慢性疼痛与抑郁症

疼痛,特别是慢性疼痛与抑郁症常常同时存在,而抗抑郁剂缓解疼痛的机制至今尚未完全澄清。把慢性疼痛作为抑郁症的症状谱之一,有利于改善患者的病情。本文试从疼痛与抑郁之间解剖结构的关联性、神经递质改变的相似性、临床表现以及治疗方面的特点对两者的关系加以综述。     

颅内肿瘤诊断的几点体会

临床诊断延误的常见原因颅内肿瘤又称脑肿瘤,是相当常见的颅内疾病,约占全身肿瘤的2%,在儿童期则约占7%。近20年来颅脑疾病的诊断水平有较大的提高,尤其是计算机X线断层照相术(CT)、磁共振成像(MRI)等的应用,能对脑肿瘤快速准确地作出判断,利于及时治疗。同其他辅助检查一样,这些成像诊断技术的检查     

高血压性脑血管功能损伤的临界关闭压评价

背景近来提出的临界关闭压在脑血流自动调节中起着关键作用,是脑循环的有效下游压,可客观反映动态调节的脑血管紧张度,即血管平滑肌收缩舒张的功能状态.目的利用临界关闭压动态评价高血压对脑微动脉平滑肌收缩功能的损伤及其与病理形态改变间的关系.设计随机对照的实验. 单位广州医学院第二附属医院神经科学研究所、中山大学附属第一医院神经科.材料实验于2002-07/2003-08在中山大学生理科学实验室进行.选择健康雄性SD大鼠160只,随机分为对照组和高血压组,每组80只.方法高血压组用双肾双夹法复制成易卒中型肾血管性高血压大鼠模型.对照组除不上银夹外,其余处理同高血压组.两组动物在术后的第2,4,6,8,10,12,14及16周8个时间点各随机选取10只进行动脉血压、临界关闭压的测定.测定完毕后在麻醉状态下取大鼠额顶叶脑组织,制成切片,定量分析脑微动脉的形态变化.主要观察指标①两组大鼠术后不同时间点动脉血压、临界关闭压.②两组大鼠术后不同时间点脑微动脉形态参数.结果160只大鼠均进入结果分析.①高血压组平均动脉压于术后第6周起明显升高,均显著高于对照组(P＜0.05).②高血压组大鼠术后脑血管临界关闭压逐步升高,于术后14,16周明显高于对照组[(63.75±7.43),(37.28±3.68)mm Hg;(67.37±15.57),(38.39±7.41)mm Hg,P＜0.05].③高血压组大鼠脑内微动脉的中膜厚度增加非常明显,于第8周后显著大于对照组(P＜0.05).④临界关闭压的升高与平均动脉压、脑内微动脉的中膜厚度呈正相关(r=0.906 93,0.811 36,P均＜0.05).并且血压升高的初期和血压较高后临界关闭压变化较明显,于血压上升明显期则改变不显著,呈倒"S"形改变(R2=0.996 2,P＜0.05).结论高血压形成后脑微动脉平滑肌的收缩程度随动脉血压的动态升高而加强,血管紧张度相应提高,并且在高血压初期和血压较高后改变比较明显.     

西比灵与阿米替林防治偏头痛疗效研究

目的：评价西比灵、阿米替林防治偏头痛的疗效。方法：采用Zung氏焦虑自评量表（SAS）及抑郁自评量表（SDS）评价偏头痛患者的焦虑和抑郁程度。将SAS或SDS评分在40分以上的偏头痛患者随机分为西比灵加阿米替林组（A组）、西比灵组（B组）和阿米替林组（C组）；比较各组间疗效的差异。结果：偏头痛患者中有抑郁者69．3％，焦虑者53．7％。治疗30天后，A组SDS及SAS评分均有所降低（P＜0．05），B组和C组则无显著改善（P＞0．05）。A组及B组治疗前后自身对照在发作次数，持续时间及对生活的影响方面评分差异均有统计学意义（P＜0．05）；C组治疗前后比较则没有统计学意义（P＞0．05）。3组间两两对比以A组防治效果最好，B组次之，C组无效。结论：西比灵加阿米替林对偏头痛有预防效果，且对其伴随的情绪障碍改善也有效。     

电针对大脑中动脉闭塞大鼠脑内神经元特异性烯醇化酶及胶质纤维酸性蛋白表达的影响

目的：研究电针治疗对脑梗死病灶周围及海马神经元特异性烯醇化酶(NSE)及胶质纤维酸性蛋白(GFAP)表达的影响。方法：采用易卒中型。肾性高血压大鼠(RHRSP)，电凝法凝闭大脑中动脉(MCAO)。MCAO后给予电针治疗，在治疗5d、2周后分别处死，行免疫组化染色，计算NSE、GFAP的阳性单位值。结果：梗死边缘NSE表达在梗死5d时处于低水平，梗死2周组增高，电针治疗2周后海马的NSE表达明显增加；梗死5d时病灶周围GFAP阳性细胞数目增多，染色加深，胞体增大，突起增粗、增长，2周时变化更明显。电针治疗5d后，梗死边缘GFAP阳性单位值明显增高。结论：早期电针治疗能够提高海马区NSE及梗死灶周围GFAP的表达，促进了缺血后脑的可塑性变化，构成了脑梗死功能恢复的物质基础。     

