原发性中枢神经系统淋巴瘤的MRI表现与病理对照

目的探讨原发性中枢神经系统淋巴瘤(primary central nervous system lymphoma,PCNSL)的MRI表现与病理学特征。方法回顾性分析18例经病理证实的PCNSL的MRI资料和病理资料。结果 18例患者均为B细胞淋巴瘤,16例为单发,2例为多发。多为圆形或类圆形,边界较清楚,瘤周水肿及占位效应轻。MR平扫T1WI等信号12个,略低信号16个,T2WI呈等低信号21个,略高信号7个;DWI呈高信号20个。14例行1H-MRS检查,11例肿瘤实质区均出现典型中度减低的NAA峰,明显升高的Cho峰,10例出现高耸的特征性的Lip峰。增强扫描,18个病灶明显团块状或结节状均匀强化,典型的出现缺口征及尖角征。13例可见瘤细胞围绕血管呈袖套样浸润。结论 PCNSL的病理学基础决定其MRI表现有一定特征性,MRI检查对于PCNSL的鉴别诊断具有十分重要的价值,对临床治疗方案的制定具有重要意义。     

中枢神经细胞瘤的CT和MRI影像学分析

目的 探讨中枢神经细胞瘤(CNC)的CT和MRI表现.方法 回顾性分析经手术病理证实的12例CNC患者的CT和MRI表现.12例均进行了MRI平扫和增强,3例同时进行了CT平扫.结果 12例CNC中有11例位于侧脑室内,其中2例位于右侧侧脑室,3例位于左侧侧脑室,以宽基底与透明隔相连;6例位于侧脑室透明隔,跨越中线向两侧生长,其中2例突入第三脑室;l例位于第四脑室出口处.肿瘤呈类圆形或不规则形的团块影,边界清楚.肿瘤在T1WI上呈等或低信号,T2WI和横断面液体衰减反转恢复序列(T2FLAIR)上呈中等至稍高信号.3例可见流空血管信号.增强扫描后,大部分肿瘤呈轻度至中度不均匀强化,仅l例明显强化.3例行CT平扫病例,肿瘤实体部分呈等或稍高密度,2例可见团块状或点状钙化.结论 发生于侧脑室内的CNC有较为特征性的CT和MRI表现,结合其好发部位、发病年龄可以在术前做出有效的诊断,而发生于侧脑室外的CNC术前诊断困难.     

脑室内中枢神经细胞瘤的MRI表现

目的：探讨脑室内中枢神经细胞瘤（CNC）的MRI影像特点,以提高对本病的认识。方法：回顾性分析经手术病理证实的CNC8例,男5例,女3例,年龄21～45岁,平均26.7岁,分析其MRI表现。结果：肿瘤均位于侧脑室透明隔或第三脑室,靠近Monro孔处,T1WI均呈等信号;T2WI信号与皮层灰质比较多为等高信号。部分肿瘤内部可见囊变、出血,边界清晰。结论：发生于青年人,位于透明隔及其附近的肿瘤,应考虑CNC的诊断可能。     

一例急性脊髓型减压病分析

急性减压病较之减压性骨坏死发病急,但大多数经过减压治疗后可痊愈。急性脊髓型减压病是由于气泡侵犯神经系统,起病急,进展快,如延误治疗则易造成严重后遗症。本文通过对我院诊断的一例急性脊髓型减压病进行分析,旨在使大家对该病有一个了解并引起重视。     

乙醇治疗急性减压病的实验观察

通过调查和动物实验指出:乙醇对急性减压病的治疗有肯定疗效.为了探索急性减压病时血小板的变化及乙醇治疗后血小板的恢复情况,我们又作了动物实验,报告如下:     

