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1.
1引言 传统上认为帕金森病是一种运动障碍性疾病,然而近来的研究表明帕金森病患者早期可出现许多非运动症状,如嗅觉减退或是嗅觉丧失、自主神经功能障碍、疼痛、过度睡眠、快速眼动睡眠行为障碍、抑郁、焦虑、认知下降及痴呆等。  相似文献   

2.
快动眼睡眠行为障碍(RBD)是一种发生于快动眼睡眠(REM)期的异态睡眠,常见于帕金森病、路易体痴呆和多系统萎缩等突触核蛋白病,并可作为上述神经系统变性病的前驱症状。RBD的确诊有赖于多导睡眠图。鉴别诊断主要包括阻塞性睡眠呼吸暂停、睡行症、夜间癫痫发作及周期性肢体运动障碍等。干预措施主要包括最大程度保护患者睡眠安全、应用氯硝西泮/褪黑素等。  相似文献   

3.
帕金森病(PD)是一种常见的神经系统变性病,其起始病理改变在黑质之外,如何在累及黑质之前尽早识别、诊断PD对于延缓疾病进展,改善患者预后具有重要意义。目前尚缺乏诊断和预测PD运动前期的理想标记物。嗅觉障碍、快动眼期睡眠行为障碍(RBD)、便秘和抑郁常见于PD运动前期,视觉障碍、自主神经功能障碍及轻度认知障碍等非运动症状也可发生于运动前期。本文对上述非运动症状对PD的早期诊断的预测价值予以介绍。  相似文献   

4.
正快动眼睡眠行为障碍(RBD)是一种异态睡眠,主要表现为快动眼睡眠(REM)期异常的肌肉失弛缓(RSWA)及梦境演绎(如唱歌、喊叫、大笑、挥拳、打人、坠床等)。根据有无病因,分为特发性RBD(iRBD)和继发性RBD(sRBD)。目前,大量研究~([1])发现特发性RBD与神经变性病关系密切,其中约90%在确诊后的数年或十数年会发展为神经变性病,如路易体痴呆、帕金森病(PD)、多系统萎缩等。而PD作为老年人常见的神经变性病,严重影响着老年人的健康与生活质量,并且PD  相似文献   

5.
早期帕金森病患者快速眼动睡眠期行为障碍研究   总被引:3,自引:0,他引:3  
目的探讨早期帕金森病患者快速眼动睡眠期行为障碍发生情况,以及帕金森病运动症状、非运动症状和快速眼动睡眠期行为障碍特点。方法共60例原发性帕金森病患者,采用统一帕金森病评价量表第二和第三部分(UPDRSⅡ和UPDRSⅢ)以及Hoehn-Yahr分期评价帕金森病非运动症状和运动症状,蒙特利尔认知评价量表评价认知功能,汉密尔顿焦虑量表和汉密尔顿抑郁量表评价焦虑和抑郁症状;中文版快速眼动睡眠期行为障碍筛查量表判断是否伴快速眼动睡眠期行为障碍,Epworth嗜睡量表(ESS)评价白天过度嗜睡程度;多导睡眠图监测睡眠障碍特征,包括下颌位相性肌电活动密度和快速眼动睡眠期肌肉失弛缓。结果 60例帕金森病患者中42例(70%)伴快速眼动睡眠期行为障碍(PD+RBD组),多导睡眠图监测其异常行为主要表现为上肢伸展抓握、肢体震颤抽搐、发笑、喊叫和怒骂等非暴力动作,仅2例出现暴力击打、蹬踢等异常行为。PD+RBD组患者年龄(P=0.024)、病程8年比例(P=0.000)、UPDRSⅡ(P=0.005)和UPDRSⅢ(P=0.001)评分、Hoehn-Yahr分期2级比例(P=0.007)、焦虑障碍(P=0.044)和抑郁障碍(P=0.001)比例,以及下颌位相性肌电活动密度(P=0.000)和快速眼动睡眠期肌肉失弛缓比例(P=0.000)均高于对照组,其中,PD+RBD组有16例(38.10%)快速眼动睡眠期行为障碍症状早于帕金森样症状5.20(3.91,6.51)年。结论年龄大、病程长、运动症状和非运动症状严重的帕金森病患者易伴发快速眼动睡眠期行为障碍,快速眼动睡眠期行为障碍可能是帕金森病的早期表现。多导睡眠图监测对早期帕金森病伴快速眼动睡眠期行为障碍的诊断有重要参考价值。  相似文献   

