猫局部脑缺血模型的建立和改进

本文探讨了O’Brien猫脑缺血模型的可靠性和可行性,采用新手术方法,经眶上缘入路,双极电凝和铜丝栓塞两种方法闭塞MCA。18只实验动物中,除1只死亡外,15/17在MCA分布区形成范围和部位基本一致的缺血性病理改变。闭塞侧脑组织含水量增加,体感诱发电位波幅显著降低。组织化学荧光观察证实电凝MCA可毁损动脉壁上的交感神经纤维,而铜丝栓塞可使其大致保持完整。后一方法较少影响植物神经对脑血管功能的调节作用,更接近人类脑梗塞后的病理改变。我们认为该模型可作为进一步研究缺血性脑血管病及神经对脑血管调节作用的理想动物模型。     

大鼠脑干缺血模型制备及早期超微结构观察

目的:制备脑干缺血动物模型并观察大鼠脑干缺血后早期组织学病理的超微结构。方法:应用两点电凝基底动脉的方法制作鼠脑干缺血动物模型。结果:病理学观察发现脑干缺血2小时即可出现超早期病理变化,并随时间的延长缺血性损害逐渐加重。结论:两点电凝基底动脉后可以造成稳定的脑干缺血,对急性脑干缺血的病理学研究有一定的价值。     

脑干听觉诱发电位对脑干缺血诊断价值的探讨

目的：探讨脑干听觉诱发电位对脑干缺血诊断价值。方法：对44例经颅多普勒检查（TCD）确定为椎基底动脉供血不足的眩晕患者（VBI组）进行脑干听觉诱发电位（BAEP）检查,并与52例经颅多普勒检查确定为脑血管痉挛的眩晕患者（对照组）脑干听觉诱发电位检查结果进行对照分析。结果：椎基底动脉供血不足的眩晕组BAEP异常率为52．27％,明显高于对照组（3．85％,P＜0．001）。VBI组BAEP各波潜伏期均长于对照组（P＜0．05）,BAEP的I波及V波波幅低于对照组（P＜0．05）。结论：脑干听觉诱发电位可作为评价脑干缺血及其程度的一个客观指标。     

海风藤对犬脑干缺血后细胞内钙含量和超微病理改变影响的研究

本研究选用犬基底动脉全段结扎脑干缺血模型，观察了海风藤对犬脑干缺血后脑组织细胞内钙含量和超微病理改变的影响，我们发现海风藤０．３ｇ／ｋｇ可明显降低犬脑干局灶性缺血后细胞内钙含量，改善缺血后神经元超微结构的损害，提示海风藤对脑干缺血具有保护作用。     

椎基底动脉缺血性卒中电生理方法早期诊断

本文系国内3个单位262例椎基底动脉缺血性脑卒中(TIA231例、梗塞31例)电生理研究的综合报道。采用脑干听觉和躯体感觉诱发电位、脑电地形图三种方法。TIA 的电生理异常发现和临床电生理前瞻性调查结果显示电生理方法对本病诊断有早期的乃至警告的意义。     

缺血性脑卒中急性期动脉溶栓治疗79例临床分析

缺血性脑卒中是由于脑动脉血管内血栓形成，栓塞或血液动力学的改变，造成相应供血区域脑组织缺血、缺氧，导致局限性脑组织缺血坏死，出现局灶性神经系统症状体征，自然预后差。[第一段]     

椎基底动脉短暂缺血性眩晕的脑干听觉诱发电位转颈试验研究

椎基底动脉短暂缺血性眩晕的脑干听觉诱发电位转颈试验研究邓远飞黄莘莘詹国华郑芷萍刘乃河椎基底动脉短暂缺血性眩晕（Ｖｅｒｔｅｂｒｏ－ｂａｓｉｌａｒｉｓｃｈｅｍｉｃｖｅｒｔｉｇｏ，ＶＢＩ－Ｖ）因体征轻微而临床诊断较为困难［１］。既往应用脑干听觉诱发电位（Ｂ...     

