猫中脑损伤后EEG,BAEP及SEP的动态监测

目的：研究中脑损伤后猫脑电图（ＥＥＧ）、脑干听觉诱发电位（ＢＡＥＰ）和体感诱发电位（ＳＥＰ）的动态变化及了解其与损伤程度和意识障碍之间的及意义。方法：用三种不同强度的直流电立体定电解损毁猫中脑网状结构造成不同程度的损伤,动态监测猫意识、ＥＥＧ、ＢＡＥＰ和ＳＥＰ的穷期人规律与中脑网状结构损伤和意识的关系。结果：中脑网状结构损伤后随着猫意识障碍的恶化与恢复,ＥＥＧ、ＢＡＥＰ和ＳＥＰ相应地发生变化,且与     

YM-14673对猫中脑损伤意识障碍的实验性治疗

目的研究ＹＭ－１４６７３对中脑损伤意识障碍的治疗作用并揭示其可能机制。方法通过立体定向电解损毁猫中脑网状结构的方法造成意识障碍的实验模型,用ＹＭ－１４６７３以高低两个不同剂量进行治疗。观察意识状态、电生理活动及超微结构的改变。结果发现ＹＭ－１４６７３对中脑损伤后意识障碍的恢复有促进作用,表现为短暂的行为觉醒反应和ＥＥＧ觉醒反应,超微结构研究发现ＹＭ－１４６７３可以使神经元内线粒体和突触小泡增多。结论ＹＭ－１４６７３对猫中脑损伤后昏迷有促进清醒作用,可能是通过增加神经元内线粒体活动而起作用的,有较好的临床应用前景     

脑干意识中枢损伤的实验研究

目的：本研究旨在探索脑干意识中枢损伤对意识状态的影响及其形态学特征，为脑干意识中枢肿瘤的手术与术后治疗提供依据。方法：建立猫脑干意识中枢电凝损毁的动物模型，用意识水平与神经系统功能缺失记分进行神经行为学评价，用Ｅｖａｎｓ蓝和ＨＥ染色做脑干损伤的大体与光镜下观察，用透射电镜和扫描电镜观察脑干损伤的超微结构表现。结果：电凝损毁脑干各部位网状结构可引起不同程度的意识障碍和神经系统功能缺失，其神经系统功能缺失记分均高于假手术组。形态学研究发现，电凝损毁的中心部位以坏死为主，周围则坏死与凋亡并存，周围的微小血管异常是重要的继发性损伤。结论：电凝损毁脑干网状结构可引起意识障碍、神经系统功能缺失、形态学上的广泛异常和迟发性神经元与胶质细胞的死亡。     

脑梗死患者的脑电图变化与有关因素—阳性诊断标准研究

目的：探讨脑梗死患者脑电图改变与有关因素的关系。方法：用ＥＥＧ阳性诊断标准对２３７例脑梗死和１４７例腔隙梗死患者的脑波进行了分析。结果；ＣＩ组在发病４周内ＥＥＧ阳性率显著高于１月后，而ＬＩ组则无统计学意义。ＣＩ组阳性率显著高于ＬＩ组。ＥＥＧ阳性与病初意识障碍或精神症状有关，然而ＥＥＧ阳性率与病变部位或瘫痪程度有关仅见于ＣＩ组：结论：阳性诊断标准能反映卒中后ＥＥＧ变化特征。     

嗜酒所致精神障碍患者的BEAM与EEG

２３例嗜酒所致精神障碍者的ＢＥＡＭ与ＥＥＧ检查结果分析提示，患者均可存在不同程度的脑功能障碍，两种检查方法相比较，ＢＥＡＭ的敏感性相对为高。     

猫持续性植物状态动物模型的建立

目的：建立猫持续性植物状态(PVS)动物模型。方法：16只成年健康家猫随机分为2组．实验组12只右颞开颅，抬起颞叶．暴露中脑及动眼神经，基本平动眼神经水平，用宽8mm、厚1mm金属毁损器横行插入中脑，深度11mm。术后饲养一个月处死动物。结果：实验组12只动物中1只因基底动脉损伤、1只因胃管内返流液误吸死亡，余10只动物均达PVS标准。结论：中脑网状结构毁损法可使猫达到PVS。     

