神经导航下经蝶窦入路显微手术切除垂体腺瘤

自2007年至今，我科采用神经导航辅助下经单鼻孔蝶窦入路显微手术切除垂体腺瘤，取得较好疗效，报告如下。1资料与方法 1.1一般资料 本组男7例，女5例；年龄18-65岁，平均年龄（36±5）岁；病程1-28个月，平均15个月。临床表现：头痛6例，闭经、泌乳5例，肢体肥大2例，视力下降8例，视野改变8例。术前常规行各项内分泌检查，     

经胼胝体入路显微外科切除丘脑胶质瘤9例

丘脑起源的肿瘤较少,占颅内肿瘤的1～5％,其中以胶质瘤较为常见。丘脑肿瘤位于大脑深部,虽然发生率不高,但由于丘脑胶质瘤位于脑中线深部,毗邻内囊、下丘脑、第三脑室等重要结构,手术难度大,手术病死率及病残率高,其治疗一直是神经外科的难题。既往认为该区肿瘤邻近重要结构不宜手术切除,但随着显微神经外科技术的不断发展,胶质瘤可得到大部甚至全部切除。我院于2005年1月～2008年12月对9例丘脑胶质瘤实施经胼胝体人路显微外科手术治疗,现对临床资料进行回顾性分析,现报告如下。     

多技术联合在丘脑胶质瘤显微手术治疗中的应用

丘脑胶质瘤毗邻第三脑室、下丘脑、内囊等大脑重要结构,是一种具有致残率高、手术难度大等特点的颅内肿瘤疾病[1],患者多有抑郁、精神呆滞、颅内压增高等问题,手术不当易致人死亡.鉴于此,本院以锥体束导航结合术中高场强磁共振技术辅助完成丘脑胶质瘤显微手术,其中锥体束导航可减少患者大脑功能结构的损伤[2],而高场强磁共振技术则能...     

神经导航下切除颅内肿瘤28例

神经导航系统又称无框架立体定向系统,它是经典立体定向技术、现代神经影像诊断技术、微侵袭手术、电子计算机技术结合的产物,是20世纪80年代后神经外科领域开展的一门新技术[1].神经导航技术为术中精确定位及脑内微创手术创造了条件.我院自2005年9月以来应用美国Stealth Station神经导航系统,完成28例颅内脑深部占位病变的手术切除,取得良好效果,现报告如下.     

神经导航下切除颅内肿瘤28例

神经导航系统又称无框架立体定向系统,它是经典立体定向技术、现代神经影像诊断技术、微侵袭手术、电子计算机技术结合的产物,是20世纪80年代后神经外科领域开展的一门新技术[1].神经导航技术为术中精确定位及脑内微创手术创造了条件.我院自2005年9月以来应用美国Stealth Station神经导航系统,完成28例颅内脑深部占位病变的手术切除,取得良好效果,现报告如下.     

丘脑胶质瘤的手术治疗

总结丘脑胶质瘤的临床特点,探讨显微手术方法和策略.方法 回顾分析5例丘脑胶质瘤患者的临床资料.经皮质入路3例,经皮质侧脑室入路2例.结果 肿瘤全切3例,次全切2例;术后症状改善2例,无明显变化2例,加重1例.无死亡病例.结论 手术方法和策略是决定丘脑手术成功的关键.     

显微外科手术治疗丘脑肿瘤

我科自1998年～2004年收治丘脑肿瘤患者9例。因丘脑肿瘤位于脑的深部,毗邻下丘脑、第三脑室和内囊等重要结构,手术切除困难,其外科治疗颇有争议。我科收治9例患者均经显微手术治疗,疗效满意,现总结如下：     

计算机辅助立体定向手术治疗超早期高血压丘脑出血

丘脑出血是高血压脑出血患者中相对较重的类型，患者有明显的偏瘫、偏身感觉减退、偏盲（三偏）症状，如优势半球出血还可出现失语．致残率较高。由于出血部位深在，开颅手术损伤较大，且需全麻，对病前有心、肺、肾等严晕疾患者多不适合。随着计算机辅助立体定向手术的发展，采用血肿单纯抽吸、血肿破碎吸引以及注药溶解血肿等方法．清除丘脑血肿已变得简单易行、创伤小．在局麻下即可施行。且早期治疗可以减轻脑组织损害，减少功能障碍及并发症，提高生存质量。本组采用计算机辅助立体定向手术治疗超早期高血压丘脑出血50例．观察其临床效果及预后。     