海风藤对犬脑干缺血后细胞内钙含量和超微病理改变影响的…

本研究选用犬基底动脉全段结扎脑缺血模型，观察了海风藤对犬脑干缺血后脑组织细胞内钙含量和超微病理改变的影响，我们发现海风藤０．３ｇ／ｋｇ，可明显降低犬脑干避灶性的因后细胞内钙含量，改善缺血后神经超微结构的损害，提示海风藤对脑干缺血具有保护作用。     

中老年眩晕的脑干听觉诱发电位研究

椎一基底动脉缺血性眩晕的脑干听觉诱发电位(BAEP)研究已有报道(游国雄,中华神经精神科杂志,1988),但对无其它椎一基底动脉缺血症状和体征的单纯性眩晕,恃別是中老年眩晕患者的BAEP研究尚不多见。本文对58例45岁以上的眩晕患者进行了DAEP检查和分析,报道如下:     

后循环缺血与眩晕

后循环又称椎基底动脉系统，由椎动脉、基底动脉和大脑后动脉（posterior cerebral artery，PCA）组成，主要向脑干、小脑、丘脑、枕叶、部分颞叶等结构供血。后循环缺血（posterior circulation ischemia,PCI）是常见的缺血性脑血管病。与前循环缺血一样，PCI也可按缺血程度和持续时间的不同分为短暂性脑缺血发作（transient ischemic attack,TIA）和脑梗死。其同义词包括椎基底动脉系统缺血、后循环TIA和脑梗死、椎基底动脉疾病、椎基底动脉血栓栓塞性疾病。     

Toxin-induced inhibition of nerve terminal growth

An in vivo model to permit the quantitative study of the effects of neurotoxins upon nerve terminal growth has been developed and used in practice to test the ability of methyl mercury chloride, leptophos, ethanol, morphine and acrylamide to inhibit nerve terminal growth. The model utilized the sympathetic innervation of rat submaxillary salivary glands. Nerve terminal growth was induced following crush of the sympathetic axons which innervated the submaxillary gland and quantified by measuring the return towards normal values of the density of sympathetic innervation in denervated glands. The nerve crush reduced the density of sympathetic innervation to a very low value but nerve growth began within 9 days and was sufficient to restore the density of innervation to approximately 70% of normal values in three weeks. Restoration of the original density of innervation took between 40 and 60 days. The major advantage of the model is its ability to detect and quantify 30% - 100% inhibition of nerve terminal growth. The major disadvantage is the time required to measure the density of sympathetic innervation though this can be minimized in a number of ways which are discussed. Acrylamide inhibited sympathetic nerve terminal growth without causing degeneration of sympathetic neurones. This demonstrates that toxins can selectively inhibit nerve terminal growth which will result in altered neuronal circuitry and abnormal function. Methyl mercury chloride, leptophos, ethanol and morphine did not inhibit sympathetic nerve terminal growth.     

Autoimmune disease and innervation

In the decades before 1987, most of the research devoted to neuronal innervation was carried out in primary and secondary lymphoid organs at very different locations. This was an important period in order to understand hard-wiring of immune organs in physiology. Between 1988 and 1997, with the appearance of specific antibodies against neuronal markers, innervation was studied in inflamed tissue of patients and of animals with autoimmune diseases. This period clearly revealed that nerve fibers of, both, the sympathetic and sensory nervous system are altered, but only small amounts of tissue have been investigated by qualitative but not quantitative techniques. Between 1998 and 2007, with the understanding that sympathetic and sensory neurotransmitters might play opposite roles in inflammation, nerve fibers of the different nervous systems have been studied in parallel using quantitative techniques. These studies have been carried out in a large number of patients with long-standing autoimmune diseases. It turned out that sympathetic nerve fibers are lost in chronically inflamed tissue, while substance P-positive nerve fibers sprout into the inflamed area. This might be important because high concentrations of sympathetic neurotransmitters are antiinflammatory whereas substance P has a proinflammatory role. The first challenge for future research is the determination of innervation in the early human autoimmune disease. The second challenge is the identification of reasons for the differential loss of sympathetic in relation to sensory nerve fibers. It might well be that nerve repellent factors specific for the sympathetic nerve fiber might play an important role for the observed differential loss. Whether, or not, a therapy can be based on these findings remains to be established.     

A dual effect of sympathetic nerve stimulation on jaw muscle spindles

In anaesthetized and paralyzed rabbits, electrical stimulation of the cervical sympathetic nerve at physiological frequencies induces in jaw muscle spindle afferents a short-latency decrease or suppression of discharge. This effect is very stereotyped in pattern and is attributed to direct sympathetic innervation of spindles. It is mediated by preganglionic S1-S2 sympathetic fiber groups. A longer-latency facilitatory effect follows, probably vasomotor in origin and mediated by S3-S4 groups. Both responses are eliminated by administration of alpha-adrenergic blocking agents. The latencies, patterns, thresholds, durations and reproducibility of these responses have been studied and the mechanisms possibly involved are discussed.     

