电刺激小脑顶核治疗急性期脑梗死的临床观察

实验证明电刺激小脑顶核可改善脑缺血损伤 ,本文观察其临床效果 ,报告如下。1　资料与方法1.1　病例选择　全部病例均为我科 2 0 0 1年 6月～2 0 0 2年 6月住院患者 ,均经 CT或 MRI证实 ,按照 1995年全国第四届脑血管病学术会议上脑梗死诊断标准而确诊。将颈内动脉系统急性期脑梗死患者 14 6例 ,随机分成治疗组(基础治疗加用脑循环治疗仪 )和对照组 (仅用基础治疗 )。治疗组 74例 ,男 4 3例、女 31例 ,年龄 4 0～ 76岁 ,平均 5 9.6 3±8.76岁。对照组 72例 ,男 4 4例 ,女 2 8例 ,年龄 38～ 75岁 ,平均 5 8.4 6± 10 .82岁 ,临床评分将各组…     

电刺激小脑顶核对急性脑梗死患者血浆CGRP的影响

近年来 ,国内外研究资料表明小脑顶核可能在脑血流量的调节方面具有重要作用。为研究电刺激小脑顶核对急性脑梗死患者的治疗作用 ,我们观察了电刺激小脑顶核对急性脑梗死患者血浆中降钙素基因相关肽 (CGRP)的影响。1　材料与方法我院神经内科住院急性脑梗死患者 6 0例 ,均符合第四届全国脑血管病学术会议制定的诊断标准 [1 ] ,并经头部 CT或 MRI证实 ,病程在 7d以内。随机分为电刺激小脑顶核治疗组和对照组 :治疗组 30例 ,男 19例 ,女 11例 ,年龄 4 9～ 74岁 ,平均 6 4 .5岁 ;对照组 30例 ,男 17例 ,女 13例 ,年龄 5 0～71岁 ,平均 6 1.…     

电刺激小脑顶核治疗急性脑梗死的临床疗效评价

我科于 1998年～ 2 0 0 0年应用脑循环功能治疗仪 ,经皮电刺激小脑顶核治疗 10 0例急性脑梗死患者 ,取得明显的疗效。现报道如下。1　资料与方法1.1　一般资料　本组 188例急性脑梗死患者均符合第四届全国脑血管病会议制定的诊断标准 ,并经头颅 CT或 MRI证实。随机分为两组 ,治疗组 (加用脑循环功能治疗仪治疗 ) 10 0例 ,男 64例 ,女 3 6例 ,年龄 4 5～ 82岁 ,平均 61.7岁 ;对照组88例 ,男 5 8例 ,女 3 0例 ,年龄 4 0～ 81岁 ,平均 60 .5岁。两组按临床神经功能缺损评分 ,治疗组中轻型 4 6例 ,中型 3 4例 ,重型 2 0例 ;对照组中轻型 4 3例…     

电刺激小脑顶核、低频电刺激和康复训练联合治疗脑卒中后吞咽障碍的研究

吞咽障碍是脑卒中后常见的并发症之一,可导致吸入性肺炎、营养不良、脱水、窒息等并发症,甚至可直接导致患者死亡,因此给予积极有效的治疗意义重大。我科自2009-10-2011-10应用电刺激小脑顶核、低频电刺激和康复训练联合治疗脑卒中后吞咽障碍疗效明显,现报道如下。     

电刺激小脑顶核对大鼠局灶性脑缺血／再灌注后Ku70表达影响的研究

目的:研究预电刺激小脑顶核对大鼠脑缺血再灌注后Ku70 mRNA的表达及其神经保护的分子机制。方法:Wistar大鼠通过原位杂交的方法及末端标记法检测Ku70 mRNA的表达及Tunel阳性细胞数。结果:①单纯造模组及毁损小脑顶核组缺血/再灌注后各时点Ku70 mRNA的表达无显著性差异,均较预刺激组及假手术组明显减少(P<0.01),预刺激组除缺血/再灌注后6h Ku70mRNAR的表达较假手术组减少(P<0.01)外,余时点与假手术组Ku70 mRNA表达无明显差异;②预刺激组Tunel阳性细胞数较未给预电刺激的两组明显减少(P<0.01)。结论:①预电刺激小脑顶核能减少缺血区神经元凋亡可能与DNA修复酶Ku70活性上调有关;②毁损小脑顶核后电刺激对脑缺血/再灌注引起的氧化性DNA损伤无保护作用。     

电刺激小脑顶核治疗偏头痛的疗效观察

我院神经内科自2004-06～2005-06,共收治偏头痛病人102例.用电刺激小脑顶核治疗,取得良好疗效,现报道如下.     

