Substantia nigra damage induced by ischemia in hyperglycemic rats

Summary Preischemic hyperglycemia induced by feeding or glucose infusion worsens the brain damage and the clinical outcome following ischemia of a given duration and density, and characteristically causes postischemic seizure activity. Light microscopy has previously showed that, in the rat, transient hyperglycemic ischemia induced by bilateral carotid occlusion in combination with arterial hypotension causes a uni- or bilateral lesion in the pars reticulata of the substantia nigra. Since this region has a central role in preventing seizure discharges the present study was carried out to determine the ultrastructural characteristics of this lesion. In rats with 10 min of transient hyperglycemic ischemia followed by recirculation for 1 to 18 h, the pars reticulata of the substantia nigra showed signs of status spongiosus, as well as extensive nerve cell alterations. These changes were observed after all recovery periods studied. The spongiotic appearance was mainly caused by swelling of dendrites and, to a lesser degree, by astrocytic swelling. The dendrites were expanded at all recovery times but the severity increased during the later periods of recirculation. These swollen dendrites contained severely expanded mitochondrias and endoplasmic reticulum. The cytoskeletal elements showed disordered lining of microtubules. Two major types of nerve cell alterations were present: a pale and a dark variety. The pale type was the most frequent cell alteration. It occurred in all experimental groups and at all time points. Redistribution of the nuclear chromatin and of cytoplasmic organelles as well as swelling of the same type as in the dendrites were the essential changes. The dark neurons were much fewer in number and occupied a peripheral position in the pars reticulata. Astrocytic foot processes appeared to be dilated around the dark neurons. Swelling of astrocyte processes was most pronounced in the 1 h recovery animals. Both types of neurons showed severe mitochondrial alterations of the type observed in dendrites. Occasionally, mitochondrial alterations were found in astrocytic processes as well. Blood vessel alterations were lacking. Previous studies have shown that in this model of ischemia the substantia nigra has a relatively well-preserved blood perfusion. In view of this the extensive histopathological lesions are surprising. We speculate that the lesions primarily involve excitotoxic damage to dendrites, with pronounced lactic acidosis playing a contributory role in causing axonal and glial pathology as well.Supported by grants from the Swedish Medical Research Council (project 12X-03020 and project 14X-263) and from the U.S. Public Health Service via the N.I.H. (grant No. 5 RO1 NS07838)     

The protective effect of vitamin E on cerebral ischemia

Using the "canine model of the completely ischemic brain regulated with a perfusion method," the effects on cerebral ischemia of vitamin E, which is known to act as an antioxidant, were investigated. After pretreatment with vitamin E by oral or intravenous administration, cerebral blood flow was reduced to 1/10th the normal state and, 1 hour later, allowed to return to normal. Subsequent changes in electrical activity were observed, and the effects of vitamin E were evaluated. In the control group, no recovery of electrical activity was seen. In the groups given vitamin E, the recovery time was significantly shortened in the dogs given 30 mg/kg of vitamin E intravenously. Furthermore, in the groups treated with vitamin E, distinct recovery of electroencephalographic potentials at 3 hours after recirculation was apparent. These effects were more favorable in the case of intravenous administration than in the case of oral administration. These experimental results indicate that the administration of vitamin E is effective in protecting the brain from cerebral ischemia.     

A golgi analysis of unlayered polymicrogyria

Summary The cytoarchitectonics of the cerebral unlayered polymicrogyria located at the borders of a bilateral porencephalic defect is characterized by minute convolutions not exteriorized by sulci, in which blood vessels and increased numbers of fibrillary astrocytes are present in the fused molecular layers. The cellular organization, based on the analysis of Golgi sections, differs among gyral, intermediate, and sulcal regions and represents variable degree of cellular damage and structural organization of the cerebral mantle injured approximately in gestational month 5. Polymicrogyria may be produced by incomplete ischemia of radial territories vascularized by cortical blood vessels penetrating at right angles from the surface which is the result of the imbalance between the impaired cerebral blood flow of occluded large prerolandic arteries, responsible for the porencephalic defect, and the arterial meningeal anastomoses.Abnormal folding in polymicrogyria may be generated by lateral differences in the cortical thickness of adjoining areas, and by the imbalance in growth rates of laterally contiguous cortical regions.Dedicated to A. Gonzalez     

