短暂性全面遗忘症的病因及认知功能的损伤

目的:探讨短暂性全面遗忘症的发病原因及其该病对患者认知功能的影响。方法:选择解放军第四五一医院2001-03/2005-05收治的经过临床确诊的短暂性全面遗忘症患者7例,其中男5例,女2例,年龄63～81(65±3.27)岁。在发病24h内分别进行经颅超声血流图、脑电图、头颅CT检查及简易心理测试、修订的韦氏记忆量表测定。结果:7例患者均进入结果分析。全部7例短暂性全面遗忘症患者头颅CT检查均未见明显异常,脑电图检查均未见明显异常波形。简易心理测试结果均在正常范围。经颅超声血流图检查结果提示全部患者均有不同程度的椎基底动脉系统血流缓慢。修订的韦氏记忆量表测定结果提示部分患者发病后会遗留部分轻度的认知功能损害。结论:短暂性全面遗忘症的发病原因与椎基底动脉供血减少有关,患者发病后会遗留部分轻度的认知功能损害。     

短暂性全面性遗忘症1例

1 病例报告 男,36岁.2002-10-08T08到单位开会,能记录会议内容,能正常活动及与别人交谈,午饭后休息一段时间,下午上班后,同事发现其反应迟钝,反复问同一个问题,对刚做过的事或说过的话忘记,16:00同事将其送到医院.患者对以上整个过程无记忆.感头晕,无感觉及肢体活动障碍.既往体健,无类似病史.查体:BP130/80 mmHg,神志清,除对8:00～16:00这一段时间无记忆外,对发病前后的事情无记忆障碍,无神经系统定位体征.入院前颅脑CT平扫未见异常,ECG未见异常.住院后行颅脑MRI、椎基底动脉彩超及脑电图均未见异常,给予706代血浆、脑多肽及噻氯鲁匹定治疗,上述症状未再复发.4 d后出院.     

短暂性全面遗忘症4例

例1,男,55岁,于2000年3月8日谈话时突然忘记谈话内容,答非所问,反复询问:"怎么回事?"2小时后恢复正常.既往体健.查体:血压113/75 mm Hg(1 mm Hg=0.133 kPa),神志清,对发病前后事情记忆得准确,惟对发病2小时所做的事情无记忆,无神经系统定位体征.脑电图(EEG):超声心动图(ECG)均为正常.头颅磁共振(MRI)多发性腔隙性脑梗死.经颅多普勒超声(TCD):椎-基底动脉供血不足.诊断:短暂性全面遗忘症(TGA).予扩血管及改善脑细胞代谢治疗,半年后随访无复发.例2,女,64岁,于2001年6月3日打麻将牌时,突然坐立不安,说话不对题,不认识周围人物,反复重复:"这是哪里?"3小时后恢复正常.既往患有糖尿病.查体:血压105/83 mm Hg,近记忆下降,无神经系统定位体征.EEG广泛轻度异常,ECG正常,头颅CT示多发性腔隙性脑梗死.TCD示椎-基底动脉紧张度增高.诊断:TGA.予扩血管,改善脑代谢治疗,半年来无复发.     

短暂性全面遗忘症的随访分析

目的：探讨短暂性全面遗忘症(transient global amnesia，TGA)和脑卒中的发病关系。方法：选择1994-10／2004-10安阳市人民医院和安阳市第二人民医院神经内科住院及门诊有详细记录且已得到随访的TGA患者16例为观察组。选择同期在两所医院就诊的高血压、糖尿病、冠心病患者16例作为对照组。嘱两组患者2～6个月复诊一次作为随访，比较两组患者随访期间脑卒中发生率。结果：观察组患者患TGA后1～10年的患者出现脑卒中的发生率[44％(7／16)]明显高于对照组[12％(2／16)]，两组比较，差异有显著性意义(χ^2=3．865，P&;lt;0．05)。结论：TGA和脑缺血有关，应将TGA患者作为脑卒中二级预防的对象。     

