经颅电刺激运动诱发电位术中监测预防脊髓缺血性损伤的实验研究

目的探讨术中经颅电刺激运动诱发电位(TceMEP)监测在脊髓髓内肿瘤切除术中对脊髓缺血性损伤的保护作用。方法将16只实验兔随机分为4组,4只/组;对照组用来确定TceMEP的最佳刺激强度,术前连续记录3h(30min/次),并于术中、术后不同时间点记录以排除麻醉、手术对诱发电位的影响;另3组分别结扎3、4、5根腰动脉,血管结扎后5min内记录TceMEP,并行运动功能评分,2d后取标本行苏木精-伊红染色。结果TceMEP波幅对缺血性脊髓损伤敏感;血管结扎后,可见波幅先降低后逐渐恢复,5min内均趋于稳定。TceMEP波幅变化与麻醉清醒后运动功能、结扎2d后运动功能和病理损伤程度均呈正相关,r分别为0.977、0.933、0.971,差异均有统计学意义(P0.01)。结论术中TceMEP可敏感地反映缺血性脊髓损伤,可在脊髓缺血可逆期内发现缺血性损伤,有助于及时采取措施,预防不可逆性脊髓损伤的发生。     

皮层体感诱发电位在不同水平脊髓缺血中的变化

目的 为术中应用皮层体感诱发电位(CSEP)监测脊髓功能,预防术后运动功能障碍提供理论依据. 方法 33只新西兰大白兔采用随机数字表法分为6组,对照组8只用于排除麻醉和手术对诱发电位的影响,余25只根据结扎左肾动脉和动脉分叉间节段性脊髓供血动脉的条数分为5组(n=5),分别为1～5根组.记录各组动物麻醉后基线诱发电位,血管结扎后急性期诱发电位,结扎后30 min、2 d后诱发电位.动物麻醉清醒后、血管结扎后2 d时进行运动功能评分,并取缺血中心区标本行HE染色. 结果 潜伏期对缺血性损伤不敏感,实验组与对照组差异无统计学意义(P>O.05);波幅变化复杂,对运动功能特异性差,2、3、4根组均观察到急性期波幅先降低又逐渐恢复趋势,波幅的变化可以反映脊髓的病理损害程度和运动功能. 结论 缺血急性期CSEP波幅变化复杂,对运动功能特异性差,波形记录的信号需要平均化过程,造成结果 解释的延迟,术中应联合运动诱发电位对脊髓功能进行监测.     

脊髓运动诱发电位监测在手术中的应用

目的 评价脊髓运动诱发电位监测在脊柱脊髓手术中的作用.方法 通过连续短脉冲头皮电刺激,应用硬膜外电极于脊髓记录18例脊柱脊髓疾病患者手术过程中的运动诱发电位.根据日本整形外科协会(JOA)评分标准对患者手术前后神经功能进行评价.结果 以手术中首次记录到的脊髓运动诱发电位D1波波幅和潜伏期作为参照值,8例脊柱侧弯患者施行脊柱矫形手术过程中记录到的脊髓运动诱发电位D1波波幅和潜伏期均无异常变化;10例行椎管内及脊髓手术患者,手术中脊髓运动诱发电位D1波波形改变、波幅降低,改变手术方向或经短暂休息后恢复正常.根据JOA评分,手术后所有患者感觉和运动功能均较手术前明显改善,差异有统计学意义(Z=-2.646,P=0.008;Z=-2.828,P=0.005).结论 手术中脊髓运动诱发电位监测可及时、客观地反映神经功能,有效避免手术中神经损伤及手术后神经功能障碍.在监测过程中,头皮电刺激记录到的脊髓运动诱发电位D1波波形清晰、稳定,且不受外界因素的影响.     