脑梗死患者血浆神经肽Y、降钙素基因相关肽、神经降压素、胃动素动态变化及其临床意义

观察脑梗死(CI)患者神经肽Y(NPY)、神经降压素(NT)、胃动素(MTL)、降钙素基因 相关肽(CGRP)浓度变化及其临床意义。方法选择C162例,用放免法检测血浆NPY、NT、MTL与CGRP浓度。结果NPY、NT与MTL浓度显著高于对照组(P<0.0001);于发病后24h内显著升高,7d内达高峰,8～15d开始下降,15d后仍在较高水平。NPY浓度重型与大灶组显著高于轻型(P<0.05)与小灶组(P<0.01);发病积分≥6分组显著高于<6分组(P<0.05);高血压组显著高于正常血压组(P<0.05)。NT与MTL浓度重型组显著高于中(P<0.05)、轻型组(P<0.01);高血糖组显著高于正常血糖组(P<O.01)。CGRP浓度显著低于对照组(P<0.0001),发病24h内即显著降低,2～7d进一步降低,8～15d开始升高,15d后逐渐升至正常水平。重型与大灶组显著高于轻型(P<0.0001)、中型(P<0.01)与小灶组(P<0.01);伴发病积分≥6分组显著低于<6分组(P<0.05)。结论CI患者NPY、NT、MTL、CGRP浓度变化以7d内最显著,15d后逐渐恢复正常水平;四种浓度监测可作为判断CI患者病情严重程度、病灶大小及伴发病的实验室指标。     

Congenital Pseudarthrosis of Femur and Sciatic Nerve Palsy with Congenital Constriction Band Syndrome: Report of the First Case in Literature

Congenital constriction band syndrome has varied clinical presentations ranging from small, incomplete skin deep constriction band to in utero amputation. Pseudarthrosis of underlying bone most commonly tibia has been reported by many authors. We report the first case of congenital pseudarthrosis of the femur with congenital constriction band syndrome. Nine-day-old female presented with the constriction band in the left thigh with open pseudarthrosis of the femur. The left femur had gross recurvatum deformity and the posterior apex of the pseudarthrosis was exposed via skin ulceration. She had an ipsilateral paralytic clubfoot. She was treated with single-stage excision of constriction band and Z-plasty. Spontaneous union of the femur was achieved at 3 months. Procurvatum deformity of the femur improved gradually over 3 years. This happens to be the first and only reported case of congenital pseudarthrosis of the femur with sciatic nerve palsy due to congenital constriction band.     

Distal rectus femoris surgery in children with cerebral palsy: results of a Delphi consensus project

PurposeThe purpose of this study was for an international panel of experts to establish consensus indications for distal rectus femoris surgery in children with cerebral palsy (CP) using a modified Delphi method.MethodsThe panel used a five-level Likert scale to record agreement or disagreement with 33 statements regarding distal rectus femoris surgery. The panel responded to statements regarding general characteristics, clinical indications, computerized gait data, intraoperative techniques and outcome measures. Consensus was defined as at least 80% of responses being in the highest or lowest two of the five Likert ratings, and general agreement as 60% to 79% falling into the highest or lowest two ratings. There was no agreement if neither threshold was reached.ResultsConsensus or general agreement was reached for 17 of 33 statements (52%). There was general consensus that distal rectus femoris surgery is better for stiff knee gait than is proximal rectus femoris release. There was no consensus about whether the results of distal rectus femoris release were comparable to those following distal rectus femoris transfer. Gross Motor Function Classification System (GMFCS) level was an important factor for the panel, with the best outcomes expected in children functioning at GMFCS levels I and II. The panel also reached consensus that they do distal rectus femoris surgery less frequently than earlier in their careers, in large part reflecting the narrowing of indications for this surgery over the last decade.ConclusionThis study can help paediatric orthopaedic surgeons optimize decision-making for, and outcomes of, distal rectus femoris surgery in children with CP.Level of evidenceV     

