小脑幕裂孔疝继发大脑后动脉梗塞3例

<正>小脑幕裂孔疝继发大脑后动脉梗塞临床少见,其发病机制复杂,预后险恶,2007年4月至2009年7月,我院收治此类病人3例,现结合文献,就其发病机制及治疗方面的问题探讨如下。     

小脑幕裂孔切开联合大骨瓣减压术治疗小脑幕切迹疝的临床研究

目的研究小脑幕切开联合大骨瓣减压治疗小脑幕切迹疝的疗效与应用价值。方法60例脑外伤或脑出血导致的小脑幕切迹疝病人随机分为小脑幕裂孔切开组（行大骨瓣减压术同时切开小脑幕裂孔）和非小脑幕裂孔切开组（仅行大骨瓣减压术）,每组30例。术后48h复查CT,对比组间脑干周围池改善率。对比组间应激性溃疡发生率、病死率、术后2周与4周的GCS评分,及术后26周的GOS评分。结果术后48h头颅CT显示脑干周围池改善率小脑幕裂孔切开组显著高于非小脑幕裂孔切开组。小脑幕裂孔切开组病死率、应激性溃疡发生率低于非小脑幕裂孔切开组。GCS评分术后2周时小脑幕裂孔切开组显著高于非小脑幕裂孔切开组,术后4周时小脑幕裂孔切开组显著高于非小脑幕裂孔切开组。术后26周的GOS评分小脑幕裂孔切开组高于非小脑幕裂孔切开组。结论小脑幕裂孔切开联合大骨瓣减压治疗小脑幕切迹疝优于单纯大骨瓣减压,显著降低病死率,改善预后。     

小脑幕裂孔切开联合大骨瓣减压治疗小脑幕切迹疝

目的研究小脑幕裂孔切开联合常规大骨瓣减压手术在小脑幕切迹疝病人中的临床疗效与实际应用价值。方法120例术前已发生小脑幕切迹疝的重型颅脑损伤及脑出血病人,按照患者入院顺序依次分为3组：标准大骨瓣减压组、内减压组和小脑幕裂孔切开组,每组40例,分别按照不同的手术原则进行手术。术后48h复查头颅CT,比较各组间的死亡率及脑干周围池改善率,对比各组间术后2周、4周GCS评分及术后24周GOS评分。结果术后小脑幕裂孔切开组死亡率显著低于标准大骨瓣减压组（P〈0.05）,但与内减压组比较无统计学显著性差异（P〉0.05）。脑干周围池改善率,小脑幕裂孔切开组显著高于大骨瓣减压组及内减压组（P〈0.01）。术后2周、4周GCS评分及术后24周GOS评分小脑幕裂孔切开组显著优于大骨瓣减压组及内减压组（P〈0.01）。结论小脑幕裂孔切开联合常规大骨瓣减压术治疗小脑幕切迹疝疗效肯定,可以显著降低病人的死亡率和伤残率,改善其预后,值得临床推广。     

小脑幕缘切开术中引流环池脑脊液对颅脑损伤合并小脑幕切迹疝患者颅内压的影响

目的研究小脑幕缘切开术中引流环池脑脊液对降低颅脑损伤合并小脑幕切迹疝患者颅内压的作用。方法将40例颅脑损伤合并小脑幕切迹疝患者按随机数字表法分为两组。观察组（20例）在术中对环池脑脊液充分引流并计量,对照组（20例）术中对环池脑脊液不进行引流,两组术后监测颅内压5d,比较引流前后颅内压及侧脑室内压力的变化。结果观察组术后不同时间颅内压均值均低下对照组（P〈0．05）。观察组小脑幕缘切开前至环池脑脊液引流结束时侧脑室内压力下降均值较对照组下降均值高（P〈0.05）：结论小脑幕缘切开术中对环池脑脊液充分引流能恢复脑脊液循环通路,降低颅内压,提高减压效果。     

小脑幕缘切开治疗脑疝

一、对象与方法 1. 一般资料:男,24例,女,12例,年龄12～53岁,平均38.6岁,均系车祸伤.头颅CT显示颅内幕上占位致小脑幕切迹疝.     

