自发性小脑出血86例临床分析

目的探讨小脑出血的病因、临床表现及治疗方法。方法对1999~2005年我院收治的86例小脑出血患者的临床资料进行回顾性分析。结果该病51~80岁为高发年龄段,占77.8%。小脑半球的出血71例,占82.6%,蚓部出血15例,占17.4%。1组为出血未破入脑室型31例,2组为小脑出血仅破入第四脑室32例,3组并发为幕上脑室系统(三脑室、侧脑室等)出现积血或扩张23例。58例保守治疗,有效率为82.8%,病死率17.2%。28例外科手术治疗,有效率为75%,病死率25%。脑疝为主要病死原因。结论根据小脑出血量及脑室系统改变进行分组有利于临床表现及病情变化的评价,及时正确的采取不同的治疗方案,降低病死率。     

脑出血破入脑室的治疗体会

目的：探讨高血压脑出血破入脑室的治疗方法并降低死亡率。方法：该组40例高血压脑出血破入脑室的病人用开颅血肿清除，血肿内引流、脑室外引流等手术方法加术后脑室内尿激酶注入、腰穿等方法。结果：优9例占22．5％，良15例占37．5％，差6例占15％，朱醒1例占2．5％，死亡9例上22．5％。结论；根据病情选择适当的治疗方法是降低死亡率的有效方法。     

高血压性脑出血破入脑室的CT和预后

经CT证实的223例高血压性脑出血中,破入脑室者死亡53例,死亡率(48.18％),较未破入脑室者(15.04％)明显为高(P<0.01)。破入脑室组高死亡率是和破入脑室血肿的量、脑室内血肿的分布以及破入途径密切相关。出现高度占位效应、破入脑室的积血量超过20ml、脑室出血呈Ⅳ或Ⅴ型分布则预后极差。     

脑脊液双向引流加尿激酶灌注治疗高血压脑出血破入脑室

高血压脑出血是临床常见的疾病,出血破入脑室时病情更加严重,死亡率高,可达42％～83％,存活者多留有严重的神经功能障碍。我院采用脑脊液双向引流结合尿激酶灌注治疗高血压脑出血破入脑室39例,取得了较好的效果。     

继发性脑室内出血（附48例分析）

报告继发性脑室内出血４８例临床资料。病因以高血压性脑出血为主占８３．３％，原发出血部位以基底节最多占６４．５％，破入脑室的脑实质内血肿量依次为脑叶、基底节、丘脑、小脑。根据脑实质内血肿量的多少及波及脑室程度的不同分别采用内科治疗、侧脑室穿刺引流、锥颅血肿抽吸、血肿抽吸加脑室引流，死亡率２９．１％。     

双通道微创术治疗脑出血破入脑室系统临床观察

目的应用双通道微创术治疗脑出血破入脑室系统的临床观察。方法选择1999-07～2003-04我科住院病人28例，均经CT证实为脑出血破入脑室系统。结果微创术效果好，死亡率14.3％。结论双通道微创术治疗脑出血破入脑室系统，提高生存率，减少血肿对脑组织的继发性损害，减少并发症及后遗症。     

高血压小脑出血破入脑室手术治疗分析

目的探讨高血压小脑出血破入脑室的手术时机、手术方式及治疗体会。方法回顾分析郑州市第一人民医院2017-01—12收治的26例高血压小脑出血破入脑室患者的临床资料,3例单纯行脑室外引流术,15例单纯行枕下开颅血肿清除术,8例联合脑室外引流+枕下开颅血肿清除术。结果按GOS评分评价治疗效果,恢复良好16例,重度残疾5例,植物生存1例,死亡4例。结论小脑出血的手术应结合出血部位、出血量、脑积水情况及临床表现等综合考虑,尽早采取个体化手术方式。合理的手术时机和手术方式,可改善患者的预后。     

丘脑出血继发罕见皮肤营养障碍

高血压性丘脑出血占脑出血的13％～31％，因出血部位、出血量以及是否破入脑室不同，其临床表现差异很大。现报道1例丘脑出血破入第三脑室和侧脑室后继发下肢皮肤营养障碍患者。     

64例高血压性脑出血破入脑室的预后分析

我院近四年来收治的高血压性脑出血破入脑室的64例患者,现从临床及CT两方面分析影响脑室出血预后的因素,以期有效合理的治疗,降低病死率。1临床资料与方法1.1一般资料1998-04～2002-04,我院经CT证实的高血压性脑出血破入脑室者64例,其中男40例,女24例,平均年龄59.4岁,占同期脑出血的48.64%。1.2临床表现64例患者中昏迷40例(占62.5%),头痛30例(占46.9%),头晕18例(28.1%),呕吐46例(71.9%),有明确高血压病史51例(79.7%),舒张压在16kPa(120mmHg)以上者28例(43.8%)。1.3CT所见1.3.1出血部位:基底节区出血18例(本组28.1%);丘脑出血18例(28.1%)…     