Sciatic nerve stimulation increases the degree of histopathological damage in lumbosacral segments after short lasting spinal cord ischemia in rabbit

To characterize the influence of primary afferent activation on the development of histopathological changes in the spinal cord after reversible ischemia, the left sciatic nerve was stimulated at the intensity of myelinated fibers before, during and for 1 h after 10 min of abdominal aortic ligation in halothane anesthetized rabbits. In control animals, only 10 min of spinal cord ischemia or sciatic nerve stimulation was employed. One hour after reperfusion all animals were perfusion fixed with 4% paraformaldehyde. Histopathological analysis using the suppressive Nauta method revealed significantly higher number of argyrophilic neurons in dorsal horns and in the intermediate zone in animals in which spinal cord ischemia was combined with sciatic nerve stimulation in comparison with the animals with spinal cord ischemia, but without stimulation. These histopathological changes corresponded with signs of irreversible damage analyzed on the ultrastructural level. Stimulation of sciatic nerve, but without ischemia did not evoke any detectable neuronal changes. The data from the present study suggest that increased activity of spinal cord neurons evoked by peripheral nerve stimulation can be an important factor in determining the extent of irreversible damage after short lasting ischemia.     

Sympathetic innervation of the upper and lower regions of the uterus and cervix in the rat have different origins and routes

The origins and routes of the postganglionic sympathetic nerve supply to the upper and lower uterus and to the cervix were investigated in the rat by using denervation procedures combined with immunohistochemistry and retrograde tracing. The sympathetic nerve fibers of the upper part of the uterus arise from the ovarian plexus nerve. They mainly originate (90%) from neurons of the suprarenal ganglia (SRG) and of the T10 to L3 ganglia of the paravertebral sympathetic chain. Fluoro-Gold injections into different regions of the upper uterus showed that the SRG neurons mainly provide innervation to the tubal extremity (52%) rather than to the uterine portion below this area (26%). Very few neurons of the celiac ganglion or the aorticorenal ganglia participated in this innervation. Most of the sympathetic innervation of the lower uterus and the cervix (90%) originates from neurons of the paravertebral ganglia T13 to S2, principally at the L2–L4 levels. By using immunocytochemistry, we show that very few tyrosine hydroxylase–positive neurons of the pelvic plexus project to these areas, where they represent only 3% of the sympathetic nerve supply. Again, very few neurons of the inferior mesenteric ganglion (IMG) supply the lower uterus and the cervix. The comparison between retrograde tracing experiments in intact animals and after the removal of the IMG shows that very few sympathetic postganglionic axons from the paravertebral chain pass through the IMG to reach the lower uterus and the cervix. In contrast, these axons mainly project to splanchnic nerves bypassing the IMG to connect with the hypogastric nerves. In addition, some axons supplying the lower uterus follow the superior vesical arteries and then reach the organ. Taken together, these results show that the upper region of the uterus receives a sympathetic innervation that is different in origin and route from that of the lower uterus and the cervix. Such a marked region-specific innervation suggests that nerve control of the myometrial activity may be functionally different between the oviduct and the cervical ends of the uterus. J. Comp. Neurol. 399:403–412, 1998. © 1998 Wiley-Liss, Inc.     

Overexpression of nerve growth factor in skin causes preferential increases among innervation to specific sensory targets

The impact of increased levels of skin-derived nerve growth factor (NGF) neurotrophin on sensory and sympathetic innervation to the mouse mystacial pad and postero-orbital vibrissae was determined. Consistent with an approximate doubling of neuron number in trigeminal and superior cervical ganglia, many components of the sensory and sympathetic innervation were substantially enhanced. Although the increased number of neurons raised the possibility that all types of innervation were increased, immunohistochemical analysis indicated that enhanced NGF production had a differential effect upon sensory innervation, primarily increasing unmyelinated innervation. This increased innervation occurred in specific locations known to be innervated by small, unmyelinated fibers, suggesting that NGF modulated sensory innervation density, but not targeting. In contrast, sympathetic innervation was not only increased but also was distributed to some aberrant locations. In the intervibrissal fur of the mystacial pad, both the number of sensory axons and branches appeared increased, whereas in vibrissal follicle sinus complexes, only branching increased. In some areas, sensory ending density was lower than expected based upon the size of the source nerve bundles suggesting that many axons and branches were surviving but failing to form functional endings. Furthermore, the immunochemical profile of innervation was altered in some sensory populations as demonstrated by the coexistence of RT-97 neurofilament labeling in calcitonin gene-related peptide (CGRP) positive axons, by the loss of substance P colocalization in some CGRP axons, and by an absence of neuropeptide Y labeling in tyrosine hydroxylase positive sympathetic axons. Collectively, these results indicate that the NGF mediated increase in neuron number may be selective for particular sets of innervation and that increases among some populations may result from phenotypic switching. J. Comp. Neurol. 387:489–506, 1997. © 1997 Wiley-Liss, Inc.     