颅脑创伤小脑幕切迹疝前驱期临床征象分析

目的探讨小脑幕切迹疝的前驱期临床征象,提高重型颅脑损伤的救治率。方法回顾分析我科小脑幕切迹疝病人的病历资料,总结脑疝发生前的临床表现和辅助检查,寻找小脑幕切迹疝前驱期较常见的临床征象。结果发生小脑幕切迹疝前主要临床表现有:GCS评分下降,识障碍程度加深,尿失禁,剧烈头痛,频繁呕吐,躁动。结论意识障碍程度加深、尿失禁、剧烈头痛、频繁呕吐、躁动为脑疝前驱期的特征性临床表现。患侧脑室、侧裂合并脑基底池的受压变窄为脑疝前驱期的特征性CT表现。有上述临床特点者应立即复查头CT,以便及时开颅手术,提高救治率。     

小脑幕切开术对重型颅脑损伤并脑疝的临床研究

目的 探讨小脑幕切开术在救治重型颅脑损伤合并小脑幕切迹疝的临床疗效.方法 将94例重型颅脑损伤合并小脑幕切迹疝病例分为两组,对照组常规清除颅内血肿大骨瓣减压,观察组在上述基础上加小脑幕切开术,观察两组临床效果及并发症.结果 观察组中恢复良好21例,中残15例,重残8例,植物生存2例,死亡2例.疗效优于对照组,P＜0.01.结论 重型颅脑损伤并脑疝患者行小脑幕切开术能有效缓解小脑幕切迹疝引发的继发性脑干损伤,有效降低致死率和致残率.     

小脑幕切迹脑膜瘤的显微外科手术治疗

目的探讨小脑幕切迹脑膜瘤的显微外科手术治疗技巧。方法对9例经显微外科治疗的小脑幕切迹脑膜瘤的临床资料进行回顾性分析。结果9例患者中肿瘤全切除8例，1例次全切除，无手术死亡病例。无脑脊液漏及颅内感染发生。9例患者平均随访9个月，术后均恢复良好，生活能够自理，未见肿瘤复发。结论显微外科手术是治疗小脑幕切迹脑膜瘤的有效方法。根据患者术前影像学资料的特征．选择恰当的手术入路．术中良好的病变显露及术后并发症的及时处理是小脑幕切迹脑膜瘤显微外科手术治疗成功的关键。     

小脑幕切开术治疗急性外伤性小脑幕裂孔疝

目的探讨小脑幕切开术在颞叶钩回疝中的作用和效果。方法在2003年3月至2006年11月间,在骨瓣减压及清除颅内血肿后,主要应用小脑幕切开减压术救治了25例重型颅脑损伤合并颞叶钩回疝患者。结果术后CT显示,中线基本回复正常23例(92.0%),脚间池出现8例(88.9%),环池恢复21例(91.3%),四叠体池显示7例(87.5%)。临床治疗效果:恢复良好14例(56.0%);中残5例(20.0%);重残3例(12.0%);植物生存1例(4.0%);死亡2例(8.0%),分别继发于脑干损伤和肺部感染而死亡。结论应用小脑幕切开减压术可以使颞叶钩回疝快速复位,从而能更好地缓解因脑疝引起的继发性脑干损伤。     

小脑幕裂孔疝致大脑后动脉梗塞（二例报告）

小脑幕裂孔疝致大脑后动脉梗塞（二例报告）候永宏，曹美鸿文献中曾提出颅内压增高致小脑幕裂孔疝的患者，可因同侧大脑后动脉受压而致其供血区出现梗塞（１）。但国内外文献中未见确切的临床病例报告。现报道二例经ＣＴ证实的病例。病例报告例１男性，１１岁。因反复发作...     

胚胎型大脑后动脉与复发脑梗死相关性分析

目的研究胚胎型大脑后动脉与脑梗死复发之间的关系。方法回顾性收集2020年1月-2021年10月在包头医学院第二附属医院神经内科住院患者1017人,根据纳入和排除标准后943人进入分析研究,其中初发脑梗死620例,复发脑梗死323例。对比两组临床资料及胚胎型大脑后动脉发生率。对复发脑梗死相关危险因素进行单因素分析,进一步应用多因素Logistic回归方法进行独立危险因素分析。结果复发性脑梗死胚胎型大脑后动脉发生率明显高于初发型脑梗死(P<0.01),二元Logistic回归显示胚胎型大脑后动脉、高血压病、糖尿病、冠心病、家族史与脑梗死的复发相关,计算OR值分别为2.481、1.486、1.652、2.402,P值均<0.05。结论复发性脑梗死患者的胚胎型大脑后动脉发生率高于初发型脑梗死,胚胎型大脑后动脉是复发性脑梗死独立危险因素。     

胚胎型大脑后动脉与复发脑梗死相关性分析

目的研究胚胎型大脑后动脉与脑梗死复发之间的关系。方法回顾性收集2020年1月-2021年10月在包头医学院第二附属医院神经内科住院患者1017人,根据纳入和排除标准后943人进入分析研究,其中初发脑梗死620例,复发脑梗死323例。对比两组临床资料及胚胎型大脑后动脉发生率。对复发脑梗死相关危险因素进行单因素分析,进一步应用多因素Logistic回归方法进行独立危险因素分析。结果复发性脑梗死胚胎型大脑后动脉发生率明显高于初发型脑梗死(P<0.01),二元Logistic回归显示胚胎型大脑后动脉、高血压病、糖尿病、冠心病、家族史与脑梗死的复发相关,计算OR值分别为2.481、1.486、1.652、2.402,P值均<0.05。结论复发性脑梗死患者的胚胎型大脑后动脉发生率高于初发型脑梗死,胚胎型大脑后动脉是复发性脑梗死独立危险因素。     