电刺激小脑顶核对大鼠脑缺血/再灌注后氧化性DNA损伤的保护作用

目的预电刺激小脑顶核对大鼠脑缺血/再灌注后DNA氧化性损伤的保护作用, 以了解电刺激小脑顶核对实验性脑缺血及再灌注后神经保护的分子机制.方法健康雄性Wistar大鼠106只, 体重(250±30)g, 随机分为4组: (1) 单纯造模组; (2) 预刺激组; (3) 毁损小脑顶核组; (4) 假手术组.毁损小脑顶核组大鼠用鹅膏氨酸毁损两侧小脑顶核, 预刺激组、毁损小脑顶核组大鼠均以电刺激器刺激左侧小脑顶核, 前3组大鼠用线栓法成功制作可复流的MCAO模型2 h后再灌注.在再灌注后6、24、48 h将大鼠断头取脑, 取第3片提取DNA或RNA.DNA样品经酶解后上高效液相-电化学检测器检测8-ohdG.RNA样品通过RT-PCR的方法探测rOOG1 mRNA的表达.结果 (1) 大鼠脑缺血/再灌注后缺血区8-ohdG堆积.预刺激组再灌注各时点的8-ohdG含量均较单纯造模组及毁损小脑顶核组减少(P＜0.01); (2) 单纯造模组及毁损小脑顶核组脑缺血/再灌注后rOGG1的转录水平相似, 再灌注后6 h其rOGG1 mRNA几乎检测不到, 随时间的延长其转录水平有所增加, 但仍较假手术组及预刺激组低(P＜0.01).预刺激组再灌注后6 h其rOGG1 mRNA的表达量与假手术组无显著性差异, 但再灌注后24及48 h其rOGG1 mRNA的表达量均较假手术组增加(P＜0.01).结论 (1) 大鼠脑缺血/再灌注后脑缺血区存在DNA氧化性损伤; (2) 预电刺激小脑顶核减少缺血区神经元凋亡可能与DNA修复酶活性上调有关.     

电刺激小脑顶核治疗视网膜中央动脉阻塞疗效的观察

目的：观察电刺激小脑顶核（ＣＦＮ）治疗视网膜中央动脉阻塞（ＣＲＡＯ）患者的疗效。方法：选择四例不同病程的视网膜中央动脉阻塞患者,用脑循环治疗仪进行治疗,治疗前后检测亮力、眼底、视野、视网膜电图。结果：经电刺激小脑顶核治疗后,两例患者治愈,一例患者好转,一例患者改善。结论：用电刺激小脑顶核治疗视网膜中央动脉阻塞地一种安全、有效的新方法。     

电刺激小脑顶核治疗急性脑梗死75例临床疗效观察

目的:观察电刺激小脑顶核治疗急性脑梗死的临床疗效。方法:150例急性脑梗死患者(n=75)随机分为A,B两组。A组(n=75),常规治疗基础上接受电刺激小脑治疗,10d1个疗程,而B组对照组(n=75),仅按常规治疗。然后观察其疗效并与对照组作比较。结果:发现接受电刺激组患者疗效明显优于对照组。治疗组在10d以及三个月时神经功能缺损评分和日常生活活动能力评分均高于对照组。治疗组有效率高于对照组,两组比较有统计学差异(10dp<0.05,三个月p<0.01)。结论:电刺激小脑顶核治疗有利于急性脑梗死患者神经功能早期恢复。     

