巨细胞动脉炎:颞动脉活检光镜研究

目的 探讨中国人巨细胞动脉炎(GCA)颞动脉活检的病理学特征和意义。方法 诊断为GCA的患者20例，非GCA患者7例为对照；以临床症状、颞动脉活检、类固醇激素治疗及随访结果作为诊断标准。结果 20例患者被诊为GCA，其中16例符合美国风湿病学会(ACR)的GCA诊断标准，18例显示活跃期血管炎，14例显示跳跃性损害，灵敏度、特异度和阳性预告值分别为90．0％、83．3％～94．8％。结论 提示颞动脉活检对GCA的诊断和治疗都具有重要意义。     

巨细胞动脉炎患者血管白介素6与信号传递子和转录激活子3的表达水平及其相关性

目的 研究巨细胞动脉炎(GCA)患者血管白介素-6(IL-6)与信号传递子和转录激活子3(STAT3)蛋白的表达水平及其相关性.方法 用免疫组化方法,检测20例GCA和6例其他神经系统疾病患者(对照组)颞动脉中IL-6和STAT3蛋白的表达.同时记录GCA患者6项与炎症有关的指标,分为炎症指标≥3项组(7例)与≤2项组(13例).并分析 IL-6与STAT3蛋白表达水平的相关性.结果 GCA组颞动脉IL-6阳性细胞评分、STAT3阳性细胞数分别为(2.85±0.75)分及(40.71±9.90)个/高倍视野,显著高于对照组[(2.00±0.63)分,(30.73±10.84)个/高倍视野](均P＜0.05);GCA组炎症指标t≥3项组IL-6、STAT3蛋白的表达水平显著高于炎症指标≤2项组(P＜0.01,P＜0.05);IL-6与STAT3蛋白表达水平呈正相关(r=0.883,P＜0.05).结论 GCA患者血管IL-6、STAT3蛋白表达水平显著增高;两者表达水平呈正相关;提示IL-6可促进STAT3的表达.     

颞动脉炎47例临床资料分析

目的总结颞动脉炎的临床特征及病理改变。方法收集国内报告的44例及本院治疗的3例。共47例(其中29例进行活检)资料进行分析。结果头痛46例(97.9%);视力障碍12例(25.5%);低热(6/14,42.9%);脑神经麻痹13例(27.7%),其中动眼神经8例、外展神经2例、面神经2例、听神经1例;合并风湿性多肌痛6例;合并脑梗死5例、脑出血2例。血沉80.6%(29/36)增快,C反-应蛋白71.4%(5/7)增高。颞动脉均增粗、变硬。颞动脉活检29例,28例证实为颞动脉炎。皮质内固醇治疗效果良好。结论颞动脉炎临床并不十分罕见,掌握其临床特征,多可诊断。颞动脉活检可确诊,皮质类固醇治疗效果良好。     

28例原发性中枢神经系统血管炎活检确诊病例回顾性分析

目的总结原发性中枢神经系统血管炎活检确诊病例的临床特点、治疗效果及远期预后,分析其危险因素,为本病的诊断治疗提供临床指导。方法采用病例回顾性研究方法,对我院收治的28例原发性中枢神经系统血管炎活检确诊病例,分别统计患者年龄、性别、病理结果、病程进展、影像学表现、治疗及预后情况,分析总结经验。结果 28例患者中男性16例,女性12例;年龄16～60岁;就诊至确诊的时间平均为6个月;首发症状表现为慢性头痛的患者18例;病理伴有脱髓鞘10例,伴有胶质细胞增生6例;糖皮质激素冲击+环磷酰胺治疗27例,其中开颅手术切除3例均好转。28例患者经治疗好转15例,携带12例,死亡1例。预后不良患者多为确诊前病程较长,确诊时KPS评分低于60分,治疗前已出现行为认知异常及短期内(0.3～1个月)病情即复发。结论原发性中枢神经系统血管炎患者容易误诊误治,病因不明且多因耽误治疗而预后差,建议早期活检病理确诊并及时糖皮质激素冲击治疗,对于占位效应明显的患者应积极手术切除治疗。     