Circle of Willis anatomy as a predictor of posterior cerebral artery territory infarction in the presence of tentorial herniation

Twenty-two brains in which tentorial herniation was present were examined to see whether the circle of Willis anatomy was a predictor of posterior cerebral artery territory infarction. This factor was considered in the context of the patients' known survival interval. Three brains in which tentorial herniation was not present were included as negative controls. Of the 22 brains in which tentorial herniation was present, 12 showed posterior communicating arteries smaller than the P1 segments of the posterior cerebral arteries; posterior cerebral artery territory infarction occurred in 8 of these. In these cases the survival interval was greater than 24 h (40 h to 2 months). In the 4 cases in which no infarction was seen the survival interval was less than 14 h. In 10 of the 22 cases the posterior communicating arteries were larger than, or equal in size to, the P1 segments of the posterior cerebral arteries and no infarction was seen in the posterior cerebral artery territories. No infarction was seen in the three control brains. These were trauma cases with no tentorial herniation. Statistical analysis indicated there was a true relationship between the sizes of the arteries and the occurrence of infarction. It cannot be excluded that other factors may have relevance in terms of whether infarction occurs. However, from the results of this study it appears that one can predict whether infarction in the posterior cerebral artery territory will occur as a complication of tentorial herniation by consideration of the anatomy of the circle of Willis in relation to the survival interval. The reasons for the presence or absence of posterior cerebral artery territory infarction have not previously been satisfactorily explained.     

Hemiplegia in posterior cerebral artery strokes

Hemiplegia is an unusual presenting feature of posterior circulation strokes. We report five cases who presented with hemiplegia and in whom CT scans revealed evidence of infarcts in posterior cerebral artery territory.     

Pure superficial posterior cerebral artery territory infarction in The Lausanne Stroke Registry

Objective: To determine the patterns of clinical presentation, lesion topography, and etiology in patients with ischemic stroke limited to the superficial territory of the posterior cerebral artery (s-PCA). Methods: In the Lausanne Stroke Registry (LSR, 1983–1998), we determined the patterns of clinical presentation, lesion topography and mechanisms of stroke, among 117 patients with s-PCA infarction (s-PCAI) on brain imaging. Results: s-PCAIs accounted for 30.5 % of all PCA territory ischemic strokes. The presumed etiology was embolism in 64 (54.5 %) patients [cardiac in 51 (43.5 %) and arterial in 13 (11 %)], indeterminate in 38 (32 %), PCA atherothrombosis in 4 (3.4 %), migraine in 4 (3.4 %), other rare causes in 4 (3.4 %), and multiple potential sources of embolism in 3 (2.5 %). The clinical findings were hemianopsia in 78 (67 %), quadrantanopsia in 26 (22 %), and bilateral visual field defects in 8 (7 %). Motor, sensory, or sensorimotor deficits were detected in 14 (12 %), 8 (6.8 %), or 8 (6.8 %) patients, respectively. Neuropsychological dysfunction included memory impairment in 20 (17.5 %; with left [L], right [R], or bilateral [B] lesions in 15, 2, or 3 patients, respectively), dysphasia in 17 (14.5 %; L/B: 14/3), dyslexia with dysgraphia in 5 (4 %; L/B: 4/1), dyslexia without dysgraphia in 10 (8.5 %; L/B: 8/2), hallucinations in 12 (10 %; L/R/B: 5/5/2), visual neglect in 11 (9.5 %; L/R: 2/9), visual agnosia in 10 (8.5 %; L/B: 7/3), prosopagnosia in 7 (6 %; R/B: 4/3), and color dysnomia in 6 (5 %; L: 6). Conclusions: s-PCAIs are uncommon, representing less than a third of all PCA infarctions. Although embolism is the main cause in 60 % of patients, identification of the emboli source is often not possible. In 1/3 of cases, the stroke mechanism cannot be determined. Neuropsychological deficits are frequent if systematically searched for. Received: 31 July 2001, Received in revised form: 23 November 2001, Accepted: 4 December 2001     

Isolated lateral thalamic infarction: the role of posterior cerebral artery disease