等容血液稀释对大鼠局灶性脑缺血作用的研究

以血液稀释治疗血栓栓塞性脑缺血为目的,采用大脑皮层局部血流量(rCBF)、脑组织含水总量以及脂质过氧化物含量(LPO)为重要指标,共71只大鼠的实验研究,结果表明:大脑局灶性缺血24小时后经血液稀释治疗2小时,血细胞压积由49.4±3.5%降至39.3±3.77%,rCBF增加19.95%(n=16,P<0.005),脑组织含水量及LPO含量,对照组与稀释组分别为81.39±1.56%(n=12),79.00±1.08%(n=13,P<0.001);645.57±106.72nmol/100mgpro(n=11),360.47±117.46nmol/100mgpro,(n=14,P<0.001)。提出血液稀释可增加rCBF,减轻脑水肿,降低LPO。     

舌下神经-面神经直接侧端吻合的应用解剖学研究

目的:为舌下神经-面神经直接侧端吻合提供解剖学依据。方法:①在21例防腐固定的成人头颈部标本上,测量面神经干及其颞骨内乳突段、鼓室段长度;面神经干分叉处至舌下神经颈部的最短距离。②3例新鲜标本取舌下神经及面神经干行组织学检测,测定其神经束数目和横切面积。③2例标本摹拟术式设计。结果:舌下神经干在寰椎水平为单束形式,横切面积为(8.5±0.3)mm2;面神经干在出茎乳孔处为单束形式,横切面积为(5.1±0.2)mm2;面神经干的长度为(15.7±2.0)mm,颞骨内面神经乳突段的长度为(14.6±1.5)mm、鼓室段的长度为(9.6±1.2)mm;面神经干分叉处至舌下神经颈部的最短距离为(17.2±2.3)mm。结论:舌下神经-面神经直接侧端吻合治疗面瘫具有可行性。     

Lymphocyte concanavalin A capping in hereditary cerebral haemorrhage with amyloidosis — Dutch type

Summary Lymphocyte capping with concanavalin A was studied in 11 patients with hereditary cerebral haemorrhage with amyloidosis (Dutch type) and 10 controls. No difference in capping was found between patients and controls. Abnormal lymphocyte concanavalin A capping has been reported in patients with the Icelandic type of cerebral amyloidosis and in patients with Alzheimer's disease, a disease in which cerebral amyloid angiopathy can also be found. The results suggest a difference in pathogenesis between the Dutch type of cerebral amyloidosis and the other amyloid diseases.Members of the Amyloid Research Group, Leiden     

Differential vulnerability of microtubule components in cerebral ischemia

Summary Differential vulnerability of the major components of microtubules was examined in ischemic gerbil brains by a light microscopic, immunohisto-chemical method using monoclonal antibodies for microtubule-associated protein (MAP) 1A and MAP2, polyclonal antibody for MAP1 and 2 as well as monoclonal antibody for -tubulin. Progressive cerebral ischemia during unilateral carotid occlusion for 5, 15 and 120 min and reperfusion for 3, 12 and 48 h following bilateral carotid occlusion for 10 min were studied. Ischemic lesions in the subiculum-CA1 region were visualized by all antibodies after ischemia for 5 min but the antibody for -tubulin was less sensitive. The antibody for -tubulin was also less sensitive than antibodies for MAPs for detection of early postischemic lesions. Differential sensitivity was also observed in the cerebral cortex and other brain regions. Microtubules in myelinated axons were more stable than those in dendrites. The observed loss of immunohistochemical reactivities for MAPs and -tubulin may have been caused by activation of calcium-dependent proteolytic enzymes such as calpains. The discrepancy between MAPs and -tubulin could be due to differences in affinities or topographic distributions of these proteins within microtubules.Supported by the grant NS-06663 from the National Institutes of Health, U.S. Public Health Service