK801+LID组大鼠刻板动作明显减少,SNr脑电图波频较LID组增加(P<0.05),与正常组比较无显著性差异(P>0.05)。LID组可见到间断少量的高大波,类似于异常放电波。其余三组未见波形改变。结论:SNr神经元异常放电与LID的发生有关,干预SNr神经元异常电活动可以抑制LID的发生。     

Valproic acid-induced hyperammonemic encephalopathy with triphasic waves

PURPOSE: To examine a patient with valproic acid (VPA)-induced hyperammonemic encephalopathy accompanied by triphasic waves. METHODS: A 61-year-old male patient with epilepsy experienced disturbance of consciousness after VPA dose was increased because of poor seizure control. The electroencephalogram (EEG) taken on admission revealed triphasic waves and high-amplitude delta-activity with frontal predominance. Although serum hepatic enzymes, such as AST and ALT, were normal, serum ammonium level was high at 96 microg/dl (normal range, 3-47 microg/dl). Serum amino acid analysis showed multiple minor abnormalities. Administration of VPA was discontinued immediately after admission, while other anticonvulsants were continued. RESULTS: The patient's condition was improved on the fourth day of admission. An EEG, serum ammonium level, and amino acid profile were normal on the eighth day. Based on VPA administration, serum ammonium levels, and results of amino acid analysis, this patient had VPA-induced hyperammonemic encephalopathy. CONCLUSIONS: Our case indicates that caution is required if triphasic waves appear in VPA-induced hyperammonemic encephalopathy.     

Effect of bone marrow stromal cell transplantation to the hippocampal CA1 region on electroencephalographic activity in epileptic rats

BACKGROUND： Animal experiments have confirmed that bone marrow stromal cell （BMSC） transplantation can serve as a treatment for epilepsy. OBJECTIVE： BMSCs derived from green fluorescent protein （GFP） mice were transplanted into the hippocampal CA1 region of epileptic rats. The aim of the study was to record electroencephalogram （EEG）, analyze survival and migration of BMSCs, and validate the effect of BMSC transplantation for the treatment of epilepsy. DESIGN, TIME AND SETTING： A randomized block design experiment was performed at the Institute of Neuroscience, Kunming Medical College from March 2005 to February 2006. MATERIALS： Homozygous C57BL/6CrSlcTgN （acr-EGFP） OsbC 14-Y01-FM 131 mice, 8-12 weeks of age, were selected for preparation of cell suspension. Sprague Dawley rats were selected for establishing epilepsy models. METHODS： Rats were randomly divided into 4 groups： control （n = 8）, model （n = 8）, normal saline （n = 24）, and BMSC （n = 24）. In the model, normal saline, and BMSC groups, epilepsy was established with penicillin （3 × 10^7 U/kg i.p. ×7 days）. Rats in the BMSC group received a BMSC suspension derived from green fluorescent protein mice into the fight hippocampal CA1 region. Rats in the vehicle control group were injected with the same volume of normal saline into the hippocampal CA1 region. MAIN OUTCOME MEASURES： The electroencephalogram was used to monitor brain activity. Survival and migration of the transplanted BMSCs was observed using fluorescence microscopy at 1, 2, and 4 weeks after transplantation. RESULTS： In BMSC group, fluorescent cells were observed at the transplantation site and in the adjacent tissue, as well as in the tissue surrounding the needle tract, indicating the migration of implanted cells. Fluorescent cells were not detected in the vehicle control group. The electroencephalogram of the control animals exhibited 7-9 Hzα waves, with a wave amplitude 〈 50 μV. In the model and vehicle control groups random spike-and     

Electrophysiological correlates of sleep delta waves

Recent studies have disclosed several oscillations occurring during resting sleep within the frequency range of the classical delta band (0.5–4 Hz). There are at least 3 oscillations with distinct mechanisms and sites of origin: a slow (<1 Hz) cortically-generated oscillation, a clock-like thalamic oscillation (1–4 Hz), and a cortical oscillation (1–4 Hz). The present paper reviews data on these oscillations and the possible mechanisms which coalesce them into the polymorphic waves of slow wave sleep. Data stem from intracellular (over 500 single cell and 50 double impalements) and field potentials recorded from the cortex and thalamus of cats (120 animals) under ketamine and xylazine anesthesia. Other experiments were based on whole night EEG recordings from humans (5 subjects). The frequency of the slow oscillation both in anesthetized animals and in naturally sleeping humans ranged between 0.1 and 1 Hz (89% of the cases being between 0.5 and 0.9 Hz). The slow (<1 Hz) oscillation is reflected in the EEG as rhythmic sequences of surface-negative waves (associated with hyperpolarizations of deeply-lying neurons) and surface-positive K-complexes (representing excitation in large pools of cortical neurons). Through its long-range synchronization, the slow oscillation has the ability to trigger and to group thalamically-generated spindles and two delta (1–4 Hz) oscillations. Finally, it is argued that the analysis of the electroencephalogram should transcend the spectral analyses, by taking into account the shape of the waves and, when possible, the basic mechanisms that generate those waves.     

Diencephalic projections from the midbrain reticular formation.

(1) Physiologically guided stereotaxic coagulation was placed so as to avoid major through pathways in the midbrain reticular formation of 7 cats. Diencephalic degeneration resulting from this was traced by the Nauta method. (2) Preterminal degeneration was found in: the intralaminar nuclei and the posterior group (PO); the ventral group of thalamic nuclei; the ventral thalamus, including the zona incerta, subthalamus and fields of Forel; and the lateral hypothalamus. (3) The results are discussed in relation to somatomotor reactions, reticular influences on the electroencephalogram and telencephalic representation of pain.     

吗啡成瘾大鼠的行为学及脑内核团形态学改变的研究

目的研究吗啡成瘾对大鼠学习、记忆、情感等行为学的影响及脑内核团的形态学变化。方法将64只大鼠随机分成吗啡成瘾组和对照组,应用Morris水迷宫、开野实验、隔离残杀实验,观察大鼠学习、记忆、攻击性等行为学变化和脑内海马、伏核及内侧额前皮质在光镜和电镜下的形态学变化。结果成瘾组和对照组部分实验项目中存在统计学差异(P<0.05);在成瘾大鼠伏核、海马、内侧额前皮质观察到细胞器减少、线粒体肿胀、染色质边集、核固缩甚至坏死等形态学变化。结论长期使用吗啡可导致脑内结构的损害,同时可导致大鼠的探索行为及攻击性等行为变化。