原发性中枢神经系统淋巴瘤的MRI表现

目的 探讨原发性中枢神经系统淋巴瘤的MRI影像学表现,以提高对该病的诊断准确率。方法 回顾性分析8例经手术及病理证实的原发性中枢神经系统淋巴瘤患者的MRI影像学资料。结果 本组8例患者共14个病灶,其中4例为单发病灶,4例为多发病灶。病灶部位包括额叶、颞叶、岛叶、枕叶、胼胝体、侧脑室周围脑白质、脑室室管膜及室管膜下、小脑蚓部,且多位于幕上,仅1个位于幕下。MRI显示T1WI呈等或低信号、T2WI呈等或略高信号,仅1例病灶合并出血、2例有囊变,均未见钙化,瘤周均有水肿,增强扫描呈明显均匀强化。结论 原发性中枢神经系统淋巴瘤的MRI表现具有特征性,掌握其MRI特点有助于提高诊断的敏感性及准确性。     

乙醇治疗急性减压病疗效观察

目的观察乙醇治疗急性减压病（acute decompression sickness,ADCS）的疗效。方法给予12例ADCS患者52度白酒（乙级大曲）100-150ml,加入等量的5％葡萄糖溶液中,于10min内口服完毕,然后观察并记录ADCS相关症状和体征消失的时间。结果6例ADCS患者,其潜水深度≤30m,潜水时间≤108min,重复潜水≤2次,饮酒后15min症状和体征明显好转,30min症状和体征基本消失,60min左右完全消失恢复正常。其余6例ADCS患者于饮酒后25min症状和体征明显好转,50min左右症状和体征基本消失,140min内左右完全消失恢复正常。结论饮酒治疗ADCS疗效肯定,无明显不良反应,是有效代替加压的治疗方法。     

反复潜水后急性减压病的临床分析

目的分析反复潜水后急性减压病患者的临床特点，探讨在常规按个体化治疗方案不能实施的情况下同时治疗多个患者的方案选择。方法统计影响疗效和复发率的因素及临床症状，依照症状和体征对所加压力的反应情况选择治疗方案，根据不同治疗方案分A组、B组、C组、D组。结果本组治愈90例（78．26％），好转25例（21．74％），无效0例，复发19例（16．52％）。（1）年龄、工龄、潜水深度、水下工作时间及初发或再发与疗效呈正相关（P〈0.05或P〈0.01），并且年龄、工龄、劳动强度、潜水深度、初发或再发、疼痛程度与复发否也呈正相关（P〈0.05或P〈0.01）；而潜伏期与疗效及复发否呈负相关（P〈0.01）；（2）年龄、潜水深度、初发或再发与疼痛程度呈正相关（P〈0.05，P〈0.01）；潜伏期与疼痛程度呈负相关（P〈0．05）；（3）治疗方案、工龄、潜水深度和潜伏期4个因素可解释疗效变化的48．0％：（4）不同治疗压力中D组、C组、B组治愈率较A组明显提高，而复发率明显低于A组，差异均有统计学意义（P〈0.01，P〈0.05）；（5）相同治疗压力不同治疗时间中D组治愈率明显高于B组，复发率明显低于B组；（6）相同治疗压力相同治疗时间中D组治愈率较C组治愈率明显提高。结论在氧舱条件受限的情况下，其治疗应首选D组的吸氧Ⅳ方案，不必过分拘泥于每个个体症状和体征对压力的反应情况同时进舱。并且根据患者的临床症状适当延长高压下停留时间，一般不超过120min。     

乙醇治疗急性减压病疗效观察

目的观察乙醇治疗急性减压病（ADCS）的疗效。方法给予12例ADCS患者52度白酒（乙级大曲）100～150 ml,加入等量的5%葡萄糖溶液中,于10 min内口服完毕,然后观察并记录ADCS相关症状和体征消失的时间。结果6例ADCS患者,饮酒后15 min症状和体征明显好转,30 min症状和体征基本消失,60 min左右完全消失恢复正常。其余6例ADCS患者于饮酒后25 min症状和体征明显好转,50 min左右症状和体征基本消失,140 min左右完全消失恢复正常。结论饮酒治疗ADCS疗效肯定,无明显不良反应,是有效代替加压的治疗方法。     

减压病的防护

减压病又称潜函病、潜水夫病、潜水员瘫痪、高压病等。该病是人从气压高处转到气压低处由于下降过快,幅度太大,使血液和组织内原来溶解的气体释放出来,形成气泡而导致的病理反应。我国沿海地区随着建设事业的发展,水产业的养殖、捕捞以及筑港、船舶维修业等不断发展,依据工作需要,潜水作业工人不断增加,工作中接触有害物理因素机会增多,容易引起减压病。到1985年末累计,仅大连市300多名潜水作业工人经体检发现,高气压危害突出,曾患有减压病者达84名,占全市从业人数的28％,在近4年体检中,每年还发现有新病人。减压病,轻者常见有皮肤癌     

