第41例——进行性记忆力减退、行动迟缓伴幻视

患者男性,82岁。主因进行性记忆力减退11年,行动迟缓5年,意识不清6 h,于1999年5月17日入院。患者自1988年逐渐出现记忆力减退,表现为时常叫不出子女名字,常用物品不易找到,购物时常忘记付款。     

丘脑动静脉畸形致双侧丘脑病变后痴呆1例

1病例介绍患者女性,29岁,因"性格改变,记忆力减退3天"于2019年10月29日入院。患者于入院前3 d无明显诱因出现性格改变,以淡漠为主,伴记忆力减退;伴有前额部持续性胀痛、恶心、非喷射性呕吐;无肢体无力、麻木、抽搐等症状;自发病以来,睡眠明显增多。为求进一步诊治收入我科。     

Creutzfeld-Jakob病1例报告

患者,女,56岁,退休工人。主因记忆力减退、精神障碍、走路不稳21个月,神志不清、全身抽搐3小时于2005年3月6 日由急诊收入院。患者入院21个月前(2003年6月),出现懒散、失眠、多疑、记忆力减退,呈渐进性加重。两个月后(2003年8月22     

遗传性弥漫性白质脑病合并轴索球样变1例报告及文献复习

<正>1临床资料患者,女,29岁。因"右侧肢体麻木6m,记忆力减退4m,言语欠清2m"于2019年2月1日入院。现病史:患者缘于6m前,无明显诱因及原因出现右足麻木,时有头晕,4m前出现记忆力减退,伴右侧偏身麻木,2m前出现言语欠清且记忆力明显下降,无法正常工作。发病以来体重无明显变化,二便正常。患者2015年曾行肺结核手术且有输血史。2018年6月开始接种乙肝疫苗。否认家族中有遗传倾向疾病。神经系统查体:意识清楚,轻度构音障碍,计算力、记忆     

SWI表现为弥漫性粟粒样病灶的肺癌脑转移一例报道及文献复习

患者 女性,58岁,因"进行性记忆力减退、反应迟钝1个月"于2009年6月25日入院.患者入院前1个月出现记忆力减退,对事件记忆模糊,反应迟钝,伴头晕,进行性加重,无头痛、抽搐.     

肌萎缩侧索硬化-帕金森痴呆叠加征（附1例报道）

肌萎缩侧索硬化症(amyotrophic lateral sclerosis,ALS)是神经科的常见疾病,而同时伴有运动减少、肢体震颤、记忆力减退、认知功能障碍、性格改变的病例较少见,我院近日收治1例病例,现报告如下。病例资料一般情况:患者男性,74岁。因左上肢震颤5年,记忆力减退、双上肢无力1年,于2004年4月19日入院。患者5、6年前出现左上肢静止性震颤。逐渐出现表情淡漠,动作缓慢、行走前冲、步子变小、转身困难,书写困难。2002年12月出现发作性头晕,伴视物旋转、耳鸣、记忆力减退,不能独自外出买菜,且性格改变、抑郁,经常为小事与老伴争吵。自2003年2月以…     

以腹痛、记忆力减退为首发症状的M3型急性白血病一例

临床资料患者,男性,37岁,因"腹痛半个月,头痛、记忆力减退10余天,发热7 d"于2008年6月18日收入院.患者半个月前腹痛,无恶心呕吐,无腹泻或便秘,无呕血及便血,在当地医院诊治(具体不详)无好转,13 d前出现头痛,12 d前记忆力减退,中午不能记忆早餐内容,出门找不到回家的路,当地医院MRI示颅内多发性病变(诊治不详).6 d前发热,最高达38℃,并出现呃逆,入我院神经内科.既往体健.     

口服平息散中毒致脑功能障碍1例报道

1 临床资料 男性,43岁,国家公务员,本科文化,因"进行性记忆力减退半年,伴发作性行为异常2月余"于2007年12月12日入院.患者半年前无明显诱因下出现记忆力减退,表现为近事遗忘,远期记忆尚可.随后患者记忆力继续恶化,直至不能回忆当日甚至前一刻事件.     

梅毒性痴呆一例报告

患者52岁的男性患者。因进行性记忆力减退、反应迟钝、性格怪异2年，抽搐1h于2002年4月入院。患者2年前始出现记忆力减退，以近记忆力减退最明显。初始表现为忘记说过的话及刚做过的事，但尚能完成买菜、做饭等日常家务。此后症状逐渐加重，常忘记回家的路，反应迟钝，整日发呆，不能从事原来的驾驶员工作，买东西不会计算。性格     

肾上腺脑白质营养不良一例

<正>患者男性,15岁,主因双眼视物不清、记忆力减退进行性加重2年,于2012年6月18日入院。患者2年前出现双眼视物不清,认为是因患者喜玩电脑游戏而出现近视,予佩戴约-300度眼镜,但视力仍下降,换为-400多度的眼镜仍视物不清,并相继出现记忆力、计算力减退,学习成绩下降,由原来的班内前十名变为倒数几名,以上两组症状呈进行性加重。6个月前逐渐表现反应迟钝,行走不稳,尤其爬坡时明显,不能上体育课,容易疲劳。于入     

Diagnostic Difficulties and Treatment Implications

Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.     

Cognitive Dysfunction Associated with Antiepileptic Drug Therapy

Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.     

Carbamazepine Efficacy in Adults With Partial and Generalized Tonic-Clonic Seizures

Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.     

Etiologic and Preventive Aspects of Epilepsy in the Child–Bridging the Gap Between Laboratory and Clinic

Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

Predisposing and Causative Factors in Childhood Epilepsy

Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.     

Anticonvulsant Drugs and Cognitive Function: A Review of the Literature

Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

Effects of NMD A- and AMPA-Receptor Antagonists on Different Forms of Epileptiform Activity in Rat Temporal Cortex Slices

Summary: Lowering extracellular magnesium induces different patterns of epileptiform activity in rat hippocampus and entorhinal cortex. Short recurrent epileptiform discharges in the hippocampus are stable over time, whereas seizurelike events (SLEs) in the entorhinal cortex, the subiculum, and the neighboring neocortex develop into late recurrent discharges which are not blocked by clinically employed antiepileptic drugs. We tested the sensitivity of the different epileptiform discharge patterns to. /V-methyl-D-aspartate (NMDA)- and non-NMDA-receptor antagonists. As NMDA-receptor antagonist we used dextrorphan, ket-amine, and 2-aminophosphonovalerate (2APV); as α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)-receptor antagonist we employed the quinoxaline derivative glutamate 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The findings show that the different patterns of epileptiform activity, including the late recurrent discharges, are sensitive to all NMDA-receptor antagonists. However, when dextrorphan was employed to suppress seizure-like events, later recurrent discharges did not develop during the remaining time course of the experiment. CNQX reversibly suppressed recurrent discharges in the hippocampus and SLEs in the entorhinal cortex. However, late recurrent discharges become insensitive to CNQX, even at a high concentration of 60 μM m. This finding suggests a prominent role for NMDA receptors in the generation of late recurrent discharges.