6.
正多系统萎缩(Multiple System Atrophy,MSA)是一散发性、成人起病的运动障碍疾病,也是一种神经退行性疾,其临床表现复杂多变,以帕金森综合征、小脑性共济失调、自主神经功能障碍为主要表现。近年研究表明,该病也常常合并睡眠障碍,包括失眠、快速眼动期睡眠行为障碍(REM Sleep Behavior Disorder,RBD)、阻塞性睡眠呼吸暂停综合征(Obstructive Sleep Apnea-hypopnea Syndrome,OSAS)、日间过  相似文献   

7.
睡眠障碍为帕金森病非运动并发症的常见临床症状,其中异态睡眠是近年来帕金森病相关睡眠障碍的研究热点.包括快速眼动睡眠期行为障碍、觉醒障碍和睡眠相关运动障碍;而觉醒障碍则可分为白天过度嗜睡和睡眠发作,睡眠相关运动障碍包括不宁腿综合征和周期性腿动.其中,快速眼动睡眠期行为障碍和白天过度嗜睡可以发生在帕金森病运动症状之前,并有可能成为帕金森病的早期生物学标志.此外,部分异态睡眠的发生与抗帕金森病药物有关.因此,了解帕金森病患者的睡眠障碍,不仅有助于改善帕金森病患者生活质量,而且可使早期筛查帕金森病易感人群、尽早开展神经保护治疗成为可能.  相似文献   

8.
<正>帕金森病(PD)又称震颤麻痹,是一种常见的神经系统退行性疾病,以静止性震颤、肌强直、运动减少和姿势步态异常等运动症状为主要临床表现[1-5],并伴有嗅觉减退、睡眠障碍、自主神经功能减退、认知功能障碍等非运动症状。主要病理改变为中脑黑质多巴胺能神经元进行性变性坏死,并出现标志性的蛋白包涵小体(路易小体),其主要生化改变为纹状体多巴胺递质显著降低[3]。虽然经过两个世纪的深入研究,但  相似文献   

9.
正纯自主神经功能衰竭(pure automatic failure, PAF)是一种以直立性低血压(orthostatic hypotension,OH)为主要临床表现的罕见的自主神经系统退行性疾病。帕金森病(Parkinson's disease, PD)、路易体痴呆(dementia with Lewy body, DLB)和多系统萎缩(multiple system atrophy, MSA)等突触核蛋白病患者早期可能会出现与PAF极其相似的自主神经症状,提高对该病的认识并进行鉴别诊断十分重要。同时,PAF数年后有转变为上述疾病的可能,如何预测PAF患者的转归,  相似文献   

10.
快速眼球运动睡眠期行为障碍(rapid-eye movement sleep behavior disorder,RBD)不仅是一种睡眠障碍疾病,而且与帕金森病(Parkinson's disease,PD)、路易体痴呆(dementia with Lewy bodies,DLB)、多系统萎缩(multiple system atrophy,MSA)等α-突触核蛋白病密切相关,通常被认为是这些疾病的早期预警.研究表明,RBD可在α-突触核蛋白病症状发作前数年至数十年出现,并预测神经变性病和认知功能障碍.本文就RBD的流行病学、临床特征及疾病进展等进行综述,进一步了解RBD与α-突触核蛋白病的关系,为临床早期诊断提供帮助.  相似文献   

11.
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.  相似文献   

12.
Diagnostic Difficulties and Treatment Implications   总被引:1,自引:0,他引:1  
Robert J. Gumnit 《Epilepsia》1987,28(S3):S9-S13
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.  相似文献   

13.
Cognitive Dysfunction Associated with Antiepileptic Drug Therapy   总被引:7,自引:5,他引:2  
Eileen P.G. Vining 《Epilepsia》1987,28(S2):S18-S22
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.  相似文献   

14.
B. J. Wilder 《Epilepsia》1987,28(S2):S1-S7
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.  相似文献   

15.
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.  相似文献   

16.
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.  相似文献   

17.
Hepatic Considerations in the Use of Antiepileptic Drugs   总被引:5,自引:4,他引:1  
Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.  相似文献   

18.
Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.  相似文献   

19.
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.  相似文献   

20.
Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity   总被引:5,自引:1,他引:4  
G. Trube  R. Netzer 《Epilepsia》1994,35(S5):S62-S67
Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.  相似文献   

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