卡马西平对脑电活动影响的动态观察与定量研究

目的探讨卡马西平对脑电活动的影响。方法应用定量药物脑电图（ｑｕａｎｔｉｔａｔｉｖｅｐｈａｒｍａｃｏ－ＥＥＧ，ＱＰＥＥＧ），采用功率谱分析方法，对癫痫患者和健康人单次口服卡马西平前后的脑电背景活动变化进行动态观察与定量研究，与此同时同步测定该药的血清浓度。结果随着血药浓度的升高，θ频段功率百分比逐渐增加，α２频段功率百分比逐渐降低；当血药浓度达峰值时，上述变化分别达到最高和最低。结论卡马西平的定量ＥＥＧ效应在不同频段及不同脑区存在着不均衡分布     

猫中脑损伤后细胞凋亡及相关基因表达的意义

目的　为探索脑干损伤后影响伤情进展的分子基础。方法　建立猫中脑损伤的实验动物模型； 应用末端标记法检测损伤后的细胞凋亡； 应用原位杂交观察神经生长因子和热休克蛋白７０（ Ｈ Ｓ Ｐ７０） ｍ Ｒ Ｎ Ａ 的表达水平； 应用神经功能缺失记分观察猫神经行为学的改变。结果　不同类型的中脑损伤可以在早期诱导 Ｎ Ｇ Ｆ 和 Ｈ Ｓ Ｐ７０ ｍ Ｒ Ｎ Ａ 的表达增强， 与神经元损伤后自身保护及修复能力的产生、代偿机制的形成有关。中脑损伤后可以引起其程序性细胞死亡， 其峰值在损伤后的４８ ～７２ 小时， 这个变化时相与神经行为学上的迟发加重相一致。结论　中脑损伤后 Ｎ Ｇ Ｆ 和 Ｈ Ｓ Ｐ７０ ｍ Ｒ Ｎ Ａ 的表达水平可以反映神经元损伤的程度和自身代偿与修复的能力； 程序性细胞死亡是神经元损伤后迟发加重的重要基础。     

轻型颅脑损伤临床与脑电图监测分析

目的；研究脑ＣＴ检查为阴性的轻型颅脑损伤的脑电图（ＥＥＧ），脑电地形图（ＢＥＡＭ）变化特点及其临床价值，方法：对近两年１０８例无ＣＴ影像学改变的轻型颅脑损伤进行早期动态ＥＥＧ和ＢＥＡＭ监测。结果：异常发迹者达８８．８９％，其中７９．１７％为异常的θ波和δ波，伤后三天内测得的阳性率显著高于三三后；并发现脑生物电异常变化沿受力轴线分布，结论：早期反复测定ＥＥＧ、ＢＥＡＭ的变化是反映轻型脑损伤早期脑功能     

刺激延髓对脑血流量及颅内压的影响以及地塞米松的治疗作用

目的：研究刺激延髓网状结构对脑血流量及颅内压的影响。方法：电解毁损家兔下丘脑背内侧核和中脑网状结构基础上电刺激延髓网状结构，毁损或刺激前静脉注射地塞米松５ｍｇ／ｋｇ，观察颅内压、脑血流量和脑含水量变化。结果：刺激单侧延髓网状结构后颅内压和脑血流量呈短暂可逆性增加，脑含水量无变化；强刺激双侧延髓网状结构后颅内压进行性上升，脑血流量先增加后减少，脑含水量增加。后者应用地塞米松后颅内压增高、脑血流量减少和脑水肿均减轻。结论：破坏下丘脑和中脑以及刺激延髓都将导致大脑血管紧张性降低。大剂量地塞米松可减轻脑水肿而防止颅内压进行性上升。     

Effects of benzodiazepines on PGO firings and multiple unit activity in the midbrain reticular formation in cats.

