帕金森病患者的情感淡漠及其与抑郁和认知障碍的关系

目的了解帕金森病患者情感淡漠发生状况,并对情感淡漠与抑郁、认知功能的关系进行分析。方法采用修订的情感淡漠评定量表(MAES)评定56例帕金森病患者的情感淡漠症状,并以统一帕金森病评定量表(UPDRS)、汉密尔顿抑郁量表(HAMD)、简易智力状态检查(MMSE)、画钟测验(CDT)、词语流畅性测验(VFT)评定患者的病情、抑郁情绪及认知功能。对情感淡漠的相关因素进行Logistic回归分析。结果 56例帕金森病患者中情感淡漠发生率为44.64%(25/56),其中情感淡漠单独发生率为30.35%(17/56),同时伴有抑郁者占14.29%(8/56)。情感淡漠组和非情感淡漠组之间UPDRS的日常生活评分(UPDRS-Ⅱ)、运动评分(UPDRS-Ⅲ)和Yahr评分以及MMSE评分的差异均有统计学意义(P0.05),情感淡漠组的CDT和VFT成绩也明显低于非情感淡漠组(P0.01)。情感淡漠影响因素的Logistic回归分析中,依次进入方程的是CDT、VFT、Yahr、MMSE、多巴胺受体激动剂和UPDRSⅢ。结论帕金森氏病的情感淡漠发生率较高,情感淡漠独立于抑郁症状,并与认知功能损害相关。     

高频重复经颅磁刺激对帕金森病患者情绪障碍及P300电位的影响

研究背景以往研究显示高频重复经颅磁刺激可以明显改善帕金森病患者运动功能,但帕金森病晚期非运动性症状给患者带来更为严重的影响,因此研究高频重复经颅磁刺激治疗帕金森病患者情绪和认知功能障碍等非运动性症状的临床疗效具有重要意义。方法共纳入65例诊断明确的帕金森病患者,根据统一帕金森病评价量表(UPDRS)、汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)和P300波,评价高频重复经颅磁刺激对患者精神行为和情绪、日常生活活动能力及运动功能的改善作用。结果与治疗前相比,帕金森病患者UPDRS总评分(t=10.872,P=0.000)和UPDRSⅠ(t=4.538,P=0.023)、UPDRSⅡ(t=8.846,P=0.012)、UPDRSⅢ(t=9.114,P=0.000)评分降低。患者焦虑和抑郁发生率由治疗前的52.46%(32/61)降至29.51%(18/61),认知功能障碍发生率由治疗前的42.62%(26/61)降至32.79%(20/61),HAMA(t=3.692,P=0.000)和HAMD(t=4.241,P=0.000)评分显著降低,但幻觉发生率由治疗前的18.03%(11/61)升至29.51%(18/61)。P300波潜伏期(t=5.924,P=0.000)和波幅(t=8.512,P=0.000)与治疗前比较,差异均有统计学意义。结论高频重复经颅磁刺激能够减轻帕金森病患者焦虑和抑郁状态,改善其认知功能。     

帕金森病认知障碍及相关因素分析

目的 探讨帕金森病认知障碍及其影响因素.方法 127例原发性帕金森病患者,收集年龄、发病年龄、病程、受教育时间、既往史、个人史和家族史等一般资料.采用帕金森病统一评价量表第3部分(UPDRSⅢ)和Hoehn-Yahr分级评价运动性症状严重程度;帕金森病统一评价量表第2部分(UPDRSⅡ)和日常生活活动能力问卷(ADL)评价日常生活活动能力;简易智能状态检查量表(MMSE)和蒙特利尔认知评价量表(MoCA)评价轻度认知障碍;Fuld物体记忆评价(FOM)、快速词汇测验(RVR)、积木测验(BD)和数字广度测验(DS)评价短时记忆、长时记忆和语言能力、视空间结构能力及注意力和瞬时记忆;汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)评价抑郁和焦虑症状.结果 帕金森病患者普遍存在轻度认知障碍,与受教育时间(r=0.510,P=0.000)和ADL评分(r=0.452,P=0.000)呈正相关,与年龄(r=-0.466,P=0.000)、发病年龄(r=-0.418,P=0.000)、UPDRSnl评分(r=-0.330,P=0.000)、Hoehn-Yahr分级(r=-0.431,P=0.000)、HAMD评分(r=-0.229,P=0.000)和HAMA评分(r=-0.222,P=0.000)呈负相关,而与病程无相关性(r=0.012,P=0.893);其中以受教育时间和Hoehn-Yahr分级对认知功能影响最为显著(R2=0.260,0.388).结论 帕金森病患者早期即存在轻度认知障碍,可影响日常生活活动能力.蒙特利尔认知评价量表是筛选轻度认知障碍患者便捷、有效的方法.     