252例高血压丘脑出血的临床分析

目的 探索丘脑出血的临床、CT表现与预后的关系,并提出自己的分类。方法 通过临床与CT动态观察本院1994-03～2002-05所收252例丘脑出血病人及其预后。结果 丘脑出血破入脑室形成Ⅲ脑室铸型者死亡率较高(96％),向内下后影响 脑干及丘脑下部者死亡率接近100％,而局限者死亡率较低(6％)。结论 本分类办法可较准确预测丘脑出血预后,并对丘脑出血所致临床表现的机制作出解释。     

Transient cerebellar mutism after evacuation of a spontaneous vermian haematoma

Cerebellar mutism after surgery for posterior fossa tumours in children is a well-described, though rare, entity. Most of these tumours are located in the region of the cerebellar vermis extending to the hemispheres. The authors report a case of cerebellar mutism in an 8-year-old boy who underwent surgical evacuation of a spontaneous vermian haematoma. We feel that his mutism was an extreme form of cerebellar dysarthria. Received: 30 January 1998     

Cerebellar efferent fibers around the dentate nucleus

Summary In patients with olivo-ponto-cerebellar atrophy (OPCA), the deep cerebellar white matter showed evidence of severe degeneration and gliosis. However, the circumferential white matter enclosing the dentate nucleus was less involved. In addition, the Holzer stain verified the presence of mild gliosis inside the wrinkled band of the dentate gray matter. In contrast, dentato-rubro-pallido-luysian atrophy (DRPLA) affected the mantle layer covering the dentate nucleus. The fibers encircling the dentate nucleus, which degenerate in DRPLA and are spared in OPCA, are anatomically noticeable to be dentatofugal pathways. Moreover, the afferent fibers from the cerebellar cortex and other systems may reach the dentate nucleus partly from the medial aspect via the hilus, as was noted in cases of OPCA.     

Fusion of the cerebellar hemispheres ventral to the brainstem: a rare hindbrain-related malformation

Introduction New variations of cerebellar malformations are being increasingly recognized using modern neuroimaging techniques. Until now only dorsal cerebellar fusion syndromes, such as the rhombencephalosynapsis and its variations have been recognized.Case report We report on a 17-month-old male infant presenting with an exceptional hindbrain related malformation characterized by midline fusion of the cerebellar hemispheres ventral to the brainstem and causing symptoms due to brainstem compression.Discussion and conclusion A more detailed understanding of the cerebellar embryogenesis is required to unravel the underlying mechanisms leading to this type of cerebellar malformation, which cannot easily be integrated into the common classification systems. Both the morphological features and the clinical presentation are different from those of other cerebellar structural abnormalities. If this type of congenital malformation is detected more frequently in the future, it seems reasonable that it should be added to the list of cerebellar malformations as a distinct type.     

The vascularization of the human cerebellar cortex

The blood vessels of the cerebellar cortex were studied by two methods of injection: india-ink and low viscosity resin (Mercox). The study is divided into two parts: (a) Pial vessels; few in number at the cerebellar surface, the pial vessels are quite dense, forming vascular laminae, within the sulci. Pial vessels do not frequently anastomose. (b) Intracortical vessels closely resemble those of the cerebral cortex. They may be divided into three categories: short, middle and long. There exist three vascular layers within the cerebellar cortex: superficial, middle and deep. The superficial vascular layer is situated within the molecular layer, the middle within the Purkinje cell layer, and the deep within the granular layer. It is therefore possible to establish a correlation between these vascular layers and the cortical cytoarchitecture. We accorded particular attention to the vascularization of the Purkinje cells. Arteries parallel to the cerebellar surface (parallel arteries) are in close relationship to the Purkinje cells whereas capillaries and veins are scarce. It is highly probable that the majority of Purkinje cells obtain nutritive elements by these parallel arteries. Possible implications in physiology and pathology are subsequently discussed.     

The reliability of cerebellar brain inhibition

ObjectiveConnectivity between the cerebellum and primary motor cortex (M1) can be assessed by using transcranial magnetic stimulation to measure cerebellar brain inhibition (CBI). The aim of the present study was to determine the intra- and inter-day measurment error and relative reliability of CBI. The former informs the degree to which repeated measurements vary, whereas the latter informs how well the measure can distinguish individuals from one another within a sample.MethodsWe obtained CBI data from 83 healthy young participants (n = 55 retrospective). Intra-day measurements were separated by ~ 30 min. Inter-day measurmenets were separated by a minimum of 24 h.ResultsWe show that CBI has low measurement error (~15%) within and between sessions. Using the measurment error, we demonstrate that change estimates which exceed measurment noise are large at an individual level, but can be detected with modest sample sizes. Finally, we demonstrate that the CBI measurement has fair to good relative reliability in healthy individuals, which may be deflated by low sample heterogeneity.ConclusionsCBI has low measurement error supporting its use for tracking intra- and inter-day changes in cerebellar-M1 connectivity.SignificanceOur findings provide clear reliability guidelines for future studies assessing modulation of cerebellar-M1 connectivity with intervention or disease progression.     