短暂性全面遗忘症的随访分析

目的:探讨短暂性全面遗忘症(transientglobalamnesia,TGA)和脑卒中的发病关系。方法:选择1994-10/2004-10安阳市人民医院和安阳市第二人民医院神经内科住院及门诊有详细记录且已得到随访的TGA患者16例为观察组。选择同期在两所医院就诊的高血压、糖尿病、冠心病患者16例作为对照组。嘱两组患者2～6个月复诊一次作为随访,比较两组患者随访期间脑卒中发生率。结果:观察组患者患TGA后1～10年的患者出现脑卒中的发生率犤44%(7/16)犦明显高于对照组犤12%(2/16)犦,两组比较,差异有显著性意义(χ2=3.865,P<0.05)。结论:TGA和脑缺血有关,应将TGA患者作为脑卒中二级预防的对象。     

短暂性全面遗忘症38例临床分析

短暂性全面遗忘症 (ｔｒａｎｓｉｅｎｔｇｌｏｂａｌａｍｎｅｓｉａ ,ＴＧＡ)系突然发生的短暂性近记忆障碍 ,不伴神经系统的其他症状体征 ,一般 2 4小时内恢复。临床少见 ,近 10年来我院发现 3例 ,国内文献报告 35例 ,本研究对这 38例进行总结分析 ,现报告如下。1　临床资料1.1　一般资料　本组 38例患者 ,男 2 8例 ,女 10例 ,年龄在2 2～ 88岁 ,其中 5 0岁以上 30例。既往有高血压病史 2 2例 ,有冠心病心房纤颤病史 2例 ,有偏头痛病史 4例 ,有类似发作病史 4例。 2例发作前有反复头晕病史。1.2　诱发因素　 11例有体力活动或情绪改变 ,如…     

短暂性全面遗忘症的临床与PET成像研究

目的:研究短暂性全面遗忘症(transient global amnesia.TGA)患者脑代谢状况,并探讨其发病机理,方法:对3例临床下诊断为TGA的患者,分别行简易心理测试(MMSE)及脑核磁共振成像(MRI),在恢复后不同时间以18F标记的脱氧葡萄糖(18F-FDG)为示踪剂行脑正电子发射型计算机断层扫描(positron emission tomography,PET)成像,并对其图像与 病史进行对照研究.结果:3例患者MMSE测试及MRI扫描均未见异常,PET成像显著,1例正常,另外2例发现与记忆相关相关结构有不同程度的低代谢.结论:TGA的发病机制离缺血的病理生理过程,其脑代谢状况与症状持续时间密切相关,尽早终止其发作是必要的.     

短暂性全面遗忘症3例局部脑血流显像观察2年随访

目的探讨短暂性全面遗忘症(TGA)的发生与局部脑血流(rCBF)改变的关系。方法对3例临床诊断为TGA患者行单光子发射计算机体层摄影(SPECT)rCBF显像检查。结果2例患者SPECT显像示左海马区血流灌注减低,1例示双侧额叶血流灌注减少。3例患者随访24个月,均无再次遗忘发作,复查SPECT显像示血流灌注正常。结论TGA的发生可能与额叶及海马局部血流灌注减低有关。     

短暂性全面遗忘症20例脑电图分析

目的探讨短暂性全面遗忘症的脑电图表现。方法比较短暂性全面遗忘症患者与正常人的脑电图表现,对其病理机制及治疗进行探讨。结果短暂性全面遗忘症患者的脑电图异常率明显高于对照组,两组比较,差异显著(P<0.05),不同年龄短暂性全面遗忘症患者脑电图异常差异无显著性。结论短暂性全面遗忘症患者的脑电图有明显异常,可根据其异常对患者进行个体化治疗,脑电图表现对探索其病因及病理机制有一定的指导意义。     

