脑基底节区对称性低密度病变的CT诊断

目的：为提高CT对双侧脑基底节区对称性低密度病变的诊断水平。方法：我们对14例资料完整的病例进行回顾性分析。肝豆状核变性3例，脑炎、脑外伤、脑梗塞与维生素B1缺乏症各2例，霉变甘蔗中毒、一氧化碳中毒与甲醇中毒各二例。结果：CT表现为双侧脑基底节区对称性低密度，呈片状、椭圆形或扇形，可伴有其他部位的低密度区、脑萎缩、脑软化灶、儿童脑发育不全、脑梗塞。结论：强调诊断结合临床病史和其他检查的重要性。肝豆状核变性有肝肾的损害，维生素B1缺乏症用VitB1诊断性治疗有效，脑外伤、一氧化碳及霉变甘蔗中毒等均有明确的病史。一氧化碳中毒常伴脑白质脱髓鞘改变。苍白球黑质色素变性MR检查有特征性，呈短T2低信号。     

双侧基底核对称性低密度病变的CT诊断

目的 分析CT上表现为双侧基底核对称性低密度的各种疾病，以加深对该CT表现的认识。资料与方法 搜集16例，其中肝豆状核变性5例，EB病毒性脑炎3例，一氧化碳中毒8例。均行CT平扫。结果 16例均表现为双侧基底核（壳核、苍白球和尾状核）对称性低密度，其中1对、2对或3对核团同时受累。结论 CT上表现为双侧基底核对称性低密度的疾病很多，其中肝豆状核变性，EB病毒性脑炎和一氧化碳中毒具有一定CT特征。了解具有以上CT表现的疾病范畴对于鉴别诊断具有重要意义。     

肝豆状核变性的颅脑CT诊断(附39例报告)

目的分析肝豆状核变性的颅脑CT征象,进一步提高对W ilson病的认识及诊断的正确率。方法全部病例均行脑CT扫描,回顾性分析其CT征象及临床表现。结果31例壳核出现对称性带状或弓状向外新月形低密度区,形如“八字”或“展翅蝴蝶”样;3例尾状核头见卵圆形低密度区;4例丘脑见对称性卵圆形低密度区;1例脑实质内未见异常密度但有脑萎缩表现。全部病例均有不同程度的脑沟裂增宽等脑萎缩表现。结论肝豆状核变性颅脑CT最多见征象是脑萎缩与基底节低密度灶,特别是双侧豆状核区对称性低密度灶最具有特征性。     

双侧基底节区对称性低密度病变的临床与CT分析

目的探讨双侧基底节区对称性低密度的CT诊断价值.材料和方法回顾性分析肝豆状核变性5例、中毒性病变7例、Wemicke脑病2例、Huntingtion氏大舞蹈病1例、kigh病1例和Hauervorclen-spatz氏病1例的CT平扫表现及临床意义.结果17例中,CT显示双侧豆状核低密度7例、苍白球6例、双侧豆状核伴胼胝体1例、壳核伴外囊2例、壳核伴尾状核1例;双额顶叶低密度5例、单侧壳核出血1例、大脑萎缩4例和小脑萎缩1例.结论CT平扫显示双侧基底节区对称性低密度可见于多种疾病,必须密切结合其他征象和临床,才能作出准确的诊断.     

一氧化碳中毒的CT诊断

目的探讨一氧化碳中毒的脑部CT特征。方法回顾性分析了18例一氧化碳中毒病人的脑部CT征象。结果双侧苍白球对称性低密度与脑白质低密度为最常见征象,前者占所有病例56%,具有特征性。脑皮质、海马、小脑病理改变也可发现。结论脑CT检查有助于临床确立诊断。     

脑内基底节区对称性低密度或异常信号的发病机理及CT-MR诊断

目的：分析基底节区对称性低密度或异常信号的发病机理，加深对其CT-MRI表现的认识。方法：30例病人均行CT及MRI横轴位扫描。结果：CT平扫均表现为两侧基底节区的对称性低密度，MRI T1WI呈对称性低信号，T2WI呈高信号。结论：MRI能更多地显示受累的部位，同时了解具有以上CT-MRI表现的疾病范畴，对于鉴别诊断具有重要意义。     

小儿急性中毒性脑病的CT诊断及临床表现

目的：研究婴幼儿急性中毒性脑病的CT及临床表现，以便明确诊断。资料和方法：选择有明确感染及药物接触史的18例1—10岁儿童，行头颅CT检查并结合临床症状，观察其CT表现。结果：急性冲毒性脑病主要CT表现为弥漫性脑水肿，部分患者基底节丘脑区呈对称性低密度区，个别患者基底节区和大脑多发钙化斑，晚期出现脑萎缩、软化灶。结论：CT诊断尚缺乏特异性，必须密切结合临床表现，对估计预后有一定帮助。     