帕金森病患者的情感淡漠及相关因素研究

目的了解帕金森病(PD)患者情感淡漠的发生率,并对其相关因素进行探讨。方法收集2006年8月至2008年3月在我院神经内科门诊就诊和住院的PD患者60例,采用统一PD评定量表(UPDRS)及自制的一般情况调查表对患者的神经功能状态、病情严重程度及人口学资料进行评测。使用修订的情感淡漠评定量表(MAES)、抑郁自评量表和汉密尔顿抑郁量表(17项版本)以及精神状态简易速检表(MMSE)分别对患者的情绪状态及认知功能进行评定,采用Logis-tic回归分析调查情感淡漠发生的相关因素。结果 60例PD病人中,35例(58.3%)出现情感淡漠,其中单纯情感淡漠14例(23.3%),同时伴有抑郁者21例(35.0%)。相关性分析显示,服药情况、合并认知障碍、UPDRS运动评分这3个因素与患者伴发的情感淡漠相关(P0.05)。结论情感淡漠是PD的常见临床表现,它可能是PD的一种核心症状,它的发生与患者并存的认知障碍和运动障碍的程度密切相关。     

帕金森病痴呆相关影响因素分析

目的 探讨帕金森病痴呆的相关影响因素.方法 根据英国帕金森病学会脑库帕金森病临床诊断标准和美国精神障碍诊断与统计手册第4 版痴呆诊断标准,对简易智能状态检查量表评分<24 分且帕金森样症状早于痴呆症状至少> 2 年的帕金森病患者进行社会人口学(性别、年龄、受教育程度、职业分类)、饮酒、吸烟、饮茶、发病年龄、病程、既往史和帕金森病相关评价量表调查.采用单因素非条件Logistic 回归分析和多因素Logistic 逐步回归模型进行分析.结果 单因素分析显示,帕金森病痴呆患者年龄、帕金森病统一评价量表第3部分(UPDRSⅢ)评分均高于非痴呆者(P < 0.05);震颤型帕金森病患者发生痴呆的概率较低(OR = 0.364,95%CI:0.139 ～ 0.953);抑郁是帕金森病痴呆较强的危险因素(OR = 2.647,95%CI:0.963 ～ 7.000).多因素分析显示,进入回归方程的因素分别为年龄、受教育程度、UPDRSⅢ评分、震颤型(OR = 1.203,0.790,4.264,0.068).结论 年龄、受教育程度、UPDRSⅢ评分、震颤型、抑郁等是帕金森病痴呆的相关影响因素.     

轻度认知功能障碍、焦虑及抑郁对帕金森病患者生活质量的影响

目的探讨轻度认知功能障碍(MCI)、焦虑及抑郁等对帕金森病(PD)患者生活质量的影响。方法选取诊治的103例PD患者,收集年龄、病程、受教育年限、统一帕金森病评定量表第三部分(UPDRSⅢ)评分、蒙特利尔认知评估量表(MoCA)评分、汉密尔顿抑郁量表(HAMD)评分及汉密尔顿焦虑量表(HAMA)评分和39项PD生存质量调查表(PDQ-39)评分等资料,分析上述指标与PDQ-39评分的相关性。结果相关性分析结果显示,年龄、病程、HAMA评分、HAMD评分、MoCA评分和UPDRSⅢ评分均与PDQ-39评分呈显著相关;多元线性逐步回归分析结果显示,年龄、HAMA评分、HAMD评分和MoCA评分是影响PDQ-39评分的主要因素(P 0. 05);影响PDQ-39评分的因素大小依次为HAMD评分、HAMA评分、MoCA评分和年龄。结论 MCI、焦虑及抑郁是影响PD患者生活质量的重要因素,且以抑郁的影响最大。     