吸烟对精神分裂症男性患者精神病理症状的影响

目的 分析吸烟对精神分裂症临床精神病理症状的影响,探索精神分裂症患者高比例吸烟的原因.方法 收集慢性精神分裂症吸烟患者(332例)和非吸烟患者(95例)共427例,首次发病(以下简称首发)精神分裂症吸烟患者(22例)和非吸烟患者(41例)共63例,均为男性;使用阳性和阴性症状最表(PANSS)评定其临床精神病理症状.结果 (1)在慢性精神分裂症患者巾,吸烟组PANSS阴性症状分量表中的情感交流障碍得分[(3.9±1.5)分]、被动或淡漠得分[(3.6±1.6)分]及其总分[(24.0.±8.2)分]低于非吸烟组[分别为(4.4.±1.7)分、(4.0±1.7)分和(26.3.±9.5)分;P<0.05];PANSS阴性症状分量表7个条目得分及其总分、一般精神病理分量表总分和PANSS总分与患者每天的吸烟量呈负相关(P<0.05～0.01);阴性症状分量表中的情感交流障碍[比值比(OR)=0.832,95%可信区间(95%CI)=0.691～0.980,P=0.029]和一般精神病理分量表中的紧张(OR=0.534,95%CI=0.363～0.786,P=0.001)进入Logistic模型.(2)在首发精神分裂症患者中,吸烟组在阴性症状分量表中的情绪退缩得分[(2.7±1.3)分]、被动或淡漠得分[(2.7 ±1.3)分]低于非吸烟组[分别为(3.5±1.3)分和(3.5±1.4)分;P<0.05];一般精神病理分量表中的动作迟缓与患者每天的吸烟量呈负相关,自知力缺乏与吸烟量呈正相关(均P<0.05);PANSS一般精神病理分量表中的动作迟缓(OR=0.589,95%CI:0.350～0.989,P=0.045)进入Logistic模型.结论 吸烟对阴性症状的正性作用可能是精神分裂症患者高比例吸烟的原因之一.     

奥氮平与氯氮平治疗精神分裂症对照研究

目的　研究奥氮平治疗精神分裂症的疗效及安全性。方法　分析 6 1例用奥氮平治疗 6周的精神分裂症病例 ,并与 6 1例用氯氮平治疗的精神分裂症病例作对照 ,采用阳性及阴性症状量表 (PANSS)的减分率评价疗效 ,用副作用量表 (TESS)评价 6周末的副作用。结果　 6周末PANSS量表总分、阳性症状分、阴性症状分和一般病理分与治疗前比较 ,两组差异均有非常显著性 (P <0 .0 1) ,但两组间差异无显著性 (P >0 .0 5 )。于 2周末两组间除一般病理分外 ,余差异均有极显著性 (P <0 .0 1) ;于第四周末一般病理分差异也有非常显著性 (P <0 .0 1) ;副作用两组间比较 ,奥氮平组明显小于氯氮平组。结论　奥氮平治疗精神分裂症疗效好、起效快、副作用小。     