Effects of benzodiapines administered by the intraperitoneal route on PGO firings and multiple unit activity in the midbrain reticular formation in chronic cat preparations were investigated at various levels of consciousness. Changes in the sleep-wakefulness cycle induced by direct injection of benzodiazepines into the reticular formation were also investigated. Benzodiazepines markedly decreased multiple unit activity in the midbrain reticular formation during each stage of sleep, but had little effect during behavioral and EEG arousal. Benzodiazepines did not affect PGO firing rate, but attenuated all increase of multiple unit activity following PGO firings. The bilateral injection of benzodiazepines into the midbrain reticular formation induced an increase of arousal and a decrease of slow wave sleep, but did not change the amount of paradoxical sleep. It is concluded that benzodiazepines show a mixture of depressant and facilitatory effects, which seem to vary with the state of consciousness of the animal.     

Microstructural changes in memory and reticular formation neural pathway after simple concussion

Patients with concussion often present with temporary disturbance of consciousness. The microstructural and functional changes in the brain associated with concussion, as well as the relationship with transient cognitive disorders, are currently unclear. In the present study, a rabbit model of simple concussion was established. Magnetic resonance-diffusion tensor imaging results revealed that the corona radiata and midbrain exhibited significantly decreased fractional anisotropy values in the neural pathways associated with memory and the reticular formation. In addition, the apparent diffusion coefficient values were significantly increased following injury compared with those before injury. Following a 1-hour period of quiet rest, the fractional anisotropy values significantly increased,and apparent diffusion coefficient values significantly decreased, returning to normal pre-injury levels. In contrast, the fractional anisotropy values and apparent diffusion coefficient values in the corpus callosum, thalamus and hippocampus showed no statistical significant alterations following injury. These findings indicate that the neural pathways associated with memory and the reticular formation pathway exhibit reversible microstructural white matter changes when concussion occurs,and these changes are exhibited to a different extent in different regions.     

Single-cell and multiunit activity in freely moving rats after corticosterone administration

With the purpose of correlating possible electrophysiologic changes in the brain with the negative feedback effect of glucocorticoids on neuroendocrine functions, the effects of corticosterone on multiunit (MUA) and single-cell activity in freely moving rats were studied in the hypothalamus, amygdala, and midbrain reticular formation. The hormone changed the MUA in all regions studied causing mainly an increase in the rate of firing. In the hypothalamus there was a predominance in overall inhibition, when the sensory responsiveness to acoustic stimulation was compared before and after corticosterone administration. No such effect was observed in the amygdala and midbrain reticular formation. The hormonally induced changes in MUA in the hypothalamus were confirmed by analysis of single-cell activity in the freely moving rats which showed also changes in the pattern of firing, as demonstrated by autocorrelations. These findings in the hypothalamus are significant and may represent the electrophysiologic correlates of changes in corticotrophin releasing factor in this region.     

Delayed response deficits in squirrel monkeys with unilateral lesions in the midbrain reticular formation

Electrophysiological experiments suggest that the midbrain reticular formation plays a role in visual attention. However, behavioral tests of this hypothesis have been few and their results inconsistent. Squirrel monkeys with unilateral lesions in the midbrain reticular formation were compared to control animals in their performance on a delayed-response task and a visual pattern discrimination. Nystagmus, adduction of limbs, and lack of visual responsivity were noted a few days after the lesion was made, but these symptoms were transient and were not seen during delayed response testing. The monkeys with lesions had delayed response deficits when the baited food well was contralateral to the lesion and responses were delayed 10 sec or longer. They did not differ significantly from controls on the delayed response task when the baited food well was ipsilateral to the lesion or in learning the visual pattern discrimination. The delayed response task presumably measures the ability to maintain orienting responses, overtly or covertly, during the delay interval. This experiment suggests that the midbrain reticular formation facilitates orienting responses over long delays.     

Effects of Unilateral Lesion in the Midbrain Reticular Formation on Kindled Amygdaloid Convulsion in Cats

Daily stimulation of the amygdala in cats resulted in progressive development of electroclinical seizures culminating in a generalized convulsion (kindling). An electrolytic lesion in the midbrain reticular formation, ipsilateral to the stimulated amygdala, markedly elevated the generalized seizure-triggering threshold and reduced susceptibility to pentylentetrazol challenge. In contrast, globus pallidus lesions had no appreciable effect upon the generalized seizure-triggering threshold and appeared to enhance susceptibility to pentylentetrazol. The results support the hypotheses that (1) the midbrain reticular formation participates significantly in the kindled amygdaloid seizures and (2) the effects of lesions in the midbrain reticular formation do not depend upon the presence of forebrain bisection.     