Background and purpose: Lateral thalamic infarction (LTI) is usually caused by small vessel disease (SVD), i.e., occlusion of the deep perforator. However, focal atherosclerotic posterior cerebral artery disease (PCAD) may produce LTI via thrombotic occlusion of the perforator. We aimed to investigate the prevalence of PCAD in LTI and differences in clinical and imaging findings between LTIs associated with PCAD and SVD. Methods: We retrospectively evaluated 58 consecutive patients with isolated LTI who underwent diffusion‐weighted imaging (DWI) and MR angiography (MRA) within 7 days after stroke onset. Patients were divided into two groups: those with PCAD and those with SVD. Clinical syndromes were divided into pure sensory stroke (PSS) and sensory stroke plus (SS‐plus), i.e., the concomitant presence of motor dysfunction or ataxia. Clinical and imaging findings were compared between these two groups. Results: Of the 58 patients, 13 (22.4%) had PCAD. PSS was more frequently associated with SVD than with PCAD (57.8% vs. 23.1%, P = 0.032). Initial DWI lesion volume (cm³) was significantly larger in PCAD than in patients with SVD (0.38 ± 0.13 vs. 0.33 ± 0.22, P = 0.025). Among the 23 patients (39.7%) who underwent follow‐up DWI, patients with PCAD showed a significantly greater increase in subacute lesion volume than those with SVD (P = 0.019). Although National Institutes of Health Stroke Scale scores did not differ at admission (P = 0.185), they were significantly higher at discharge in PCAD than in patients with SVD (P = 0.012). Conclusions: Our data suggest that PCAD is an important cause of LTI, being related to SS‐plus, larger lesion volume, and worse clinical outcomes.     

Health status and life satisfaction after decompressive craniectomy for malignant middle cerebral artery infarction

Objectives –  To study the long-term outcome in patients with malignant middle cerebral artery (MCA) infarction treated with decompressive craniectomy. The outcome is described in terms of survival, impairment, disabilities and life satisfaction.
Materials and methods –  Patients were examined at a minimum of 1 year (mean 2.9, range 1–6) after the surgery and classified according to the Glasgow Outcome Scale (GOS), the National Institutes of Health Stroke scale (NIHSS), the Barthel Index (BI), the short-form health survey (SF-36) and the life satisfaction checklist (LiSat-11).
Results –  Eighteen patients were included. The long-term survival was 78%. The mean NIHSS score was 13.8 (range 6–20). No patient was left in a vegetative state. The mean BI was 63.9 (5-100). The SF-36 scores showed that the patients' view of their health was significantly lower in most items compared with that of a reference group. According to the LiSat checklist, 83% found their life satisfying/rather satisfying and 17% found their life rather dissatisfying/dissatisfying.
Conclusion –  We conclude that the patients remained in an impaired neurological condition, but had fairly good insight into their limitations. Although their life satisfaction was lower compared with that of the controls, the majority felt that life in general could still be satisfying.     

大脑后动脉远端动脉瘤的血管内介入治疗

目的 探讨大脑后动脉远端动脉瘤的血管内介入治疗方法及特点.方法 10例动脉瘤,P2段6例(囊状2例、梭形2例、夹层2例)、P2-P3交界处1例(夹层)、P3段3例(夹层).对于囊状动脉瘤采用弹簧圈栓塞并保留载瘤动脉的方法;梭形动脉瘤采用支架重建瘤腔的方法;P2段及P2-P3交界夹层动脉瘤采用弹簧圈栓塞并闭塞载瘤动脉的方法;P3段夹层动脉瘤采用Glubran胶栓塞并闭塞载瘤动脉的方法.结果 随访半年至1年,预后良好.DSA复查9例,未见动脉瘤复发.结论 对于大脑后动脉远端动脉瘤,根据动脉瘤的类型及部位采用不同的血管内介入治疗方法,短期随访可以获得较好的疗效.     

伴有一侧胚胎型大脑后动脉的Percheron动脉梗死二例临床与影像分析

目的 Percheron动脉属于丘脑穿动脉的一种少见的先天变异,伴有一侧胚胎型大脑后动脉的Perch eron动脉梗死报道罕见.我们报告2例,旨在提高认识以利于早期诊断和治疗.方法 回顾性分析2例Percheron动脉梗死的临床表现、影像特征、治疗及预后.结果 1例急性昏迷,1例发作性视物不清后意识不清合并眼球垂直运动障碍.2例磁共振弥散加权成像(DWI)示双侧丘脑旁正中高信号,其中1例合并中脑“V”字型高信号;2例右侧大脑后动脉(PCA) P1段均显示发育不良,即胚胎型PCA.结论 典型的临床症状、丘脑旁正中部对称DWI高信号及中脑“V”字征有助于Percheron动脉梗死的诊断及治疗.一侧胚胎型PCA可能是Percheron动脉梗死的潜在变异因素.     

Spectrum of superficial posterior cerebral artery territory infarcts

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.