电刺激运动诱发电位监护在脊柱脊髓手术中的应用

目的观察运动诱发电位在脊柱脊髓手术监护中的应用效果。方法对30例脊柱脊髓手术患者采用经颅电刺激-四肢肌记录肌活动电位，行术中脊髓机能监测，其中对采用经颅电刺激-四肢肌记录无效者，配合经脊髓硬膜外刺激-四肢肌记录肌活动电位。结果30例采用经颅电刺激-四肢肌记录方法，其中26例于术中和术后都记录到了正常的运动诱发电位波形。其余4例改为使用经脊髓硬膜外刺激-四肢肌记录方法后，共29例患者的运动诱发电位获得记录。结论采用经颅电刺激，并配合经脊髓硬膜外刺激-四肢肌记录肌活动电位，使术中对脊髓内部运动传导通路机能监测的有效率得到了提高。     

脊髓运动诱发电位在脊髓肿瘤手术中的监测应用

目的探讨脊髓运动诱发电位(SCMEP)在脊髓肿瘤手术中监测的应用价值.方法采用硬膜外电极在椎管内直接刺激脊髓记录脊髓运动诱发电位(SCMEP)监测脊髓肿瘤手术,并对17例肿瘤患者的手术监测的记录结果进行回顾性分析.结果SCMEP由于病变部位及性质、刺激电极与记录电极间的距离不同,波幅及潜伏期的差异较大,电极安放后与手术结束时的结果个体对照,相差不显著(P=0.083;P=0.387).7例术中波幅降低超过预警值20%,5例经短暂休息或改变手术方向后,波幅恢复正常.结论SCMEP的波幅变化是提示脊髓损伤的可靠性灵敏指标,对辅助医生进行手术安全操作,缩短手术时间,提高手术质量,减少术后神经功能障碍起到重要作用.     

颅内前循环动脉瘤术中诱发电位监测效果评估

目的 探讨全静脉麻醉下经颅电刺激运动诱发电位(TES-MEPs)联合体感诱发电位(SEP)监测颅内前循环动脉瘤手术及预防缺血性卒中的应用价值.方法 47例颅内动脉瘤夹闭手术患者,术中行SEP和TES-MEPs联合监测,以神经功能检查作为评价指标,比较术前和术后神经功能的改变和诱发电位变化之间的关系.结果 43例神经功能未见显著改变,4例神经功能出现不同程度下降,其中3例MEP及SEP同时出现波幅下降＞50%或消失,且手术结束时未恢复至基线水平,与术后神经功能障碍发生具有一致性.结论 术中监测指标的改变可较早地获得脑缺血的证据,联合SEP与MEP监测有利于降低术后缺血性脑卒中的发生.     

不完全性脊髓缺血损伤动物模型的建立及价值

目的 探讨不完全性脊髓缺血损伤动物模型的建立方法,为不完全性脊髓缺血损伤机制研究提供理想的载体. 方法 24只新西兰大白兔按照随机数字表法分为对照组及3根组、4根组,每组8只.对照组用于排除麻醉和手术对运动诱发电位的影响;3根组、4根组分别结扎3根、4根腰动脉.各组麻醉后记录基线诱发电位,手术/结扎后30 min、2d、7d记录诱发电位;麻醉清醒后、手术/结扎后2d、7d进行运动功能评分;手术/结扎后7d后取缺血中心区标本进行HE染色,镜下观察. 结果 3根组动物结扎后30 min诱发电位波幅与对照组比较差异有统计学意义(P＜0.05),结扎后2d、7d与对照组比较差异无统计学意义(P＞0.05);4根组动物结扎后30 min、2d、7d3个时间点诱发电位波幅与对照组比较差异均有统计学意义(P＜0.05).3组动物手术/结扎后30min、2d、7d3个时间点的潜伏期与对照组比较差异均无统计学意义(P＞0.05).各组动物运动功能评分结果与诱发电位波幅变化一致. 结论 结扎3根腰动脉可以造成可逆性不完全性脊髓缺血损伤,结扎4根腰动脉可以造成不可逆性不完全性脊髓缺血损伤.     