电刺激小脑顶核治疗急性脑梗死的临床疗效观察

目的 研究电刺激小脑顶核治疗急性脑梗死的临床疗效。方法 60例急性脑梗死患者，随机分为治疗组和对照组，治疗组患者在常规内科治疗的基础上，同时接受电刺激小脑机核治疗，观察其临床疗效、TCD及血液流变学各项指标。结果 治疗组患者总有效率为93．3％，对照组患者总有效率为83．3％，两组比较有显著性差异（P＜0．05），同时治疗组治疗前后血液流变学指标（全血高切粘度、血浆比粘度、RBC聚集指数、血学方程K值及血细胞比容等）比较，均有显著性差异（P＜0．05）。结论 电刺激小脑顶核治疗急性脑梗死有显著疗效。     

小脑顶核电刺激对脑卒中患者情感障碍的影响

目的探讨小脑顶核电刺激治疗对脑卒中后抑郁患者抑郁症状的影响。方法脑卒中后抑郁患者78例,随机分成治疗组41例和对照组37例,所有病人均接受常规治疗,治疗组在此基础上加用小脑顶核电刺激,治疗2周,治疗前和治疗后2周、3个月、6个月应用汉密顿抑郁量表评定抑郁症状。结果治疗组治疗后汉密顿抑郁量表评分改善,低于治疗前和对照组(P<0.05)。结论小脑顶核电刺激可减轻脑卒中抑郁症状,对患者情绪障碍的恢复有促进作用。     

小脑顶核电刺激合并高压氧治疗颅脑损伤

目的探讨小脑顶核电刺激合并高压氧治疗颅脑损伤恢复期患者的疗效。方法将颅脑损伤患者随机分为治疗组42例和对照组40例。治疗组接受小脑顶核电刺激并用高压氧治疗，对照组接受高压氧治疗，分别在治疗前后采用日常生活活动能力评分量表（ADL）进行功能评定，根据临床四级疗效标准进行疗效评定。结果治疗组治疗后ADL评分较前明显提高（P〈0．01），且与对照组相比差异有统计学意义（P〈0．05），治疗组总有效率80．95％明显高于对照组的52．22％（P＜0．05）。结论小脑顶核电刺激合并高压氧能有效提高高压氧对颅脑损伤恢复期患者的疗效。     

小脑顶核电刺激合并高压氧治疗颅脑损伤

目的探讨小脑顶核电刺激合并高压氧治疗颅脑损伤恢复期患者的疗效。方法将颅脑损伤患者随机分为治疗组42例和对照组40例。治疗组接受小脑顶核电刺激并用高压氧治疗,对照组接受高压氧治疗,分别在治疗前后采用日常生活活动能力评分量表(ADL)进行功能评定,根据临床四级疗效标准进行疗效评定。结果治疗组治疗后ADL评分较前明显提高(P<0.01),且与对照组相比差异有统计学意义(P<0.05),治疗组总有效率80.95%明显高于对照组的52.22%(P<0.05)。结论小脑顶核电刺激合并高压氧能有效提高高压氧对颅脑损伤恢复期患者的疗效。     

电刺激小脑顶核防治血管性痴呆的实验研究

目的探讨电刺激小脑顶核(FNS)对血管性痴呆(VD)的防治作用.方法采用反复低血压和双侧颈总动脉阻断法建立VD大鼠模型,双侧小脑顶核植入电极进行FNS,用跳台试验、程控穿梭箱试验和神经病理学检查评价FNS对VD大鼠的防治效果.结果反复全脑缺血前2 d给予FNS 1次或缺血后即刻给予FNS治疗7 d均可明显减轻脑缺血后2周大鼠的学习和记忆障碍(P＜0.01),并使脑缺血后大脑皮层和海马神经元丢失显著减少(P＜0.01).脑缺血11周后给予FNS治疗7 d,虽不能减轻脑缺血后大脑皮层和海马神经元的丢失P＞0.05),但可明显改善大鼠的学习和记忆障碍(P＜0.05).结论FNS对VD大鼠具有明确的防治效果,但减轻缺血神经元损害可能只是其防治作用的机制之一.     