60例男性完全性脊髓损伤患者的认知行为筛查

目的:研究完全性脊髓损伤(SCI)患者的认知功能情况以及简易精神状态检查量表(MMSE)和北京版蒙特利尔认知评估量表(MoCA)在完全性SCI患者认知功能障碍筛查中的应用价值。方法:筛选60名男性完全性SCI患者作为研究组,并进一步分为四肢瘫组(22名)和截瘫组(38名);同期招募附近社区30名健康男性作为对照组。对3组用MMSE、北京版MoCA、汉密尔顿焦虑量表(HAMA)和汉密尔顿抑郁量表(HAMD)评估;采用多因素回归分析法对完全性SCI患者的认知功能进行相关性分析。结果:与对照组相比,四肢瘫组及截瘫组的MoCA评分之反向平方根、焦虑和抑郁得分均升高(P<0.05),MoCA的语言项目和延迟回忆项目得分均降低(P<0.05),MMSE评分差异无统计学意义。四肢瘫组与截瘫组对比,上述指标均无显著性差异。多因素回归分析结果显示年龄、文化程度和抑郁与完全性SCI患者MoCA评分显著相关(P<0.05)。结论:年龄、文化程度和抑郁是完全性SCI患者认知功能的影响因素;MoCA量表更适合应用于完全性SCI患者认知功能障碍的初筛。     

Marijuana-induced transient global amnesia

A 6-year-old boy accidentally became intoxicated with marijuana secondary to ingesting cookies laced with marijuana. He presented with retentive memory deficit of sudden onset that was later diagnosed as transient global amnesia. Transient global amnesia as a result of marijuana intoxication is an extremely rare event.     

The diagnosis and management of transient global amnesia in the emergency department

Transient Global Amnesia (TGA) is a benign and temporary loss of anterograde memory with the preservation of remote memories and immediate recall. TGA was first described in 1956 and since then epilepsy, transient ischaemic attacks (TIA), migraine and now intracranial venous stasis have been implicated in its aetiology. Precipitants of TGA include physical exertion and valsalva-like manoeuvres. In order to diagnose TGA the criteria created by Hodge and Warlow in 1990 can be used. This requires the episode of memory loss to be witnessed and involve anterograde amnesia. The patient must not have any evidence of neurological signs or deficits, features of epilepsy, active epilepsy or recent head injury. Finally the episode must have resolved within 24 h. In this case study the patient's symptoms are mistakenly attributed to a TIA. There is no increased risk of TIA or CVA in patients who have had TGA and there are no increased levels of mortality amongst these patients. In this article we aim to help doctors working in the emergency department to diagnose and manage TGA.     

The link between reversible cerebral vasoconstriction syndrome and transient global amnesia

Reversible cerebral vasoconstriction syndrome (RCVS) and transient global amnesia (TGA) are acute and self-limiting intra-cerebral conditions. Although previously studied as independent phenomena, there are increasing reports of co-occurrence of these two pathologies. We report a 55-year-old male who presented to the hospital with recurrent thunderclap headaches over the course of 1 week with sudden onset of anterograde memory loss. His medications included a selective serotonin reuptake inhibitor and intermittent use of pseudoephedrine. On examination he was amnestic to recent events and notably perseverating. Magnetic resonance imaging of the brain without contrast showed a small, punctate focus of restricted diffusion in the left hippocampus. He was diagnosed with TGA based on his clinical presentation. His headaches and amnesia resolved over the next 12 h throughout the course of his stay with acetaminophen and oral verapamil and he was discharged. Repeat computed tomography angiogram at 2 weeks revealed diffuse and segmental narrowing of the anterior and posterior intracranial circulation, which resolved on follow-up imaging at 3 months, confirming RCVS. The acute and reversible nature of these conditions and increasing reports of co-occurrence suggests a common pathophysiologic link. We review the literature highlighting similar cases and the presumed pathophysiology.     

Transient global amnesia

Transient global amnesia is a benign, self-limiting disorder primarily involving a disturbance of memory. It occurs in late middle and older aged adults. Patients with this syndrome do not have a history of head trauma, drug or alcohol intoxication, hypoglycemia or psychologic dysfunction. Once the episode has cleared, there are no residual deficits except amnesia for the events which occurred during the episode. This article includes a case presentation in addition to discussion of the clinical features, etiology, treatment and nursing interventions for the patient with a transient global amnesia episode.     

Transient global amnesia

Transient global amnesia is often attributed to a seizure, vascular cause, or migraine, but the outcome is usually benign. The presence of migraine and important risk factors for stroke necessitates close patient monitoring. Anti-platelet therapy should be considered.