神经电生理监测技术在脊髓髓内肿瘤切除术中的应用

目的探讨神经电生理技术联合监测对预防脊髓髓内肿瘤切除术中脊髓神经功能损伤的意义。方法回顾性分析26例脊髓髓内肿瘤的病例资料,均行手术切除治疗,术中应用体感诱发电位(SEP-P40)和运动诱发电位(MEP-ABP)监测。结果术后2周随访脊髓神经功能JOA评分改善10例,不变13例,下降3例。JOA评分改善者,手术前后SEP-P40潜伏期、波幅改变及MEP-ABP潜伏期改变均具有统计学意义(P0.01)。JOA评分不变者,手术前后SEP-P40潜伏期、波幅改变及MEP-ABP潜伏期改变均无统计学意义(P0.05)。结论脊髓髓内肿瘤切除术中使用神经电生理联合监测能及时反映神经功能变化,术中电生理指标变化与病人术后神经功能改变一致。联合监测可提高术中操作的安全性,能避免或减少并发症。     

脊髓手术中诱发电位监测

本文介绍了近年来发展的经颅电或磁刺激运动诱发电位、多点记录的躯体感觉诱发电位、脊髓诱发电位、诱发肌电及神经干诱发电位等脊髓传导通路的监测技术;并对术中诱发电位监测的目的、脊髓病变手术中诱发电位的改变作了综述。其中以经颅电刺激运动诱发电位和多点记录的体感诱发电位较适合我国国情。     

术中神经电生理监测在椎管肿瘤手术中的应用

脊髓肿瘤患者在手术过程中常常会因手术机械性损伤直接导致的脊髓损害和脊髓缺血间接导致的脊髓损害而加重原有的脊髓、神经损伤或造成新的医源性损伤,严重者可导致感觉、运动和大小便功能永久性障碍。因此,在脊髓手术中避免对脊髓造成损伤至关重要。近年来,随着神经电生理监测技术的发展,在全麻脊髓肿瘤手术中开展神经电生理监测以保护脊髓传导通路的完整性,术后躯体感觉、运动功能,尿道及肛门括约肌功能的正常已取得了很好的效果。     

Deteriorating stroke model: histopathology, edema, and eicosanoid changes following spinal cord ischemia in rabbits

Secondary motor dysfunction is often observed following ischemic episodes in the central nervous system. To study potential mechanisms of postischemic motor deterioration, we developed a rabbit spinal cord ischemia model that has characteristics similar to the clinical condition termed deteriorating stroke. In this model, 70% of the rabbits regained substantial motor function by 4 hours after complete hindlimb paralysis during lumbar spinal cord ischemia; however, over the next 20 hours motor function steadily declined to the point where only 30% of the rabbits had minimal hopping function. The role of eicosanoids in spinal cord ischemia was studied by radioimmunoassay of several prostaglandins (6-keto-PGF1 alpha, PGE2, and TxB2) in the spinal cord. After 5 minutes of reperfusion, TxB2 levels were markedly elevated (p less than 0.05) while 6-keto-PGF1 alpha levels did not change. The TxB2:6-keto-PGF1 alpha ratio was also significantly increased. After 30 minutes of reperfusion, PGE2 levels were also elevated (p less than 0.05). Tissue edema measured by microgravimetry was also increased after 30 minutes of reperfusion in both gray and white matter. By 4 hours of reperfusion, rabbits regained near-normal hindlimb motor function while PGE2, 6-keto-PGF1 alpha, TxB2, and tissue water content were back to normal. However, by 18 hours of reperfusion, when hindlimb function was deteriorating, TxB2 levels were elevated again, and edema in gray and white matter was increased as was the number of necrotic neurons observed by light microscopy. These results suggest that the secondary deterioration of motor neurologic function was due to the excess formation of TxA2 primarily in the late reperfusion phase. However, further studies are necessary to elucidate the relation of TxA2 with ischemic neural injury.     

Neuroprotective effects of infliximab in experimental spinal cord ischemic injury

Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia–reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin–eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups (p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups (p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant (p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model.     