Cerebellar ataxia in patients with Leber's hereditary optic neuropathy

We report the cases of a mother and son with Leber's hereditary optic neuropathy (LHON), where a point mutation of mitochondria DNA from guanine to adenine on nucleotide position 11778 was verified. Both also had cerebellar ataxia and dysarthria and in both cases cerebellar atrophies were detected by computed tomography or magnetic resonance imaging. It was not possible to elucidate the relationship between LHON and the cerebellar atrophy, but it should be kept in mind that various neurological complications may occur in LHON.     

Long-Term Synaptic Plasticity in Cerebellar Stellate Cells

Inhibitory transmission controls the action potential firing rate and pattern of Purkinje cell activity in the cerebellum. A long-term change in inhibitory transmission is likely to have a profound effect on the activity of cerebellar neuronal circuits. However, little is known about how neuronal activity regulates synaptic transmission in GABAergic inhibitory interneurons (stellate/basket cells) in the cerebellar cortex. We have examined how glutamate released from parallel fibers (the axons of granule cells) influences postsynaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors in stellate cells and modulates γ-aminobutyric acid (GABA) release from these neurons. First, we found that burst stimulation of presynaptic parallel fibers changes the subunit composition of post-synaptic AMPA receptors from GluR2-lacking to GluR2-containing receptors. This switch reduces the Ca²⁺ permeability of AMPA receptors and the excitatory postsynaptic potential amplitude and prolongs the duration of the synaptic current, producing a qualitative change in synaptic transmission. This switch in AMPA receptor phenotype can be induced by activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors and involves PICK1 and the activation of protein kinase C. Second, activation of presynaptic NMDA receptors triggers a lasting increase in GABA release from stellate cells. These changes may provide a cellular mechanism underlying associative learning involving the cerebellum.     

Pure post–stroke cerebellar cognitive affective syndrome: a case report

Abstract. Cerebellar pathology commonly shows important motor signs and less evident cognitive dysfunction. The cerebellar cognitive affective syndrome is characterised by impairment on executive function, spatial cognition, language and behaviour. We report the case of a man with acute onset of transitory motor features and severe mental disorders. Cranial CT and brain MRI revealed extended cerebellar lesions. Neuropsychological assessment disclosed deficits of attention, executive function and memory. Auditory event–related potentials showed abnormal P300. These data suggest a pure cerebellar cognitive affective syndrome and strengthen the hypothesis of cerebellar cognitive function modulation.     

Cerebellar Changes in Partial Seizures: Clinical Correlations of Quantitative SPECT and MRI Analysis

Summary: Purpose: To determine the frequency and patterns of periictal cerebellar hyperperfusion, whether it is associated with increased cerebellar atrophy, and whether cerebellar hyperperfusion and cerebellar atrophy are associated with predisposing clinical factors or with the outcome of epilepsy surgery.
Methods: Periictal and interictal SPECT scans and volumetric brain magnetic resonance imaging (MRI) were quantitatively analyzed in 54 consecutive patients with medically refractory partial epilepsy. Their histories were reviewed and their postsurgical outcomes assessed.
Results: Significant periictal cerebellar hyperperfusion was found in 26 (48.1%) patients, of whom 18 had CCH, two had homolateral cerebellar hyperperfusion (HCH), and six had symmetrical bilateral hyperperfusion (BCH). No relation found between the site of the SPECT seizure localization and the presence or type of cerebellar hyperperfusion. CCH was more common when the injected seizure involved unilateral clonic motor activity (p < 0.05). A smaller MRI relative cerebellar volume (cerebellar volume/cerebral volume) was correlated with a greater seizure frequency (R_s= -0.30; p < 0.05) but not with the duration of epilepsy. There was no difference in the cerebellar volumes between the different patterns of cerebellar perfusion (p > 0.05). However, patients without a focal structural MRI lesion had significantly smaller cerebellar volumes (p < 0.05). In patients who underwent epilepsy surgery (n = 31), there was a trend for those without excellent outcomes to have smaller relative cerebellar volumes than did those with excellent outcome (10.6 vs. 11.8%; p = 0.08).
Conclusions: Periictal changes in cerebellar perfusion, particularly CCH, are common in patients with intractable partial epilepsy. However, periictal hyperperfusion does not appear to be a major contributor to the development of cerebellar atrophy.