肝豆状核变性的颅脑CT分析

目的 :分析肝豆状核变性的颅脑CT表现 ,评价CT对肝豆状核变性的临床诊断价值。方法 :对临床及实验室检查证实的 110例肝豆状核变性患者均进行颅脑CT平扫 ,部分给予增强扫描。结果 :颅脑CT无异常发现 2 0例 ,有异常发现 90例 ,阳性率为 81.8%。主要表现为各灰质核团区显示低密度影和 /或脑萎缩改变。其中双侧或单侧豆状核 5 2例 (单侧 8例 ) ,双侧丘脑 2 9例 ,双侧大脑脚 4例 ,桥脑 2例 ,双侧尾状核头 2例 ,双侧侧脑室旁 2例 ,双侧额叶 2例 ,双侧小脑齿状核 1例。脑萎缩 60例 ,仅表现为脑萎缩者 2 2例。结论 :颅脑CT对肝豆状核变性有很高的诊断价值 ,可为临床提供诊断和治疗依据。     

慢性酒精中毒性脑病的CT诊断

目的评估CT诊断慢性酒精中毒性脑病的价值。材料与方法分析15例CT和临床证实慢性酒精中毒性脑病的CT表现。结果(1)胼胝体变性15例;(2)伴双侧豆状核低密度7例,内囊／外囊和侧脑室周围白质低密度8例;(3)脑萎缩8例。结论胼胝体变性是慢性酒精中毒性脑病CT重要的表现,CT结合临床能明确诊断。     

皮质下动脉硬化性脑病的CT表现及其鉴别诊断

皮质下动脉硬化性脑病(SAE)亦称Binswanger′s病。SAE典型CT表现为两大脑白质弥散性相互融合的低密度灶,常两侧对称,脑室周围明显。低密度灶显著侧可有脑室扩大。早期病灶限于额叶,以后向侧脑室、枕叶和中央半卵圆中心区方向扩展。脑室常中度扩大,侧脑室边缘不整。成人脑CT出现室周围大脑白质弥散性低密度灶见于以下病理情况:①脑室内阻塞性脑积水;②脑室外阻塞性脑积水;③伴脑水肿的高血压脑病;④化疗引起的脑白质病;⑤放射性脑白质病;⑥脑室周围播     

小儿维生素B1缺乏性脑病的CT诊断价值

目的 :探讨维生素B1 缺乏性脑病的CT表现特征和诊断价值。方法 :对临床确诊的 12例维生素B1 缺乏性脑病患儿行颅脑常规CT扫描 ,并对其颅脑CT表现及临床资料进行综合分析。结果 :其中对称性的低密度见于尾状核和豆状核 7例 ,豆状核 3例 ,豆状核及颞叶 2例。经CT诊断的该组病例治疗取得明显的效果 ,5例治疗 1周后CT复查 ,2例基底节病灶消失 ,3例病灶明显减小。 2例患儿出现脑瘫后遗症 ,CT显示基底节区有对称性的囊变灶。结论 :小儿维生素B1 缺乏性脑病患儿 ,其颅脑CT表现两侧基底节区对称性的低密度改变有一定特征性 ,CT对该病诊断以及预后判断有重要价值。     

婴儿维生素B1缺乏性脑病的CT诊断(附25例分析)

目的 :探讨婴儿维生素B1缺乏性脑病的CT表现特点 ,提高临床诊断水平。方法 :回顾性分析 2 5例经临床证实的婴儿维生素B1缺乏性脑病患者的临床和CT资料。结果 :2 5例脑CT扫描均显示为双基底节 (壳核、苍白球、尾状核 )对称性低密度影 ,呈圆形或斑片状 ,可伴有脑白质低密度病变、脑萎缩、脑软化。结论 :CT对婴儿维生素B1缺乏性脑病的诊断具有重要价值。     

Usefulness of 99mTc ethyl cysteinate dimer brain SPECT to detect abnormal regional cerebral blood flow in patients with acute carbon monoxide poisoning

99mTc ethyl cysteinate dimer (99mTc-ECD) brain single photon emission computed tomography (SPECT) was used to detect abnormal regional cerebral blood flow (rCBF) in patients with acute carbon monoxide (CO) poisoning. Ten patients with acute CO poisoning and no past histories of psychoneurological disorders were enrolled in this study. After oxygen treatment, all of the 10 patients were investigated using 99mTc-ECD brain SPECT and brain computed tomography (CT) scan. Brain CT scan findings were normal in all of the 10 patients. 99mTc-ECD brain SPECT showed the hypoperfusion lesions of the basal ganglia and brain cortex in five and seven patients, respectively. Only three of the 10 patients had normal 99mTc-ECD brain SPECT findings. This study suggests that, in comparison with brain CT scan, 99mTc-ECD brain SPECT is a better tool for the early detection of hypoperfusion brain lesions in acute CO poisoning in patients with normal brain CT findings.     

Basal ganglia volumes following CO poisoning: A prospective longitudinal study.