实验性高血压所致的脑卒中与静息心率的关系

为探讨高血压个体中脑卒中发生与静息心率的关系。方法将易卒中型肾血管性高血压大鼠（ＲＨＲＳＰ）中，已发生脑卒中者的卒中前静息心率与未卒中者同时期静息心率进行比较；并观察不同药物抗高血压治疗后，脑卒中发生与静息心率的关系。结果高血压对照组中，已卒中大鼠卒中前心率快于未卒中大鼠同时期心率；静息心率≥３３０ｍｉｎ－１者，自发脑卒中率高于静息心率＜３３０ｍｉｎ－１者。美托洛尔减慢静息心率，显著降低ＲＨＲＳＰ的自发脑卒中率。结论静息心率是ＲＨＲＳＰ自发脑卒中的一个危险因素，能适当减慢静息心率的抗高血压治疗，可能有利于预防脑卒中。     

丁苯酞抗缺血性脑损害的靶细胞研究

目的 丁苯酞抗缺血性脑损害的细胞作用靶点.方法 培养大鼠原代脑微血管内皮细胞(BMECs)及神经元,将2种细胞联合培养或将BMECs培养液预处理神经元后,予神经元氧糖剥夺损伤(OGD),计算神经元存活率,观察丁苯酞对其影响.结果 丁苯酞不能直接提高神经元OGD损伤后的存活率,但能提高其中缺氧预处理及联合培养组的神经元OGD损伤后的存活率(P＜0.05).结论 丁苯酞对神经元的保护作用依赖于BMECs的正常功能,提示其脑保护的直接细胞靶点是BMECs.     

脑卒中组织化治疗与传统治疗的疗效和医学经济学比较

目的 探索符合我国国情的卒中治疗模式.方法 成立脑血管病专科,建立组织化的卒中病房,收集成立专科3年来我科住院病历资料完整的所有卒中病例,对普通病房与卒中病房在基本设置、诊治程序及卒中患者的住院时间、住院费用和预后方面进行了对比分析,并用方差分析和卡方检验进行了统计学检验.结果 卒中病房较普通病房有正规的基本设置和诊治程序易于实施组织化治疗,能轻度缩短住院时间,显著降低住院费用和死亡率、提高患者的好转率.结论 建立卒中病房简单、有效、可行,是符合我国国情的卒中治疗模式,有广泛的推广应用价值,具有蕈要的临床意义.     

Mixed Stroke

Purpose To summarize the chnical, autoptic and animal experimental dala of stroke, propose the concept of mixed stroke (MS) and demonstrate the enoiogy, pathogenesis, clinical mainfestations, prophylaxis and treatment of MS Background At present. stroke still is classified in the national and international academic fields as two main groups: hemorrhage and ischema In fact, thc cerebral vascular disease with hemorrhage forus and ischema focus at the same time is not rare moreover, this type of stroke has special etiology, pathogenesis and clinical manifestations. But it is always made a main dagnosis and neglected the other nature of coexistent focus on either clinical or pathological diagnosis according to traditional classification of stroke Data sources and methods Mort of pablished originsl articles about MS in our department and laboralory wcre reviewed. Resulta The clinical autoptic and animal experimental dats all prcved that hemorrhage and infarction could occur in the course of a stroke simultaneously or in suecession during a short time, which demonstrated the existence of MS It was found clinically that MS patients all had the hustory of hypcrtension and in the autoptic data the MS patients dying of stroke all had typical hypertensive changes in the heart and kidney. and had hypertensive arteriosclerosis in the cerebral arteriole and small artery. MS was cas lily thdueed in stroke-prone renovascular hypertensivc rats This kind of rats are free from genetic deficiency and arc not affected by senile factor, so their cerebral vascular foci are mainly induced by the single factor -hypertension. TThese indicate definitely that hypertensive cerebral vascular lesion is the basis inducing MS. The main lesions of hypertensive cerebral arteriole and small artery were hyalinosis and fibrinoid of the walls, and the formation of microaneurysms or hyperplasla of iniernal and external layers The math lcsions of hypertensive cerebral capillaries were increasing vascular permeability. mural damage. edema of brain tissuc surroumding the vessel. stenotie lumen and leakage of bloed cells These lcsions in varying degrees were observed at different part of thc same brain or at different length of the same vessel at the same time, on the basis of which both hemocrhagic stroke and ischemic stroke could occurr These indicate the brain of the same patient with hypertension has pathomocpliological base of hemorrhagic strokc and ischemic stroke at the same time After after acute cerebral vascular disease occurring, it can be complicated by the other opposite nature of focus during a short time owing to oppression. draw. vascular spasm, metabolic disotder. sharp fluctuation of systemic blood pressure and other factors. The MS patients often had alterations of consciousness and the sign5 of meningeal irritation. were easlily complicated by multiple system organ failure Few cascs had distinct mulufocal cerebral lesions climcally. but after a careful cxamination of the nervous system. bilateral pathologic reflexes were often found. CT or MRI is an important means to diagnose Mis and should be used in 1 -Sd after the onset The measures of treatment for MS should be more vigorous and reliable The factors aggravating pathological lesion should be paid special attention to prevent When MS suspected of occurring clinically, rational neutral measures of treatment are advisable With MS definitely diagnosed the doctors should treat the main foous positively. keep homeostasis, prevent the disorder of hypothafamic function. select proper drugs and treat mfection positively Preventing multiple system organ failure is a key to decrease the mortality of MS. Having spent many years exploring, we establish the anunal model of coexistent infarction and hemorrhage on the basis of stroke-prone renovascular hypertensive rats The incidence of MS up to 95% was found in the group. which were given an inIection of fiblinogen and resperpine. As this model can stimulate the clinical evolution of stroke very well and has very high incidence. it Is a good animal model of MS. conclusions It is essential to list MS as a type of stroke singly. Valuing and studying MS are im ponant for the whole fieid studying pathogenesis. prophylaxis and treatment of stoke.