动脉硬化性皮层下白质脑病（附22例临床及CT分析）

动脉硬化性皮层下白质脑病（附２２例临床及ＣＴ分析）唐明耀，曾祥发，张永全动脉硬化性皮层下白质脑病又称为血管性进行性皮层下脑病（Ｂｉｎｓｗａｎｇｅｒ病，简称ＢＤ），是一种主要累及脑室周围白质及顶枕白质的综合征。于１８９４年由Ｂｉｎｓｗａｎｇｅｒ首先报告...     

Binswanger病14例临床分析

本文分析１４例Ｂｉｎｓｗａｎｇｅｒ病（ＢＤ），ＢＤ的发病形式缓慢，病因多为高血压病，病灶及局限大脑白质，临床特点为渐进性痴呆，二便失禁，步态异常，ＣＴ或ＭＲ为脑室周围白质密度降低，基底节多发腔隙梗塞及脑萎缩，提出影像学改变先天症状出现。     

皮质下动脉硬化性脑病的临床与CT(附38例报告)

目的探讨皮质下动脉硬化性脑病的病因、发病机理、诊断和治疗、脑ＣＴ表现。方法回顾性分析３８例经临床及脑ＣＴ诊断为皮质下动脉硬化性脑病的患者，均作了脑ＣＴ检查。结果（１）均有６～４０年不等的高血压病史，部分伴有多年吸烟史或伴Ⅱ型糖尿病史者病情较重。（２）脑ＣＴ均表现有不同程度的白质疏松（ＬＡ）及深部白质上软化灶、侧脑室扩大；大多数同时伴有皮质的小梗死（８４％）。结论Ｂｉｎｓｗａｎｇｅｒ病的直接病因即是高血压。对有长期高血压和进展性痴呆，伴有多发性腔隙卒中者，结合脑ＣＴ改变可考虑本病诊断，及时给予治疗，可延缓病程。     

老年性痴呆智能与CT研究

现将我科治疗６５例痴呆病人报道如下。１临床资料６５例老年性痴呆病人均为１９９３年５月～２０００年５月我科住院病人。男４５例,女２０例,平均６９±８岁（６０～８１岁）。所有病人经神经心理韦氏成人智能测定及头颅ＣＴ检查。全部患者和对照组５０例均完成１１项分测验,将结果分析根据量表得出语言智商（ＶＩＱ）、操作智商（ＰＩＱ）及总智商（ＦＩＱ）。 ６５例均检查了头颅ＣＴ,并进行定量分析,脑萎缩线性定量测定,如第三脑室宽度、平均脑回宽度、尾状指数及脑室指数等,局灶性病变的大小、数量及部位,脑室周围白质疏松程…     

脑白质疏松

脑白质疏松山东医科大学附属医院神经内科（２５００１２）李义召，刘爱芬，迟兆福，郭洪志，韩丹春，李大年，崔元孝山东省立医院神经内科崔元孝脑白质疏松（Ｌｅｕｋｏａｒａｉｏｓｉｓ，ＬＡ）是一影像学诊断名词，它是由许多病因所致的在ＣＴ上显示环绕脑室的斑片状白...     

皮质下动脉硬化性脑病的临床与CT

目的 探讨皮质下动脉硬化性脑病的病因，发病机理，诊断和治疗，脑ＣＴ表现，方法 回顾性分析３８例经临床及脑ＣＴ诊断为皮质下动脉硬化性脑病的患者，均作了脑ＣＴ检查。结果 （１）均有６－４０年不等的高血压病史，部分伴有多年吸烟史或伴Ⅱ型糖尿病史病情较重。（２）脑ＣＴ均表现有没程度的白持疏松（ＬＡ）及深部白质土软化灶、侧脑室扩大；大多数同时伴有皮质的小梗死（８４％）。结论 Ｂｉｎｓｗａｎｇｅｒ的直接病因即     

大脑中动脉高密度征临床意义的探讨

大脑中动脉高密度征（ｈｙｐｅｒｄｅｎｓｅｍｉｄｄｌｅｃｅｒｅｂｒａｌａｒｔｅｒｙｓｉｇｎ，ＨＭＣＡＳ）曾被认为是大脑中动脉闭塞的最早期ＣＴ表现（见图１），但尚未被普遍接受。有人观察了５５例急性缺血性脑卒中患者，ＨＭＣＡＳ发生率为３４．５％（１９／５５...     