The allocation of nerve fibres to the anterior eye segment and peripheral ganglia of rats. II. The sympathetic innervation

The sympathetic innervation of the peripheral ganglia related to the eye, i.e. the trigeminal ganglion, the ciliary ganglion and the pterygopalatine ganglion, and of the anterior eye segment was studied in rats. Selective labelling of sympathetic nerves was obtained by means of injection of [3H]leucine into the superior cervical ganglion. Bundles of sympathetic nerve fibres were found in the trigeminal ganglion and the pterygopalatine ganglion but were absent in the ciliary ganglion. In addition individual sympathetic nerve fibres, which may have contacts with trigeminal ganglion cells, were found between the ganglion cell bodies all over the trigeminal ganglion indicating a sympathetic innervation of this ganglion. In the anterior eye segment, there appeared to be a sympathetic innervation of the ciliary cleft, the ciliary body and the iris. Within the ciliary body sympathetic nerve fibres innervate the central stroma and the stroma of the ciliary processes. Labelled sympathetic nerve fibres were also observed in the stroma of the iris and were most abundant in its periphery. Most sympathetic fibres reach the iris and ciliary body by way of the base of the ciliary body. Only few sympathetic fibres are present in the ciliary cleft. No sympathetic innervation of the cornea was found.     

Trigeminal Neuralgia Caused by an Anomalous Posterior Inferior Cerebellar Artery from the Primitive Trigeminal Artery: Case Report

A 61-year-old woman presented with typical trigeminal neuralgia (TN), caused by an aberrant posterior inferior cerebellar artery (PICA) associated with the primitive trigeminal artery (PTA). Magnetic resonance angiography and digital subtraction angiography clearly showed an anomalous artery directly originating from the PTA and coursing into the PICA territory at the cerebellum. During microvascular decompression (MVD), we confirmed and decompressed vascular compression of the trigeminal nerve by this anomalous, PICA-variant type of PTA. The PTA did not conflict with the trigeminal nerve, and the anomalous PICA only compressed the caudolateral part of the trigeminal nerve, without the more common compression at its root entry zone. This case is informative due not only to its very unusual angioanatomical variation but also to its helpfulness for surgeons preparing a MVD for a TN associated with such a rare vascular anomaly.     

小脑下后动脉切断的实验研究

目的研究切断一侧小脑下后动脉（ＰＩＣＡ）的可行性及在增加延髓后区术野显露方面的作用。方法将ＰＩＣＡ分为４段（ＰＩＣＡ１－ＰＩＣＡ４），自ＰＩＣＡ１－ＰＩＣＡ３逐段切断实验。结果ＰＩＣＡ１、ＰＩ－ＣＡ２切断后果严重，ＰＩＣＡ３切断不仅安全可行，且能充分显露自同侧内耳门－导水管下端－对侧四室壁－枕大孔这一区域，无需切开小脑蚓部。结论ＰＩＣＡ１、ＰＩＣＡ２切断后果严重，ＰＩＣＡ３切断安全可行且具有较大的临床意义，为临床开辟了新的手术入路。     

小脑动脉的临床解剖探讨

目的：为神经外科临床提供解剖学资料。方法：手术显微镜下观察５０例成人脑标本小脑动脉的起始、行径、主要分支、穿动脉及大致分布，检查各小脑动脉与出入脑干的颅神经的接触关系。结果：５０例人脑有小脑下后动脉（ＰＩＣＡ）９４支，小脑下前动脉（ＡＩＣＡ）９７支和小脑上动脉（ＳＣＡ）１１２支。２侧ＰＩＣＡ和１２侧ＳＣＡ接触三叉神经根，２侧ＡＩＣＡ接触面神经根，动脉与神经根接触多形成压迹。结论：小脑动脉的局部解剖有助于神经外科医生在颅后窝手术时，对这些动脉尤其是行程可能有变异的动脉及穿支要特别谨慎，避免损伤，并保护与小脑动脉关系密切的脑神经根；对某些脑干血管综合征患者及某些三叉神经痛、面肌痉挛患者采取相应的治疗。