前颞叶切除术或选择性海马杏仁核切除术治疗顽固性内侧颞叶癫痫患者神经心理功能改变的研究

目的 探讨前颞叶切除术(ATL)或选择性海马杏仁核切除术(SAH)治疗顽固性内侧颞叶癫痫(MTLE)患者神经心理功能的改变情况。方法 选择2010年1月-2014年12月来本院接受ATL或SAH治疗的MTLE患者60例; 根据MTLE手术部位分为左颞部MTLE组(n=35)和右颞部MTLE组(n=25); 利用神经心理功能评分系统(DST、VMPT、WMSLM、WMS视觉、BNT、视觉技能、Stroop、WCST、分类、VFT)对患者术前及术后1年神经心理功能进行评分,比较2组患者左右颞部手术前后神经心理测试及手术前后左右颞部神经心理测试差异。结果 60例MTLE患者中35例(58.33%)左颞部MTLE,25例(41.67%)右颞部MTLE; 2组患者在性别、年龄、手术方式、癫痫发作平均年龄、病程、术前WAIS评分方面无显著性差异(P>0.05); 2组患者左右颞部手术前后神经心理测试比较显示,右颞部MTLE组术后在最大学习得分、短时记忆得分、长时记忆得分、第5卡片时间、矫正、转换错误方面与术前比较有显著差异(P<0.05); 左颞部MTLE组术后在合计得分方面与术前比较有显著差异(P<0.05); 2组患者手术前后左右颞部神经心理测试比较显示,左颞部MTLE组在回忆得分、识别得分、短时记忆得分方面显著高于右颞部MTLE组(P<0.05)。结论 尽管ATL或SAH治疗顽固性MTLE患者会引起部分常见的认知副作用,但该手术治疗也可提高患者部分认知功能。     

消炎痛治疗额颞对冲性脑挫裂伤20例分析

自 1998年 4月至 2 0 0 0年 10月 2年 ,作者对收治的 2 0例枕部着地致额颞对冲性脑挫裂伤患者 ,在常规治疗 (手术 +药物 )基础上 ,实施消炎痛治疗 ,收到良好效果 ,现报道如下。1　临床资料1 1　一般资料　本组 2 0例 ,男 14例 ,女 6例 ,年龄 16～ 5 6岁 ,平均 3 6岁。自受伤至入院时间间隔 0 5～ 5ｈ不等 ,平均 2 75ｈ ,入院时均有程度不等的意识障碍 ,格拉斯格评分 5～ 8分 ,双侧病理征阳性。 12例患者发生尿潴留 ,8例尿失禁。1 2　ＣＴ所见　 2 0例患者ＣＴ表现为单侧额极多发性小点状出血者 8例 (左 6例 ,右 2例 ) ;单侧额颞多发性小点…     

大骨瓣减压合并颞肌敷贴对大面积脑梗死患者血流动力学及神经功能的影响

目的探讨大骨瓣减压合并颞肌敷贴对大面积脑梗死患者血流动力学及神经功能的影响。方法选取2014年3月～2018年3月本院收治的大面积脑梗死患者80例,依据随机数字表法分为颞肌组和减压组,每组40例,减压组给予大骨瓣减压治疗,颞肌组在此基础上给予颞肌敷贴治疗,比较两组血流动力学[大脑中动脉(MCA)、大脑前动脉(ACA)、大脑后动脉(PCA)血流速度]、梗死体积、脑损伤因子[B型脑钠肽(BNP)、S100β蛋白(S100β)]、美国国立卫生研究院卒中量表(NIHSS)、格拉斯哥预后评分(GOS)。结果颞肌组和减压组治疗后MCA、ACA、PCA血流速度明显高于治疗前,颞肌组治疗后MCA、ACA、PCA血流速度明显高于减压组,差异有统计学意义(P 0. 05);颞肌组和减压组治疗后BNP、S100β明显低于治疗前,颞肌组治疗后血清BNP、S100β明显低于减压组,差异有统计学意义(P 0. 05);颞肌组和减压组治疗7 d、14 d后梗死体积、NIHSS得分明显低于治疗前,颞肌组治疗7 d、14 d后梗死体积、NIHSS得分明显低于减压组,差异有统计学意义(P 0. 05);颞肌组GOS良好率明显高于减压组,差异有统计学意义(P 0. 05)。结论大骨瓣减压合并颞肌敷贴可有效改善大面积脑梗死患者血流动力学、梗死体积、脑损伤,有利于促进患者神经功能恢复及可改善其预后,值得临床作进一步推广。     