Central nervous system decompression sickness: latency of 1070 human cases

Many aspects of central nervous system (CNS) decompression sickness (DCS) are poorly understood, including the temporal pattern of its presentation and the pathogenic mechanisms involved in the development of the disease. Using case histories and clinical series published in the literature and retrieved from treatment center records, this study is an attempt to define the interval between surfacing from a hyperbaric exposure and the onset of symptoms of CNS DCS. The results of 1070 cases of human CNS DCS were included in the study. The results show that the disease generally occurs rapidly: over 50% became symptomatic within 10 min of returning to 1 ATA, and in only 15% of cases was the onset of symptoms delayed for more than 1 h. Cerebral DCS had a more rapid onset than spinal cord disease: 50% of cerebral cases became apparent within about 3 min and a similar proportion of spinal cord cases within about 9 min from surfacing. The influence of these results on the diagnosis and treatment of dysbaric illness, on the safety of certain diving practices, and on possible pathogenic mechanisms is discussed.     

A combined deficiency of vitamins E and C causes severe central nervous system damage in guinea pigs

A short period of combined deficiency of vitamins E and C causes profound central nervous system (CNS) dysfunction in guinea pigs. For this report, CNS histopathology was studied to define the nature and extent of injury caused by this double deficiency. Weanling guinea pigs were fed a vitamin E-deficient or -replete diet for 14 d. Then vitamin C was withdrawn from the diet of some guinea pigs. Four diet groups were thus formed: replete, vitamin E deficient, vitamin C deficient, and both vitamin E and C deficient. From 5 to 11 d after institution of the doubly deficient diet, 9 of 12 guinea pigs developed paralysis, and 2 more were found dead. The remaining guinea pig in the doubly deficient group and all animals in the other 3 groups survived without clinical impairment until the experiment was terminated at 13-15 d. Brains and spinal cords were serially sectioned and stained for examination. Only the combined deficiency produced damage in the CNS. The damage consisted mainly of nerve cell death, axonal degeneration, vascular injury, and associated glial cell responses. The spinal cord and the ventral pons in the brainstem were most severely affected, often exhibiting asymmetric cystic lesions. Several features of the lesions suggest that the primary damage was to blood vessels. These results indicate that the paralysis and death caused by combined deficiency of vitamins E and C in guinea pigs is caused by severe damage in the brainstem and spinal cord.     

Ethanol treatment for acute decompression sickness in rabbits

Rabbits developed acute decompression sickness after staying at 6 ATA for 30 min followed by decompression to 1 ATA in 20 min or less. If the rabbits received an i.v. injection of 25% ethanol upon surfacing, all survived, whereas half the untreated control group died within 15-35 min after decompressing. In ethanol-treated animals, no bubbles were seen in blood vessels of visceral organs, muscles, and subcutaneous tissues at autopsy 60 min after treatment. Decompression reduced platelet counts markedly in all rabbits, but in the control group the count stayed low, whereas with ethanol treatment the counts had reached the precompression level after 1 h and 24 h.     

原发性中枢神经系统淋巴瘤MRI表现及误诊原因分析

目的 对于原发性中枢神经系统淋巴瘤MRI表现及误诊原因进行分析.方法 2007年12月～2010年12月某医院收治的原发性中枢神经系统淋巴瘤患者,共选取15例,男7例,女8例,使用SIEMENS IMPACT 1.OT及SIEMENS Trio with Tim 3.0 T超导型磁共振成像仪.结果 15例患者中,经手术证实5例,随访证实10例.MRI诊断正确的11例,误诊4例,误诊率为26.67%.其中误诊为脑胶质瘤的1例,误诊为转移瘤的1例,误诊为脑炎的1例,误诊为脑膜瘤的1例.其中单发的6例,多发9例.发生在幕上14例,幕下1例.结论 要重视对MRI新成像方法 的应用,有利于避免误诊,为临床治疗提供帮助.     