Epidural perfusion cooling protects against spinal cord ischemia in rabbits

The protective effect of regional epidural spinal cord cooling was evaluated in a rabbit spinal cord ischemia model. Hypothermia was performed by the continual perfusion of 2–4°C cold saline in the epidural space around the ischemic lumbar segments, 4 min before and during ischemia. The spinal cord was deeply hypothermic (21°C) throughout the whole ischemie period. Ischemia was induced by the occlusion of the abdominal aorta for 40 min under normothermic or hypothermie conditions. Recovery of motor and sensory functions, spinal cord-evoked potentials, and motor-evoked potentials were then evaluated up to 24 h postischemia. After this period, choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were measured, in particular, zones of the lumbar spinal cord. AChE was also investigated histochemically. Animals in the normothermic group displayed fully developed spastic paraplegia with near complete loss of spinal somatosensory and motor-evoked potentials. AChE histochemistry showed extensive necrotic changes affecting lumbosacral gray matter. These changes corresponding with the pronounced losses of ChAT and AChE activities indicated irreversible injury of the spinal cord. In contrast, after hypothermic ischemia, animals survived without any sign of neurological impairment with almost full recovery of the spinal cord-evoked potentials. ChAT and AChE activities in the gray matter showed near control values corresponding with histochemical analysis of fully preserved gray matter. Hypothermia under the present experimental conditions efficiently protected the spinal cord against ischemic injury.     

Delayed selective motor neuron death and Fas antigen induction after spinal cord ischemia in rabbits

The mechanism of spinal cord injury has been thought to be related with tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model for spinal cord ischemia. Using this model, cell damage was histologically analyzed. Detection of ladders of oligonucleosomal DNA fragment was investigated with gel electrophoresis up to 7 days of the reperfusion. Time course expression of Fas antigen, identified as a apoptosis-regulating molecules, was also assessed in rabbit spinal cord following transient ischemia. Spinal cord sections from animals sacrificed at 8 h, 1 day, 2 days, and 7 days following 15-min ischemia were immunohistochemically evaluated using monoclonal antibodies for Fas antigen. Following 15-min ischemia, the majority of motor neuron showed selective cell death at 7 days of reperfusion. Typical ladders of oligonucleosomal DNA fragments were detected at 2 days of reperfusion. Immunoreactivity of Fas antigen were induced at 8 h to 1 day of reperfusion selectively in motor neuron cells. The expression of Fas antigen may be related to the activation of apoptosis signal in motor neuron cells after spinal cord ischemia in rabbits.     

腺苷A1受体激动剂对缺血损伤的兔脊髓神经元凋亡的影响

目的观察腺苷A1受体激动剂对脊髓缺血性损伤后的神经元凋亡的影响。方法建立兔脊髓缺血模型,给予腺苷A1受体激动剂(CPA),观察兔神经功能恢复,通过病理切片,计算脊髓前角正常神经元,再应用免疫荧光染色检测BCL-2表达水平,western-blot的方法观察caspase3、caspase9、BCL-2、BCL-X1、BAX、BAD表达水平。结果与DMSO组相比,CPA组兔神经功能明显改善。caspase3、caspase9、BCL-2、BCL-X1表达水平显著高于DMSO组,而BAX、BAD表达水平则明显降低。结论腺苷A1受体激动剂可能通过抑制神经元凋亡对脊髓缺血损伤发挥保护作用。     

缺血预适应后脊髓区域血流的改变及其对脊髓功能的保护作用

目的：探讨缺血预适应对脊髓区域血流的影响及其对脊髓功能的保护作用。方法：采用放射介入球囊栓塞方法建立脊髓缺血动物模型，氢去除电极测定脊髓区域血流，脊髓诱发电位监测脊髓功能，研究缺血预适应对脊髓缺血的保护作用。结果：缺血预适应５分钟后，脊髓局部区域血流升高，是脊髓诱发电位改变的直接原因；而脊髓区域血流的改变，可能与缺血预适后，儿茶酚胺类神经递质含量轻度升高有关。脊髓不可逆缺血损害后，单胺类递质（ＮＥ，ＤＡ，５－ＨＴ）的严重升高，将造成脊髓血管痉挛、内皮细胞裂隙、多灶出血、坏死，而使脊髓功能受损。脊髓区域血流与脊髓功能的改变密切相关；缺血预适应后，脊髓区域血流的轻度升高以及再次不可逆缺血（３０分钟缺血）后脊髓区域血流的明显改善，是缺血预适应对脊髓功能保护作用的直接原因。结论：缺血预适应可改变脊髓区域血流，增加长时间不可逆缺血后脊髓区域血流并对不可逆脊髓缺血后的脊髓功能损害有明显而确定的保护作用。     