重组组织型纤溶酶原激活物溶栓治疗急性脑梗死的疗效观察

目的　观察重组组织型纤溶酶原激活物 (rtPA)动脉或静脉溶栓治疗急性脑梗死的疗效及安全性。方法　 6 0例符合入选标准的急性脑梗死患者分为动脉溶栓组、静脉溶栓组和对照组 ,各 2 0例。动脉溶栓组给予rtPA 10～ 2 0mg ,30分钟内恒速动脉注入 ;静脉溶栓组给予rtPA总量 0 7～ 0 8mg/kg,最大剂量 5 0mg。 90分钟内静脉滴入 ;两组次日均用低分子肝素 (速避凝 4 10 0U或法安明 5 0 0 0U) ,每 12小时腹部皮下注射 1次 ,连续 7天 ;对照组应用低分子右旋糖酐 5 0 0ml加复方丹参 16ml静滴 ,每日 1次 ,连用 8天。采用欧洲卒中量表 (ESS)、Barthel指数 (BI)评价神经功能恢复状况。结果　两溶栓组疗效明显优于对照组 (均P <0 0 5 ) ,动脉溶栓与静脉溶栓组之间的疗效无明显差异 (P >0 0 5 ) ,但动脉溶栓能发现颅内外血管是否存在狭窄 ,通过实施支架成形术消除狭窄 ,预防再次的血栓形成。动脉溶栓组脑实质性出血 1例 ,非症状性脑出血 1例 ;静脉溶栓组和对照组非症状性脑出血各 1例。 3组均无死亡病例。结论　rtPA用于急性脑梗死 (发病 6小时内 ) ,无论动脉还是静脉溶栓均有效 ,且比较安全。     

Giant cell (temporal) arteritis: a treatable cause of multi-infarct dementia

Dementia occurs infrequently in patients with giant cell (temporal) arteritis (GCA). Three elderly women with biopsy-proven GCA showed abrupt cognitive decline during periods of clinically active GCA, 1 to 6 months after diagnostic temporal artery biopsy, during periods of corticosteroid taper. One patient had additional clinical signs of cerebral infarction and other ischemic phenomena. Reinstitution of higher oral doses of corticosteroids successfully prevented further cognitive losses and permitted gradual but incomplete improvement of cognitive function in 1 patient. Neuropsychologic data from 2 patients 7 to 10 months after temporal artery biopsy suggested multifocal cognitive impairment, and the 3rd patient appeared clinically to be globally, severely demented. Neuroimaging studies revealed multiple areas of infarction, predominantly in the posterior circulation territory. One patient had bilateral vertebral artery occlusions (digital subtraction angiography) and bilaterally reduced carotid system perfusion pressures (oculoplethysmography). There were no associated cardiovascular risk factors or family history of dementia in these patients.     

Axonal cytoskeleton changes in experimental optic neuritis

Axonal loss and degeneration in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE) have been suggested by brain imaging, pathological and axonal transport studies. Further elucidation of the processes and mechanisms of axonal degeneration in demyelinating diseases is therefore of potential importance in order to alleviate the permanent disabilities of MS patients. However, detailed studies in this area are impeded by the small number of reliable models in which the onset and location of demyelination can be well-controlled. In this study, microinjection of polyclonal rabbit anti-galactocerebroside (anti-Gal C) antibody and guinea pig complement was used to induce local demyelination in the rat optic nerve. We found that treatment with appropriate volumes of the antibody and complement could induce local demyelination with minimal pressure- or trauma-induced damage. Local changes in neurofilaments (NFs) and microtubules (MTs) were examined with both immunohistochemistry (IHC) and electron microscopy (EM). On day 1 after microinjection, we observed moderate NF and MT disassembly in the local demyelinated area, although in most cases, no apparent inflammatory cell infiltration was seen. The NF and MT changes became more apparent on days 3, 5, 7 after microinjection, along with gradually increased inflammatory cell infiltration. These results suggested that acute demyelination itself may induce local cytoskeleton changes in the demyelinated axons, and that the ensuing local inflammation may further enhance the axonal damage. When the lesions were stained with specific antibodies for T lymphocytes, macrophages, and astrocytes, we found that most of the cells were macrophages, suggesting that macrophages may play a greater role in inflammation-related axonal degeneration and axonal loss. These results were confirmed and further characterized on the ultrastructural level.     