手足口病患儿合并中枢神经系统损害临床特征分析

目的 分析手足口病伴发中枢神经损害患儿的临床特征,以期为该病的临床防治工作提供参考依据.方法 回顾性分析2008年3月-2012年8月医院收治的手足口病伴发中枢神经损害66例患儿临床资料,统计分析其相关的临床特征.结果 66例手足口病伴发中枢神经损害的患儿中男42例占63.6％,女24例,占36.4％,男性的发病例数显著高于女性(P＜0.05);居住在农村的患儿50例占75.8％,城市的16例占24.2％,两者之间差异有统计学意义(P＜0.05);伴发中枢神经损害的患儿年龄主要集中在＜3岁,占78.8％;中枢神经系统损害主要表现为精神萎靡、手足抖动和嗜睡或昏睡,分别占92.4％、63.6％和57.6％,其次为易惊、昏迷、烦躁不安、肢体无力、抽搐等,分别占25.8％、22.7％、21.2％、19.7％和18.2％.结论 手足口病患者伴发中枢神经损害主要集中在＜3岁的患儿,精神萎靡、手足抖动和嗜睡或昏睡是其早期最常见的神经系统损害症状,早期的诊断和积极的治疗是减低死亡率和致残率的关键.     

Acute decompression illness following hyperbaric exposure: clinical features of central nervous system involvement

Decompression illness (DCI) is a general term encompassing all pathological changes secondary to reduction of environmental pressure. This condition has two forms: decompression sickness (DCS) and arterial gas embolism (AGE) secondary to pulmonary barotrauma. Moreover, DCS is categorized as minor, such as limb and/or joint pains or skin rash (Type I), and serious, as in cardiopulmonary and/or central nervous system involvements (Type II). Cerebral and spinal injuries have been symptomatically classified into AGE and DCS. Brain scans of patients with AGE or DCS showed multiple cerebral infarctions in the terminal and/or border zones of the cerebral arteries. Brain involvements of patients in both AGE and DCS show no differences in neurological or neuro-radiological findings. From the neurological and radiological standpoint, it is therefore impossible to distinguish these two conditions. Despite established treatments for neurological DCI (both AGE and DCS), it is unclear whether US Navy treatment Table 6 is preferable to standard hyperbaric oxygen therapy such as 2.4 atmospheres pressure for 90 minutes. Japanese laws and regulations have peculiarities that permit air diving to 90 meters depth, but with explicit prohibition of the use of oxygen for decompression, albeit a limited use of mixed gas is permissible. Moreover, currently the health screening for hyperbaric workers does not include detailed examination of the cardiopulmonary or the central nervous system.     

Microbubble damage to the blood-brain barrier: relevance to decompression sickness

Decompression sickness affecting the nervous system is still a serious problem in diving, but the mechanisms involved are in dispute. Although microbubbles can be detected in the pulmonary artery on decompression using ultrasound, mammalian lungs are competent filters for microbubbles larger than 20 microns in diameter. It has been assumed that smaller bubbles released by the lungs are harmless, because there is evidence that they do not arrest in the cerebral circulation. We injected 15 +/- 5 microns diameter microbubbles in 5 ml of plasma slowly into the right carotid artery of anesthetized guinea pigs. At intervals of 1, 2, or 3 h postinjection, 2% trypan blue in 2 ml of plasma was injected into the same artery or the contralateral carotid artery. A control animal for each experiment was injected with 5 ml of plasma only, followed by the injection of dye at the same interval. After the animals were killed, the brains were examined for evidence of blood-brain barrier dysfunction. All animals at 1 h, and 9 out of 10 animals at 2 h after the injection of microbubbles, showed extravasation of the albumin-binding dye in the ipsilateral hemisphere, indicating gross blood-brain barrier dysfunction. In each of the matched controls, the barrier in the neocortex remained intact. At Hour 3 the barrier was impermeable to the trypan blue in both experimental and control animals. These experiments demonstrate that microbubbles impair the blood-brain barrier integrity to protein, causing focal edema.(ABSTRACT TRUNCATED AT 250 WORDS)