脑梗塞患者的诱发电位,经颅多普勒与CT等对照研究

对８６例脑梗塞患者的脑诱发电位和经颅多普勒（ＴＣＤ）进行分析，并与ＣＴ／ＭＲＩ检查作对照，体感诱发电位（Ｓｏｍａｔｏｓｅｎｓｏｒｙ Ｅｖｏｋｅｄ Ｐｏｔｅｎｔｉａｌ，ＳＥＰ）异常率８２．６％，脑干听觉诱发电位（Ｂｒａｉｎｓｔｅｍ Ａｕｄｉｔｏｒｙ Ｅｖｏｋｅｄ Ｐｏｔｅｎｔｉａｌ，ＢＡＥＰ）异常率７４．４％经颅多普勒（Ｔｒａｎｓｃｒａｎｉａｌ Ｄｏｐｐｌｅｒ，ＴＣＤ）为９０．７％。脑梗塞位于大脑半     

多发性脑梗塞并脑白质疏松脑室扩大的研究

本文对６６例多灶性脑梗塞并脑白质疏松、脑室扩大患者的症状、体征、ＣＴ及ＭＲＩ表现进行分析。并对头颅ＣＴ图像作双额径、双尾径及Ⅲ脑室外侧至半球外侧裂径与其相应颅腔径比率测定。结果表明有痴呆患者ＢＣ比率增加，ⅢＶ—Ｓ比率减少，与健康对照组及脑梗塞并白质疏松非痴呆组比较，差异有显著意义。     

急性脑梗塞病情与白细胞变形能力和粘附功能相关性的研究

目的探讨外周血白细胞变形能力（ＬＤ）和白细胞粘附功能（ＬＡＦ）的变化与急性脑梗塞病情的相关性。方法检测６８例急性脑梗塞患者发病后第３、７、１５、２１天和６０例健康人ＬＤ和ＬＡＦ的变化。结果急性脑梗塞患者ＬＤ明显降低，ＬＡＦ明显增高。与对照组比较有显著差异（Ｐ＜０．００１），且病程在第３天前ＬＤ和ＬＡＦ变化更明显。有并发症患者ＬＤ和ＬＡＦ变化较无并发症者更明显（Ｐ＜０．００１）。结论ＬＤ降低和ＬＡＦ增高与急性脑梗塞病情变化有关。     

Hypodensity of the cerebral white matter in patients with transient ischemic attack or minor stroke: influence on the rate of subsequent stroke. Dutch TIA Trial Study Group.

In a prospective study of 3,017 patients with transient ischemic attack or minor ischemic stroke from the Dutch Transient Ischemic Attack Trial, the presence or absence of diffuse hypodensity of the white matter on a baseline computed tomography (CT) scan of the brain was related to the occurrence of subsequent stroke. On entry, 337 patients were judged to have diffuse hypodensity of the white matter on CT; they were older (71.4 +/- 7.4 years versus 64.4 +/- 9.9 years), more often had hypertension (50% versus 41%), and more often had lacunar infarcts on CT scan (40% versus 26%) than did patients with normal white matter. Strokes, fatal or nonfatal, occurred in 51 (15%) of the patients with diffuse hypodensity of the cerebral white matter, compared to 217 (8%) in the group with normal white matter (crude hazard ratio, 2.0; 95% confidence interval, 1.4-2.7). After adjustment for age and other relevant entry variables, the hazard ratio was 1.6 (95% confidence interval, 1.2-2.2). In patients younger than 70 years the crude hazard ratio was 2.7 (95% confidence interval, 1.7-4.2). The distribution between the main subtypes of stroke was similar for patients with and those without diffuse hypodensity of the cerebral white matter: Intracerebral hemorrhage occurred in 6 and 9%, cortical infarction in 47 and 45%, and lacunar infarction in 34 and 29%, respectively. We conclude that hypodensity of the cerebral white matter in patients with transient ischemic attack or minor stroke is associated with an extra risk of future stroke, from large as well as from small vessels, and particularly in patients under 70 years old; this increase of risk is independent of other risk factors for stroke.     