Hyperosmolar syndrome and diffuse CNS dysfunction with clinical implications

In an electrophysiological study, hyperosmolality damaged the central nervous system including the cerebral cortex, hippocampus, midbrain reticular formation, pyramidal pathway, extrapyramidal pathway and anterior horn cells, and peripheral nervous system. In the experimental model in which acute changes were made, sodium ion concentration was related to the dysfunction of reticular formation. In the clinical setting, hyperosmolality with hyperglycemia is related to the individual's level of consciousness. In the clinical management of hyperosmolar syndromes, plasma osmolality should be kept below 320 mOsm/L.     

The effects of brainstem lesions on vocalization in the squirrel monkey

The present study is an attempt to find out the brain areas involved in the motor coordination of species-specific vocalization. For this purpose, high-frequency coagulations were placed in a systematic manner throughout the brainstem and posterior diencephalon in altogether 43 squirrel monkeys (Saimiri sciureus). The effect of these lesions on different call types elicited by electrical brain stimulation was studied spectrographically. It was found that bilateral destruction of the ventrolateral, ventroposterior and intralaminar thalamus, periventricular and rostral periaqueductal gray, ventral tegmental area of Tsai, nucl. interpeduncularis, nucl. ruber, anterodorsolateral midbrain tegmentum, superior and inferior colliculi, pontine gray, cerebral peduncles, medial pontine reticular formation, raphe and vestibular nuclei did not affect the acoustic structure of the calls tested. On the other hand, lesions in the ventrolateral midbrain involving the substantia nigra and overlying reticular formation, in the midbrain tegmentum just below the inferior colliculus, in the lateral pons and almost the whole medulla (minimal lesion size: 2.5 mm3) changed vocalization significantly. It is suggested that the latter areas are more or less directly involved in the motor coordination of vocalization, while the first are not.     

Blink reflex elicited by auditory stimulation in the rabbit

The pathway of the blink reflex, elicited by auditory stimulation, was investigated electrophysiologically. The reflex was recorded as microvibrations of the eyelid and was named the auditory-evoked eyelid microvibration (AMV). Pharmacophysiological studies suggest that AMV is closely related to the midbrain reticular formation and studies of electrical lesions in the midbrain reticular formation support this. Lesions in several parts of the central nervous system provide evidence that the inferior colliculus has an important role in AMV, and the cerebral cortex may have an inhibitory influence. Studies of brainstem transections indicate that the reflex pathway of AMV exists between the lower midbrain and the upper medulla. Because of its ease and simplicity, AMV is believed to be a useful test for evaluation of the function of the brainstem.     

Involvement of the midbrain reticular formation in self-injurious behavior, stereotyped behavior, and analgesia induced by intranigral microinjection of muscimol

Bilateral microinjection of muscimol (60 ng), a gamma-aminobutyric acid (GABA) agonist, into the central region of the substantia nigra (pars reticulata) produced self-injurious behavior (SIB), stereotyped behavior and analgesic-like effects in rats. Bilateral electrolytic lesions of the midbrain reticular formation ventrolateral to the periaqueductal gray matter completely blocked the SIB but had little effect on stereotyped behavior produced by intranigral muscimol. Lesions of the midbrain reticular formation reduced the antinociceptive effect of intranigral muscimol on the tail-flick but not on the hot-plate test. Bilateral microinjection of muscimol (10-100 ng) into the midbrain reticular formation produced intense stereotyped behavior and had an analgesic-like effect on the hot-plate test but not on the tail-flick test. Stereotyped behavior appeared to interfere with the paw-lick response on the hot-plate test. These data suggest that the antinociceptive effect of intranigral muscimol on the tail-flick test is mediated by fibers that project to or pass through the midbrain reticular formation and that analgesia may play an important role in muscimol-induced SIB. The midbrain reticular formation does not appear to be involved in the stereotyped behavior produced by intranigral muscimol.