神经导航下微创穿刺治疗高血压脑出血临床报告

2007至2009年我科采用德国博医来公司Brain LAB神经导航引导下应用一次性颅内血肿穿刺治疗高血压病脑出血23例,效果良好,报告如下。1资料与方法1.1一般资料23例患者中,男13例,女10例;年龄28～72岁,平均年龄51.6岁;高血压病史3～35年。出血部位：基底节出血11例,脑叶出血12例。出血量25～60 ml。入院时格格斯哥昏迷评分（GCS）6～14分,均有不同程度的肢体偏瘫,     

丘脑性失语症的临床研究

目的 探讨丘脑血管病所致的丘脑性失语症的言语特点、解剖机制及预后.方法 选择2002年6月至2008年7月我科收治的13例丘脑性失语症患者,采用汉语失语症检查法进行失语检查,同时行神经系统检查、常规实验室检查,及头颅CT、MRI检查.所有患者按原发病治疗.结果 13例患者均有自发言语减少,音量减少;3例伴命名障碍;10例伴错语;11例伴理解障碍.3例头颅CT示优势半球侧丘脑出血;头颅CT正常的10例中,9例头部MRI示优势半球丘脑腹外侧核中上部处腔隙性梗死灶、1例示优势半球丘脑背内侧核腔隙性梗死灶.所有患者于5～12天丘脑性失语的临床表现肖失.结论 丘脑性失语症有其独特的言语特点,优势半球侧丘脑腹外侧核和丘脑背内侧核可能为责任病灶区.头颅MRI对丘脑出血及梗死均敏感,能明确丘脑性失语症的病灶.经积极治疗原发病,丘脑性失语症预后较好.

Abstract：

Objective To study the language characteristics, anatomical mechanism and prognosis of thalamic aphasia caused by cerebrovascular diseases of thalamus. Methods Thirteen patients with thalamic aphasia during June 2002 to July 2008 in our department were studied. Aphasia examination, physical examination of central nervous system, routine laboratory examinations, as well as CT and MRI scanning of brain were taken. All patients were treated according to thalamic infarction or hemorrhage. Results All patients presented as sparse verbal output and low tone, 3 cases accompanied with anomia, 10 cases with paraphasia, and 11 cases with disturbance of comprehension. Thalamic hemorrhage in dominant hemisphere was detected in three cases by CT scanning. Among the other ten patients with normal CT, lacunar infarction in ventrolateral nucleus of thalamas (VL) of dominant hemisphere was detected in nine cases, while lacunar infarction in dorsomedial nucleus of thalamas ( DM ) of dominant hemisphere was detected in one case. The manifestations of thalamic aphasia disappeared after treatment for 5 ～ 12 days in all patients. Conclusions Thalamic aphasia has its own language characteristics, which is different from cortical aphasia. VL and DM in dominant hemisphere are probably the responsible lesions for it. MRI scanning of brain is sensitive toboth thalamic infarction and hemorrhage, which is good for lesion detection. The prognosis of thalamic aphasia is good.     

丘脑出血123例临床分析

目的：观察丘脑出血的临床特点，探讨早期判定预后及病死率的相关因素。方法：对123例经CT确诊丘脑出血患者的临床特征及其预后进行分析。结果：123例患者平均年龄62．7岁，既往有高血压病史82例，入院时血压高于正常91例，意识障碍38例，眼球运动障碍57例，瞳孔变化17例，感觉障碍79例，运动障碍95例，血肿破入脑室32例。存活104例，死亡19例，病死率15．4％。结论：丘脑出血临床表现严重而复杂，病死率以及严重并发症的产生与年龄、血肿大小、是否破入脑室、下丘脑及脑干是否受累有关。     