Relation between cerebral white matter damage on CT and MRI and clinical data in DRPLA (pseudo-Huntington form)]

We studied the relation between cerebral white matter damage and clinical data in nine patients with dentatorubropallidoluysian atrophy (DRPLA). All patients showed pseudo-Huntington form. The study produced five results. (1) The four of the nine patients showed diffuse hypodensity of the cerebral white matter on CT. We studied one of this four patients by MRI. The hypodensity area on CT showed marked high signal intensity by T2-weighted image on MRI. (2) The onset age was later in the patients with cerebral white matter damage as compared with the patients without this damage. (3) All patients showed subcortical dementia, which was more remarkable in the patient with white matter damage. This suggests the relation between cerebral white matter damage and progression rate of subcortical dementia in DRPLA. (4) Gait disturbance progressed more rapidly in the patients with cerebral white matter damage. (5) The homovanillic acid (HVA) and 5-hydroxyindole acetic acid (5-HIAA) concentration in CSF decreased more remarkably in the patients with white matter damage.     

Computed tomography in subacute sclerosing panencephalitis: report of 15 cases

Computerized tomographic (CT) study of the brain was performed in 15 cases of subacute sclerosing panencephalitis (SSPE). Most patients in Stage II (6/8) had cerebral edema and diffuse white matter low attenuation, and patients in Stages III and IV (5/7) had atrophy of cerebral cortex, brainstem and cerebellum. Low density areas in deep grey matter nuclei (5 cases), large focal areas of white matter hypodensity (3/15) and evidence of brainstem atrophy without cerebral atrophy (2/15) were features not hitherto described. One patient in Stage III had normal scan. Correlation of scan findings was better with the stage of the disease than with the duration of SSPE.     

Middle cerebral artery occlusion: correlation of computed tomography and angiography with clinical outcome

The clinical outcome of 40 cases with middle cerebral artery (MCA) occlusion was examined in relation to the site of occlusion and the findings on computed tomography (CT). Patients were treated conservatively without surgery. A few had decompressive craniotomy when necessary. Outcome in 7 (18%) was good, in 6 (15%) moderate, and in 15 (38%) severe; 12 (30%) died by the follow-up at 3 months. In cases with occlusion at the origin of the MCA, hypodensity on CT scan was usually localized to the basal ganglia, presumably because of collateral circulation through the anterior cerebral arteries; the outcome in these patients was not always favorable. Cases with occlusion of the trunk or branch vessels always showed marked CT hypodensity, and clinical outcome was poor. To assess quantitatively the extent of collateral circulation, the conduction time of contrast medium from the intracranial siphon (IC) to the insular portion of the MCA (M2) through the anterior cerebral arteries was calculated on serial carotid angiograms obtained within 24 hours after stroke onset. An IC-M2 time of 5 seconds was a critical indicator of whether extensive CT hypodensity would develop (the rule of 5 seconds). Furthermore, this method predicted the appearance and extent of infarction before CT revealed hypodensity. The significance of acute reconstructive surgery is also discussed.     

Comparison of CT scan and MRI findings in the diagnosis of Japanese encephalitis

Japanese encephalitis (JE) is the commonest endemic encephalitis but there are very few studies on the radiological changes and these are based on relatively small number of patients. The present study aims at comparing the CT scan and MRI findings in JE and correlate these with the reported histopathological findings. Forty two patients with JE were subjected to detailed neurological examination. Cranial CT scan was carried out in 38 and MRI scan in 31 patients. Haemagglutination inhibition test was carried out in the acute and convalescent sera. The CT scan and MRI findings have been compared. Both CT scan and MRI were available in 28 patients. In 21 patients, CT scans were abnormal and changes included thalamic hypodensity in 15, midbrain and basal ganglia hypodensity in 1 patient each, cerebral oedema in 4 and cortical atrophy with ventricular dilatation in 2 patients. MRI however was abnormal in all 31 patients including 17 with normal CT scan. Cranial MRI revealed either mixed intensity or hypointense lesion on T(1) and hyperintense or mixed intensity lesion on T(2) in thalami in all except two patients. The MRI lesions were also noted in basal ganglia in 11, midbrain in 18, pons in 8, cerebellum and cerebral cortex in 6 patients each and subcortical white matter in 2 patients. MRI was more sensitive than CT scan in revealing thalamic and extrathalamic abnormalities. Thalamic changes may be helpful in the diagnosis of JE especially in endemic area.     