小脑电刺激对脑梗塞患者抗凋亡蛋白的影响

目的:通过观察脑梗塞患者小脑顶核电刺激前后体内的抗凋亡蛋白sAPO-1/Fas及Bcl-2的含量变化,进一步探讨小脑顶核电刺激治疗脑梗塞的机制。方法:发病后3天内的急性脑梗塞病人40例,随机分为刺激组及对照组。采用SNSS评分表及ELISA方法测定小脑顶核电刺激前后的神经功能评分及血清、脑脊液中sAPO-1/Fas及Bcl-2含量。结果:(1)小脑顶核电刺激10天后的脑脊液sAPO-1/Fas含量较刺激前明显升高,也明显高于对照组;对血清sAPO-1/Fas含量也有一定的增高作用。(2)小脑顶核电刺激10天后的血清Bel-2含量均较入院时明显增高,并显著高于对照组;对脑脊液中的Bcl-2含量有一定的增高作用。(3)小脑顶核电刺激10天后的神经评分明显高于刺激前及对照组。结论:在脑梗塞急性期给予小脑顶核电刺激可明显改善神经功能评分、提高体内的抗凋亡蛋白sAPO-1/Fas及Bcl-2含量,并可能是小脑顶核电刺激治疗脑梗塞的机制之一。     

小脑顶核电刺激对脑外伤患者脑血流速度和颅内压的影响

目的　探讨小脑顶核电刺激对脑外伤患者脑血流速度和颅内压的影响。方法　选择 2 0例脑外伤患者 ,其中 7例行手术治疗。用小脑顶核电刺激方法对所有患者实施电刺激 ,应用经颅多普勒超声技术检测刺激前后大脑前、中、后动脉 (ACA ,MCA,PCA)血流速度。通过颅内压监护持续监测刺激前后颅内压的变化。结果　实施刺激后 10分钟 ,脑血流速度升高 ,2 0～ 30分钟达高峰。刺激前 ACA,MCA,PCA血流速度分别为 45 .5± 8.3cm/ s,5 3.6± 10 .2 cm / s和 36 .9± 8.4cm / s;刺激后分别为 6 0 .2± 9.6 cm/ s,6 7.2± 11.7cm/ s和 37.2± 8.6 cm/ s;ACA和MCA的血流速度在刺激后明显升高 (P <0 .0 5 )。 7例脑外伤患者小脑顶核电刺激前后颅内压无明显变化 (P>0 .0 5 )。结论　小脑顶核电刺激后可明显提高脑外伤患者颅内血流速度 ,改善脑循环 ,对颅内压变化无明显影响。     

Neuroprotective electrical stimulation of cerebellar fastigial nucleus attenuates expression of periinfarction depolarizing waves (PIDs) and inhibits cortical spreading depression

In rat, electrical stimulation of the cerebellar fastigial nucleus (FN) for 1 h reduces the volume of focal ischemic infarctions produced by occluding the middle cerebral artery (MCAO), even 10 days later. The mechanism by which this 'central neurogenic neuroprotection' salvages ischemic brain is not known but does not result from changes in cerebral perfusion. MCAO also triggers periodic periinfarction depolarizing waves (PIDs) in the ischemic penumbra, the territory of salvage. These may contribute to neuronal death and promote infarct expansion. Conceivably, FN stimulation, which can otherwise modify cortical excitability, may alter the development of PIDs. We investigated in anesthetized rats whether FN stimulation modifies PIDs expression and, if so, the threshold for evoking cortical spreading depression (CSD), a process sharing characteristics with PIDs and an index of cortical excitability. Stimulation of FN immediately or 72 h before MCAO decreased infarction volumes by approximately 45% (p<0.01), increased PID latency >10-fold, and decreased the number of PIDs by >50% (p<0.001). In normal rats, stimulation of FN increased the threshold current for eliciting CSD by 175% and slowed its propagation velocity by 35% (p<0.01 for each) immediately, but not 72 h, after FN stimulation. We conclude: FN stimulation elicits long-lasting suppression of PIDs in parallel with neuroprotection. However, PIDs suppression over time is unlikely to result from a major increase in cortical tolerance to depolarization and probably is not the principal mechanism of salvage.     