Late ipsilateral recurrence of ischemic optic neuropathy in giant cell arteritis.

A patient with arteriosclerosis, diabetes mellitus, and giant cell arteritis (GCA) treated continuously with low-dose prednisone developed anterior ischemic optic neuropathy (AION) at 5 and 13 months after clinical diagnosis of GCA. At the time of late recurrent AION, there were no systemic symptoms or elevations in acute phase reactants to signal active arteritis, yet temporal artery biopsy disclosed dramatic inflammation, forcing the presumption that the infarct was arteritic. Recurrent systemic symptoms and elevation of acute phase reactants are not reliable warning signs of reactivated GCA. In patients at high risk for corticosteroid complications, late biopsy may be a reasonable guide to corticosteroid weaning.     

Recent Advances in Diagnostic Strategies for Giant Cell Arteritis

Giant cell arteritis (GCA) is a systemic vasculitis that affects the aorta and its major branches. Involvement of the ciliary artery can result in ischemic optic neuropathy and subsequent blindness, which is typically irreversible. If GCA is suspected, treatment with glucocorticoids should be initiated promptly to prevent further vision loss. However, given the need for prolonged therapy with glucocorticoids and the morbidity associated with their use, diagnosis should be confirmed. Clinical features and laboratory findings are neither sensitive nor specific for GCA. The mainstay of diagnosis remains histopathologic examination of a section of the superficial temporal artery. Several imaging studies have been used to evaluate the temporal artery but, at present, their utility as alternatives to a temporal artery biopsy is limited. Recent advances in imaging modalities have allowed detailed noninvasive imaging of the large arteries and are a useful adjunct for the diagnosis of GCA, particularly in patients with primarily large-vessel involvement in whom temporal artery biopsy is often negative.     

The diagnosis of giant cell arteritis

Giant cell arteritis (GCA) is the most common primary vasculitis in adults older than 50 years. The potential of GCA to cause bilateral, sequential vision loss makes it often a true neuro-ophthalmic emergency. Approximately one fifth of patients with GCA will present with ophthalmic complaints alone. The diagnosis of GCA requires a high index of suspicion and a systematic approach to diagnostic testing. The combination of abnormal laboratory markers of systemic inflammation and unilateral temporal artery biopsy is usually diagnostic. Additional testing with other diagnostic modalities may be required in cases in which clinical suspicion remains high despite a negative initial workup. We systematically review the diagnostic modalities used in suspected GCA patients who present with neuro-ophthalmic symptoms and signs.     

小儿moyamoya病颞浅动脉组织学和超微结构与免疫组化研究

报告了５例小儿ｍｏｙａｍｏｙａ病（ＭＤ）颞浅动脉（ＳＴＡ）的组织学和超微结构病理，它们的变化是中膜平滑肌细胞变性、破坏，内弹力板变薄、断裂和内膜平滑肌细胞增生。这些变化与成人ＭＤ脑动脉和ＳＴＡ的病变一致。小儿ＭＤ的ＳＴＡ中能看到大量较早期和较轻的病变，如中膜平滑肌细胞空泡变性、质膜破坏、或仅见于内弹力板两侧的肌细胞坏死；内弹力板破坏轻；内膜增生轻，没有管腔狭窄，与成人不同。本文对ＭＤ动脉病变的发展过程和病因问题提出了看法。     

Low diagnostic yield with second biopsies in suspected giant cell arteritis.