丘脑梗死60例临床分析

目的：研究丘脑梗死的原因。方法分析我院2009年3月～2011年4月住院的60名患者的临床资料,观察患者的年龄、临床特征、影像学检查和治疗效果。结果46～65岁的患者比例为65.0%,主要病因是高血压动脉硬化症,大部分患者的首发症状是偏身感觉障碍,给予抗血小板凝集、改善循环和营养神经的治疗之后,多数患者可以达到好转。结论丘脑梗死多发于中老年人,患者多为丘脑梗死外侧型,疾病预后良好,经过2个月以上的治疗,基本可以达到好转或痊愈。     

对1例脑出血患者的药学监护

1例61a男性患者,因＂丘脑出血合并高血压、2型糖尿病＂入院,给予脱水、利尿、脑保护、促脑代谢、降血压、降血糖等治疗。入院后第11天患者发生吸入性肺炎,医生经验性给予哌拉西林/他唑巴坦抗感染治疗。结合患者肾功能低下、哌拉西林/他唑巴坦与依达拉奉联合应用可能出现肾衰竭加重情况,临床药师建议将抗菌药物改为头孢哌酮/舒巴坦;同时对硝苯地平合用二甲双胍出现低血糖症状进行分析,并建议两药间隔2h以上服用;并对糖尿病合并高血压患者降压药物选择进行讨论,建议将硝苯地平改为培哚普利。经合理优化治疗方案后,患者避免了肾损伤加重,血压及血糖控制平稳,病情明显好转。     

舒张压与丘脑出血预后关系的研究

目的探讨舒张压对丘脑出血患者预后的影响。方法回顾性分析我科2000年3月至2009年6月收治的200例丘脑出血患者的临床资料,以入院初始舒张压水平为分组依据,将所有患者分为低血压组(舒张压<70mmHg)﹑正常血压组(舒张压在70～90mmHg之间)及高血压组(舒张压>90mmHg),比较不同舒张压水平患者预后分布差别。结果所有丘脑出血病例中,合并低血压者20例(10.0%),正常血压者56例(28.0%),高血压者124例(62.0%),在治疗过程中继发脑出血患者18例(9.0%),均为高血压组患者;其中,低血压组死亡病例2例(10.0%),正常血压组死亡3例(5.4%),高血压组死亡11例(8.9%),与正常舒张压患者相比较,合并低舒张压病例死亡率最高,其次为高舒张压病例(P=0.030)。结论舒张压对丘脑出血患者预后的影响具有重要作用,其中,舒张压过低及过高者提示预后不良。     

76例丘脑出血患者血糖水平变化的观察研究

目的研究分析丘脑出血患者的血糖水平变化,分析血糖检测对丘脑出血患者的价值。方法选择2009年1月-2011年7月本院收治的丘脑出血患者76例为研究对象,观察患者起病后24h内的血糖变化水平。同时随访患者1年．观察发生高血糖患者与无高血糖患者的预后差异,分析导致高血糖的相关因素。结果76例丘脑出血患者发生高血糖39例,无高血糖37例。高血糖患者肥胖比例高,从发病到人院治疗时间长,与无高血糖患者比较,差异有统计学意义（P〈0．05）。高血糖患者1年内的残疾率高于无高血糖患者,差异有统计学意义（P〈0．05）。结论丘脑出血患者24h内发生高血糖比例较高,主要与患者肥胖、发病到入院的时间有关,且高血糖会直接影响患者预后。     

Caffeine and chlordiazepoxide: Effects on motor activity in the chronic thalamic rat

Summary The effects of three doses of caffeine and of chlordiazepoxide (CDX) on motor activity were tested in the chronic thalamic rat. In this preparation virtually all cortical, striatal and limbic structures were ablated. A small dose of caffeine had only a weak motor stimulant effect which was succeeded by sedation. Larger doses that are stimulatory in intact animals, depressed motor activity in the thalamic rat. Amphetamine, in contrast to caffeine, produced a substantial motor stimulation. CDX caused a dose-dependent reduction of motor activity, similar to its effect in the intact rat. It is concluded that (a) telencephalic structures are involved in mediating the stimulatory action of caffeine; (b) a sedative component of caffeine may be present, but masked, in the intact animal, and may be due to serotoninergic mechanisms; (c) the presence of limbic structures is not necessary for the sedative effect of CDX.     

Inhibitory effect of crotoxin on the pain-evoked discharge of neurons in thalamic parafascicular nucleus in rats.