Local cholinergic mechanisms participate in the increase in cortical cerebral blood flow elicited by electrical stimulation of the fastigial nucleus in rat

We sought to determine whether the increase in regional cerebral blood flow (rCBF) elicited within the cerebral cortex (CX) by electrical stimulation of the fastigial nucleus (FN) of the cerebellum is: prevented by local application of the muscarinic cholinergic receptor antagonist, atropine and temporally correlated with a stimulus-locked release of acetylcholine (ACh) from the cortical surface. Rats were anesthetized, paralyzed, ventilated, with arterial blood gases controlled and arterial pressure maintained within the autoregulated range. Bilateral craniotomies were performed over a standardized region of the sensory motor CX and superfusion devices stereotaxically positioned on the cortical surface. Cortical surface temperature, as well as pH, pCO2 and pO2 of the solutions applied to the cortex were also carefully controlled. rCBF was measured in dissected regions of frontal (FCX), parietal (PCX), and occipital cortices (OCX), caudate nucleus (CN), and hippocampus (HIPP) by the Kety principle using [14C]iodoantipyrine as indicator. Resting rCBF (ml/100 g/min) in unoperated control animals ranged from 70 +/- 5 in HIPP to 95 +/- 7 in PCX and was unaffected by bilateral craniotomies and placement of superfusion devices containing Kreb's bicarbonate buffer (vehicle) on the cortical surface. Local application of atropine (ATR, 100 microM) to the right PCX via the superfusion device did not affect resting rCBF. With FN stimulation rCBF increased bilaterally and symmetrically in all areas up to 227% in PCX. ATR application attenuated by 59% the FN-elicited increase in rCBF on the ipsilateral frontoparietal CX, without affecting blood flow in adjacent structures. ATR did not affect cortical cerebrovasodilation produced by hypercarbia (arterial pCO2 = 59.0 +/- 1.4 mm Hg). FN-stimulation resulted in a small (22%) but significant (P less than 0.05, n = 9) reduction in the release of [3H]ACh from the cortical surface, while supramaximal depolarization with 55 mM K+ increased [3H]ACh release by 251%. These studies indicate that: increases in cortical rCBF elicited by FN stimulation, but not hypercarbia, are in large part mediated by local muscarinic cholinergic receptors; resting rCBF is not tonically affected by muscarinic receptor activation; and the release of ACh from the cortical surface is, in general, reduced during FN-stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Kainic acid administration in the fastigial nucleus produces differential cardiovascular effects in awake and anesthetized rats

Kainic acid was microinjected or microdialyzed into the rostral medial aspect of the fastigial nucleus to determine its effect on mean arterial pressure and heart rate. This was carried out in both the awake and the anesthetized (α-chloralose) rat. In awake animals, kainic acid elicited an initial phasic pressor response which was followed by a long-term elevation of mean arterial pressure that lasted for the duration of the experiment (2 h). Rats anesthetized with α-chloralose exhibited only a tonic depressor response. This converted to a pressor response as the rats began to emerge from anesthesia after 2 h. Both the awake and the anesthetized rats exhibited regular phasic changes in mean arterial pressure that was superimposed on the longer term changes in the mean arterial pressure. Similar results were obtained in both the microinjected and the microdialyzed animals. Thus, stimulation of the intrinsic fastigial neurons by kainic acid evokes an elevation of the mean arterial pressure in the awake rat. This is manifested as a decrease in pressure in the anesthetized animal. Thus, stimulation of the cardiovascular region of the fastigial nucleus can increase or decrease mean arterial pressure. It is possible that the direction of the change in mean arterial pressure is dependent on the level of afferent or intrinsic fastigial neural activity.     

Brief electrical stimulation of cerebellar fastigial nucleus conditions long-lasting salvage from focal cerebral ischemia: conditioned central neurogenic neuroprotection

The cerebellar fastigial nucleus (FN) was electrically stimulated for 1 h in anesthetized rats and the middle cerebral artery occluded at various times thereafter. Stimulation of the FN but not dentate nucleus reduced the volume of the focal infarction to 50%. Protection persisted for 10 but disappeared by 30 d. Intrinsic neuronal pathways which function to condition central neurogenic neuroprotection can protect the brain from ischemic injury by processes independent of cerebral blood flow.