2例大动脉粥样硬化性脑梗死患者合并全身性低灌注后的结局

1病例简介 例1,患者,男,58岁,汉族.主因"右上肢无力37 d,加重伴意识障碍27 d"于2010年9月5日入我院.患者于人院前37 d无明显诱因突发右上肢无力,伴言语不清,尚能行走,发病当日就诊于当地医院,发病初右侧上肢血压为200/100 mm Hg,行颅脑计算机断层成像(computerized tomography,CT)示左侧半卵圆中心腔隙性脑梗死,给予抗血小板等治疗,具体用药方法和剂量不详,症状基本缓解.     

老年发病的视神经脊髓炎一例

1 病例报告 患者男性,64岁,以"双下肢无力5年,左眼失明1年,右眼视物不清2 d"于2009-08-15入院.患者2004-07突然出现双下肢无力、麻木,逐渐加重,3 d后双下肢完全不能动,同时伴大小便失禁.无发热及腰背部疼痛,双上肢活动良好.     

延髓出血1例报告

患者,男,47岁,因突发右肢体麻木、无力伴吞咽困难、饮水呛咳半天,于2009年3月入院.入院前于晨起突发右上肢麻木、无力,右手无法持物,抬举费力,右下肢拖拽伴吞咽困难、饮水呛咳、言语含糊、声音嘶哑,能够理解旁人对话,恶心、呕吐胃内容物数次,非喷射性.     

脑血管狭窄颅内支架成形术前后CT灌注成像1例

1病例简介患者,男性,62岁,因“发作性右侧肢体无力伴言语不清1年,加重5天”入院。该患者1年前无明显诱因出现右侧肢体无力,右上肢不能抬举,右下肢不能行走,伴言语不清,     

不伴眼部疼痛的双侧眼眶肌炎一例

正1病例报告患者女,53岁,研究员。主因"左眼红肿伴眼睑上抬无力4d,右眼肿胀伴眼睑上抬无力半天"于2017-02-22入院。2017-02-18无明显诱因晨起后出现左眼红肿、左眼睑上抬无力,就诊于某私人诊所,给予"氯霉素、妥布霉素地塞米松"滴眼及"头孢曲松钠"静脉输液3d后症状无明显改善。4d后患者自觉右眼睑肿胀,右眼睑上抬费力,双眼无疼痛、流泪症状,不伴发热、头痛、恶心、呕吐、复视、     

以脑卒中为首发症状的大动脉炎1例报道

<正>病例资料病史3136×××,患者女性,48岁。因"右侧肢体无力7、8年,左侧肢体无力4 d"于2013年8月19日入住菏泽市第三人民医院。现病史患者于7、8年前因活动后突然出现言语不能,由卧位变坐位时言语不能加重,平卧2 min后症状可缓解,右侧肢体无力,右上肢持物不牢,右下肢行走不稳,伴饮水呛咳,进食困难,在菏泽市立医院诊断为"大动脉炎"、"脑梗死",给予拜阿司匹林、低分子肝     

非酮症高血糖偏侧舞蹈伴一过性偏瘫一例

临床资料 患者女性,84岁,主因"右上肢不随意运动、口角抽动3 d,右侧肢体无力1 d"于2009年4月11 日入院.患者于入院前3 d无诱因出现右上肢不随意运动,右上肢时而屈曲、时而伸直、时而扭转,面部有挤眉弄眼动作,意识清楚,无肢体抽搐,睡眠时减轻;入院前1 d患者出现右侧肢体无力,上下肢均不能抬起,伴精神、进食差,小便失禁.     

视网膜小脑血管瘤病

张××,男,20岁,左眼失明、四肢无力进行性加重半年于87年4月17日入院。86年9月左眼突然视物不清,一月后右上肢无力,4月后波及右下肢,相继出现左肢无力,四肢僵硬,迈步困难,胸部     

烟雾病合并动脉瘤一例

1 病例简介 　　患者男,43岁,农民,因"复视伴左上睑下垂7 d,加重1 d"于2007年3月14日入院. 　　患者于入院前7 d无明显诱因出现复视伴左上睑下垂,可睁眼,言语欠清,伴轻微头痛,无眩晕,无恶心呕吐,无肢体无力及抽搐,无意识障碍,1 d前左眼睁眼不能.入院前2个月突发失语伴右肢活动不良,在当地医院诊断为脑梗死,治疗后好转.否认高血压,糖尿病病史.……     

颈内动脉夹层并发远端栓塞所致青年卒中1例

正1病例介绍患者男性,26岁。主诉因"被发现言语不能伴右侧肢体无力3小时15分"就诊于基层医院。患者3 d前曾有颈部按摩史及溜冰摔伤史,于2017年6月14日下午14时有左眼视物不清,未引起重视,18时被房东发现跌倒在房门口,不能言语,伴右侧肢体无力,就诊于当地医院,行头颅计算机断层扫描(computed tomography,CT)未见出血,经天河卒中区域急救网络平台     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.