Crotoxin (Cro), the principal neurotoxic component of Crotalus durissus terrificus, has been previously reported to have a behavioral analgesic effect in rats and mice. The present study investigated electrophysiologically the effect of Cro on pain-evoked unit discharge of neurons in thalamic parafascicular nucleus (Pf) and underlying mechanisms of its effect. The electrical discharge of Pf neurons was recorded with the microelectrode technique in rats. Intracerebroventricular (i.c.v.) injection of Cro at 0.25, 0.45 and 0.65 microg/kg resulted in a dose-dependent inhibitory effect on the pain-evoked discharge of Pf neurons. The discharge frequency and the discharge duration significantly (P<0.05) decreased after Cro administration. This inhibitory effect was significantly (P<0.05) attenuated after pretreatment with para-chlorophenylalanine (pCPA), or electrolytic lesion of dorsal raphe (DR) nucleus. In contrast, i.c.v. injection of atropine (muscarinic receptor antagonist, 5 microg) or naloxone (opioid receptor antagonist, 4 microg) had no effect on Cro-induced inhibition of discharge of Pf neurons. The results suggested that Cro has an analgesic effect, which is mediated, at least partially, by the central serotonergic system.     

Activation of dopamine D4 receptors modulates [3H]GABA release in slices of the rat thalamic reticular nucleus

The thalamic reticular nucleus (nRt) is innervated by dopaminergic projections from the sustantia nigra compacta (SNc) and is rich in dopamine D4 receptors, however, the functional effects of dopamine on this structure are unknown. We examined whether the D1 receptor agonist SKF 38393, or the D2 class receptor agonist quinpirole, modify depolarization evoked Ca(2+)-dependent [3H]GABA release. SKF 38393 was without effects, whereas quinpirole inhibited [3H]GABA release with an IC50 of 81 +/- 33 nM. Dose-dependence determinations of agonists (quinpirole and PD 168, 077) and antagonists (L-745,870, U-101958, clozapine and raclopride) with different affinities for different D2 class subtype receptors showed that a D4 receptor mediates quinpirole inhibition. We used methylphenidate, an agent that acts by increasing interstitial dopamine, to determine whether endogenous dopamine modulates [3H]GABA release. Methylphenidate inhibited [3H]GABA release showing that the nRt contains sufficient endogenous dopamine to activate D4 receptors. This inhibition was completely reversed by selectively blocking D4 receptors with L-745,870 or U-101958 indicating that the catecholamine receptors that modulate GABA release are D4 receptors. Given the importance of the nRt in the control of attention, sensory processing and the generation of rhythmic activity during slow wave sleep, it is possible that abnormal nRt function may generate some of the manifestations of the disorders of dopaminergic transmission.     

Cobratoxin inhibits pain-evoked discharge of neurons in thalamic parafascicular nucleus in rats: Involvement of cholinergic and serotonergic systems

The present study investigated the inhibitory effect of cobratoxin (CTX) on pain-evoked discharge of neurons in thalamic parafascicular nucleus (Pf) of rats and analyzed some of the mechanisms involved in this effect. Intracerebroventricular injection (icv) of CTX at 0.56, 1.12 and 4.50 μg/kg resulted in a dose-dependent inhibitory effect on the pain-evoked discharges of Pf neurons. The inhibition of pain-evoked discharges of Pf neurons by CTX at high dose (4.50 μg/kg) persisted at least for 2 h, while the inhibitory effect of morphine (40 μg) persisted no longer than 30 min. The inhibitory effect of CTX was reversed by pretreatment with atropine (icv, 5 μg). In contrast, icv injection of naloxone (4 μg) had no effect on CTX-induced inhibition. Furthermore, pretreatment with parachlorophenylalanine, a specific inhibitor of tryptophan hydroxylase, also significantly attenuated the inhibitory effect of CTX. The results suggested that: (a) CTX has a dose-dependent inhibitory effect on pain-evoked discharges of Pf neurons, confirming electrophysiologically the antinociceptive action of CTX; (b) the inhibitory effect of CTX has a longer duration compared to that of morphine; (c) central cholinergic and serotonergic systems, but not opioidergic system, are involved in the inhibitory effect of CTX.