Carbon monoxide (CO) poisoning may result in focal and diffuse neuropathological changes, including basal ganglia lesions. The effect of CO poisoning on basal ganglia volumes over time is unclear. We assessed basal ganglia volumes longitudinally following CO poisoning. We prospectively enrolled 73 CO poisoned patients who underwent brain MR imaging on day 1 (baseline), 2 weeks, and 6 months post-CO poisoning. Basal ganglia volumes were obtained. One patient had bilateral globus pallidus lesions at two weeks and 6 months. Of the CO-poisoned patients 28% had volume reduction in at least one basal ganglia structure by 6 months, of which 21% had putamen, 15% had caudate, 15% had globus pallidus, and 16% had total basal ganglia volume reduction. Putamen volumes were significantly smaller from baseline to six months (p = 0.02). Verbal memory and mental processing speed correlated with smaller putamen and globus pallidus volumes. Carbon monoxide poisoning results in basal ganglia volume reduction 6 months post CO poisoning. Slow mental processing speed and impaired memory correlated with smaller putamen and globus pallidus volumes. Clinicians need to be aware of basal ganglia neuropathologic changes in the absence of observable lesions following CO poisoning.     

中枢神经系统结核的CT及MRI诊断

本文报道了６７例中枢神经系统结核的ＣＴ及ＭＲＩ表现，其中结核性脑膜炎３８例，脑结核瘤１８例，结核性脑膜炎合并结核瘤５例、合并脊髓蛛网膜炎６例。头颅ＣＴ对病变显示率为８４．６％，病损类型有基底池渗出物、脑积水、结核瘤、脑梗塞、脑萎缩及基底池钙化等。增强ＣＴ扫描应列为常规检查。４例结核性脊髓蛛网膜炎ＭＲＩ扫描，显示蛛网膜下腔闭塞消失、髓内外结核瘤、脊髓受压或肿胀及晚期空洞形成，此类影像表现既往国内文献无系统报道。ＣＴ及ＭＲＩ各有长短，其定性价值仍需密切结合临床及脑脊液检查     

Cerebral blood flow and glucose metabolism measurements in a patient surviving one year after carbon monoxide intoxication.

A 29-yr-old woman was studied for 1 yr after acute carbon monoxide intoxication following an attempted suicide by inhalation of automobile exhaust fumes. The patient demonstrated impaired responsiveness to stimuli without any specific neurological deficits for 1 yr after carbon monoxide intoxication. Repeated brain magnetic resonance imaging consistently displayed only bilateral globus pallidus lesions, but no lesions in either deep white matter or cerebral cortex. Position emission tomography measurements of regional cerebral blood flow, and glucose utilization rate were made in this patient at 6 mo and 1 yr following carbon monoxide intoxication. Impairment of both blood flow and glucose metabolism were found not only in the basal ganglia but also in morphologically normal frontal cortex. The decrease in glucose utilization in the frontal cortex was greater than that in the basal ganglia. During the period of 6 mo to 1 yr, blood flow and glucose metabolism in the basal ganglia recovered to the normal range. In the frontal cortex, however, blood flow and glucose metabolism remained approximately 20% lower than the normal mean values. This prolonged dysfunction in the frontal cortex may therefore be responsible for the impaired responsiveness of the subject.     

Calcification of the basal ganglia following carbon monoxide poisoning

Summary Minor calcification of the basal ganglia was demonstrated by computed tomography in a woman, aged 66, who had survived carbon monoxide poisoning 48 years earlier. Extensive neuropathological investigations have demonstrated calcified lesions of the basal ganglia in a number of conditions, but their frequency and topographic distribution in vivo remain to be elucidated, by means of CT.     

Gd-DTPA-enhanced MR imaging of the brain in patients with meningitis: comparison with CT

Plain and Gd-DTPA-enhanced MR images of the brain were obtained in 18 consecutive patients with meningitis (eight with tuberculous, five with bacterial, three with viral, and two with fungal infections); the MR images were compared with CT scans. MR images were obtained on a 2.0-T superconducting unit with both T1- and T2-weighted pulse sequences before injection and with a T1-weighted sequence after injection of Gd-DTPA (0.1 mmol/kg) in all patients. In tuberculous meningitis, MR imaging depicted ischemia/infarct, hemorrhagic infarct of basal ganglia, meningeal enhancement at either basal cistern or convexity surface of brain, and associated small granulomas in a few more patients than CT did. In bacterial meningitis, primary foci of extracranial inflammation (i.e., mastoid, paranasal sinuses) and adjacent intracranial lesions including localized dural inflammation, subdural fluid collection, and/or brain parenchymal lesions were demonstrated much better on MR than on CT. Otherwise, MR images generally matched the CT scan. Although the plain MR images, both T1- and T2-weighted, were the most sensitive in delineating ischemia/infarct, hemorrhage, and edema, they were not as specific as Gd-DTPA-enhanced T1-weighted images and postcontrast CT scans in defining the active inflammatory process of the meninges and focal lesions precisely. We conclude that if Gd-DTPA is used, MR imaging appears to be superior to CT in the evaluation of patients with suspected meningitis. Precontrast MR is needed to delineate ischemia/infarct, edema, and subacute hemorrhage.