脑白质疏松的临床意义

分析４０例痴呆患者、１２０例无痴呆脑血管病患者及６０例临床既无痴呆也无脑血管病病史的“正常”老人ＣＴ和ＭＲＩ资料，脑白质疏松的发生率由高到低依次为痴呆（６２．５０％）、脑血管病（３４．１７％）和“正常”老人（１５．００％）。推测脑白质疏松的病理生理基础是脑室周围半卵圆区缺血、缺氧及炎症反应所致脑白质神经纤维脱髓鞘。脑白质疏松可能加重或导致智能障碍。     

初发腔隙性梗死病人与代谢综合征关系的研究

目的 探讨腔隙性梗死病人代谢综合征的患病率及与各亚型之间的关系.方法 选择138例初发腔隙性梗死患者及年龄、性别相匹配的138例初发动脉硬化性皮层梗死患者,根据有无白质损害,观察腔隙性梗死患者代谢综合征的患病率及与腔隙性梗死亚型的关系.结果 皮层梗死组代谢综合征的患病率（45.7%）高于腔隙性梗死组（35.9%）（P〈0.01）.无白质损害的腔隙性梗死患者代谢综合征的患病率高于有白质损害者,皮层梗死组代谢综合征患病率高于有白质损害的腔隙性梗死组.结论 代谢综合征的患病率与不伴白质损害的腔隙性梗死明显相关,皮层梗死的患病率高于有白质损害的腔隙性梗死,与各型梗死之间的发病机制不同有关.     

Could changes in arterioles impede the perivascular drainage of interstitial fluid from the cerebral white matter in leukoaraiosis?

Y. H. Huang, W. W. Zhang, L. Lin, J. Feng, X. X. Zhao, W. H. Guo and W. Wei (2010) Neuropathology and Applied Neurobiology 36, 237–247
Could changes in arterioles impede the perivascular drainage of interstitial fluid from the cerebral white matter in leukoaraiosis? Aims: Leukoaraiosis (LA) is the increase in fluid in cerebral white matter with hyperintensity on T2‐weighted MR imaging that occurs in 25% of individuals over 65 years of age and in Alzheimer's disease. Age, hypertension, diabetes mellitus and cardiac disease are the major risk factors for LA. Ischaemia is considered to be the cause of LA, but the aim of the present study is to assess whether changes in arterioles in LA could impede perivascular lymphatic drainage of interstitial fluid from the cerebral white matter. Methods: We quantified arteriolosclerosis and immunohistochemical changes in the extracellular matrix in arterioles of cerebral white matter in 20 hypertension autopsy cases with LA and in 10 controls. Results: The ratio of the area immunoreactive for collagen types I, III, V and VI to the cross‐sectional area of arterioles was significantly higher in LA patients compared with controls (P < 0.001). Changes were observed in collagen IV and laminin. The walls of white matter arterioles in LA were significantly thicker (P < 0.01), and lumina were significantly smaller (P < 0.01). Arterioles had a significantly higher sclerotic index [1 ? (internal/external diameter)] in LA than in adjacent cortex or control white matter (P < 0.01). Conclusions: Our results show that thickening and sclerosis of the walls of arterioles in cerebral white matter in LA are associated with the accumulation of extracellular matrix components. Although these changes may result in decreased perfusion, they could also impede perivascular lymphatic drainage of interstitial fluid from white matter in LA.     

Hereditary cerebral hemorrhage with amyloidosis-Dutch type. Clinical and computed tomographic analysis of 24 cases

Clinical and computed tomographic findings in 24 patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type were reviewed. The common initial symptoms were headache and vomiting. Computed tomographic scans showed 50 hypodense and 49 hyperdense cortical lesions and in 20 patients the scans also showed generalized white matter hypodensity. Impairment of consciousness was related to the size of the hemorrhagic lesion. Dementia, seen in 11 patients, was related to the duration of the disease and the number of focal lesions on the computed tomographic scans, but not to the presence of white matter hypodensity. It is concluded that in hereditary cerebral hemorrhage with amyloidosis-Dutch type, lobar hemorrhages account predominantly for the acute clinical syndromes. The hemorrhages often have an irregular shape and are responsible for progression of the symptoms after an acute onset. Furthermore, cerebral amyloid angiopathy leads to a generalized abnormality of the white matter, probably due to chronic hypoperfusion.