Effect of protein kinase C modulation on outcome of experimental CNS ischemia

Protein kinase C (PKC) is an important intracellular regulator, and its activity may play a central role in the modulation of neuronal ischemic damage. Staurosporine and the compound H-7 are potent in vitro inhibitors of PKC, and 1,2-oleoylacetylglycerol (OAG) is an effective activator. We administered these compounds through a spinal subarachnoid catheter and demonstrated in vivo alteration of spinal cord PKC activity. We then tested the effects of altering PKC activity in a well-established rabbit model of reversible spinal cord ischemia. Animals within each experimental group were subjected to a range of spinal cord ischemic durations by temporary occlusion of the infrarenal abdominal aorta. Compared to control, both staurosporine and H-7 significantly shortened the duration of ischemia that the animals could tolerate, without developing permanent paraplegia. OAG resulted in an insignificant lengthening of the ischemic duration that the animals could withstand. The worsening of ischemic outcome by PKC inhibitors suggests that the enzyme is important for maintaining neurologic function under ischemic conditions, possibly secondary to modulation of intracellular calcium levels.     

Phenothiazines reduce ischemic damage to the central nervous system

We found substantial alterations in reactions catalyzed by calcium/phospholipid-dependent and calcium/calmodulin-dependent protein kinases during CNS ischemia which suggested that phenothiazines, drugs capable of inhibiting these reactions, might reduce neurologic damage. To test this hypothesis, we used chlorpromazine and trifluoperazine. Both drugs reduced neurologic function deficits relative to controls in a rabbit multiple cerebral embolism model and a rabbit spinal cord ischemia model. Chlorpromazine was effective despite reduction of blood pressure, and trifluoperazine did not alter blood pressure. These findings suggest that phenothiazines may be useful for preserving neurologic function when administered shortly after the onset of CNS ischemia.     

丹参酮IIa拮抗脊髓缺血再灌注损伤：干预谷氨酸释放的上游因素

目的：探讨丹参酮调控谷氨酸转运体功能对脊髓缺血再灌注损伤的作用。方法：88只SD 大鼠结扎腹主动脉,制作脊髓缺血再灌注损伤模型。按随机数字表法将动物分为假手术组（n=8）,模型组（n=40）和丹参酮组（n=40）。分别在脊髓缺血再灌注损伤后0.5h、1h、4h、8h、12h相应时点检测各组谷氨酸转运体功能和Na+-K+−ATP酶活性。结果： ①大鼠脊髓组织谷氨酸转运体功能及Na+-K+−ATP酶活性在脊髓缺血再灌注损伤后0.5h后开始下降,4h后降到最低点,其后活性逐渐恢复,但12h后仍未及正常水平。②丹参酮组各观测点脊髓组织谷氨酸转运体功能及Na+-K+−ATP酶活性均较其它两组高。结论：①大鼠脊髓缺血再灌注损伤时脊髓谷氨酸转运体功能和Na+-K+−ATP酶活性均下降;②丹参酮可能通过保护脊髓谷氨酸转运体功能和Na+-K+−ATP酶活性的下降,从而减轻大鼠脊髓缺血再灌注损伤。     

Free and peptide-bound amino acids as indicators of ischemic damage of the rabbit spinal cord

The concentrations of free and peptide-bound amino acids aspartate (Asp), glutamate (Glu), glycine (Gly) and gamma-aminobutyric acid (GABA) were studied following ischemia and recirculation in the ventral and dorsal gray matter of the rabbit spinal cord. No changes in the concentration of amino acids following ten minutes (min) of ischemia and four days of recovery were found. The most significant change after 20 min, and especially 40 min, of ischemia was a decrease in free Asp and GABA levels in both parts of the gray matter. The relatively greater decrease in the concentration of free amino acids in the ventral horns corresponds with the greater morphological damage to this part of spinal cord following ischemia. Following 40 min of ischemia and recirculation decrease in peptide-bound Glu in the ventral horns and Asp and Glu in the dorsal horns was found.