OBJECTIVES: The clinical diagnosis of giant cell arteritis may be confirmed with a biopsy of the superficial temporal artery. Because of "skip lesions," a histologic diagnosis of giant cell arteritis may be missed with a unilateral biopsy. The authors report a study that investigates whether a biopsy of the contralateral superficial temporal artery provides any additional information for confirmation of a diagnosis of giant cell arteritis. METHODS: Available medical records of 91 consecutive patients who underwent bilateral superficial temporal artery biopsy procedures were reviewed. Information that was abstracted included sequence of biopsy procedures, length specimens, and histologic diagnosis. Microslides from all biopsy specimens were retrieved and reexamined in a masked fashion by the ocular pathologist (RCE) who had made the original diagnoses. RESULTS: Seventy-two bilateral simultaneous superficial temporal artery biopsies and 19 bilateral sequential biopsies were performed. The mean length of biopsy specimens was 23 mm, and the mean length of the total artery removed from each patient was 33 mm. The pathologist's original diagnosis and the diagnosis at reexamination were in 100% agreement. In 90 (99%) of the 91 patients, the histologic diagnoses in the left and right superficial temporal arteries were the same. This is a concordance rate of 98.9% (38 of 39 positive biopsy results) among the positive biopsy results. CONCLUSION: There is a low yield of information from a second temporal artery biopsy in patients with suspected giant cell arteritis. This suggests that patients who present to the ophthalmologist with possible giant cell arteritis will, in most cases, have a similar diagnosis on both temporal artery biopsies if the specimens are adequate.     

Giant cell arteritis (temporal arteritis): A report of four cases from north east India

Giant cell arteritis (GCA) is a common disease of the geriatric age group in the western world, with a prevalence of 0.2% in the fifty plus age group. It is an important cause of morbidity, with irreversible visual loss being the most ominous complication. This diagnosis is an important consideration in all cases of new onset headache in elderly subjects. Reports of giant cell arteritis are few and far between in the Indian subcontinent. In this report, we describe the clinical details of four cases of giant cell arteritis, detected at Guwahati, Assam. The four patients were in the 70-82 age group. Sex distribution was equal. All of them had polymyalgia rheumatica (PMR), with one case displaying an initial presentation as only PMR. Cardinal manifestation was a severe headache, frequently accompanied by scalp allodynia and abnormalities of the superficial temporal artery (STA) on examination. STA biopsy yielded histopathological confirmation in three patients. Permanent visual loss was noted in one patient. These cases highlight the importance of assessing the possibility of giant cell arteritis through appropriate clinical history, estimation of acute phase reactants and the judicious use of superficial temporal artery biopsy, to clinch the diagnosis.     

Orchestration of the inflammatory response in ischemia-reperfusion injury

Ischemia to nerve can cause fiber degeneration and reperfusion following ischemia [ischemia-reperfusion (IR)] adds the additional insult of an inflammatory response and oxidative injury. Limited information is available on the molecular mediators and their endoneurial targets. In this study, using a highly reproducible animal model of IR injury to nerve and selective immunolabeling methods [for nuclear factor kappa B (NF-kappaB), intercellular adhesion molecule-1 (ICAM-1), cytokines, and inflammatory cells] over an expanded time frame, we evaluated the temporal pattern and localization of mediators of the inflammatory response. Sixty rats were used. Nine groups (N=6 each) underwent complete hind limb ischemia for 4 h, followed by reperfusion durations of 0, 3, 12, 24, and 48 h, and 7, 14, 28, and 42 days. One group underwent sham operation (N=6). The earliest change was ICAM-1 expression in the microvessel (endothelial cell) followed almost immediately by NF-kappaB activation with axonal expression (24 and 48 h), followed by endoneurial edema and ischemic fiber degeneration (7 and 14 days). Granulocytic infiltration was followed by endoneurial infiltration of mononuclear phagocytes (14 days), expression of interleukin 6 (IL-6) (microvessels), and subsequent Schwann cell NF-kappaB expression. Granulocytes, tumor necrosis factor alpha, and IL-6-positive cells were observed primarily within the epineurium. IR results in changes in a number of interacting networks of targets and inflammatory mediators. NF-kappaB activation has a central orchestrating role involving both the axon and the Schwann cell in effecting the inflammatory response.