帕金森病患者情绪障碍研究

目的 了解帕金森病患者伴发的情绪障碍.方法 采用汉密尔顿焦虑评价量表和抑郁评价量表对100例帕金森病患者和50例对照者进行情绪障碍研究;并根据简易智能状态检查量表、帕金森病统一评价量表(UPDRS Ⅲ)和改良Hoehn-Yahr分级,分别评价帕金森病患者的认知功能和运动障碍严重程度并进行病情分级.结果 帕金森病组患者汉密尔顿焦虑评价量表评分[(14.45±8.30)分]和抑郁评价量表评分[(7.98±6.24)分]均高于对照组[(3.68±3.23)分、(2.76±3.32)分],差异均有统计学意义(P<0.01);其焦虑症状发生率为49%(49/100),高于对照组(2%),差异有统计学意义(P<0.01),但早期与中晚期患者之间差异无统计学意义(P>0.05).帕金森病组患者抑郁症状发生率(12%)虽高于对照组(2%),但组间差异无统计学意义(P>0.05);中晚期患者抑郁症状发生率高于早期者(P<0.05).帕金森病组焦虑症状主要表现为精神性焦虑及躯体性焦虑,抑郁症状则以焦虑躯体化、认知障碍、迟缓以及睡眠障碍为主;性别与肢体发病侧别对情绪障碍无明显影响,而汉密尔顿焦虑评价量表(r=0.199,P=0.049;r=0.295,P=0.005)和抑郁评价量表(r=0.196,P=0.050;r=0.274,P=0.009)情绪均与病程和UPDRSⅢ评分呈正相关.结论 帕金森病患者以焦虑情绪为主要情绪障碍症状,表现为躯体性焦虑和精神性焦虑,于疾病早期即已出现;而抑郁症状多出现于疾病的中晚期,主要表现为焦虑躯体化、认知障碍、迟缓以及睡眠障碍.     

帕金森病相关性疼痛的相关因素及其对生活质量的影响

目的探讨帕金森病(PD)相关性疼痛的相关因素及其对生活质量的影响。方法根据是否伴有疼痛将120例PD患者分为疼痛组(49例)和非疼痛组(71例)。采用PD统一评分量表(UPDRS)和Hoehn-Yahr(H-Y)分级评估患者的严重程度,采用PD生活质量量表-39(PDQ-39)测评其生活质量,用数字评分法(NRS)评估疼痛组患者疼痛程度。采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)和MMSE评价患者的焦虑、抑郁及认知情况。结果与无疼痛组比较,疼痛组H-Y分期及UPDRSⅠ、UPDRSⅢ服药后(med-on)、UPDRSⅢ服药前(med-off)、PDQ-39、HAMA、HAMD评分均显著升高(P0.05～0.01)。Spearman相关分析显示,NRS评分与H-Y分级及UPDRSⅠ、UPDRSⅢmed-off、UPDRSⅢmed-on、PDQ-39、HAMA、HAMD评分呈正相关(P0.05～0.01),与年龄、发病年龄、病程、受教育年限及UPDRSⅡ、MMSE评分无相关性(均P0.05)。线性回归分析显示,UPDRSⅡ、HAMA、NRS评分对PDQ-39有显著性影响(均P0.01)。结论 PD相关性疼痛可能与精神活动、运动症状、焦虑抑郁相关。PD相关性疼痛是影响PD患者生活质量的独立预测因子。     

帕金森病患者出现认知功能障碍的危险因素Logistic回归分析

目的探讨帕金森病患者出现认知功能障碍的危险因素,为临床预防提供参考。方法对97例帕金森病患者采用帕金森病统一评价量表(UPDRS)、蒙特利尔认知评估量表(MoCA)、汉密尔顿抑郁量表(HAMD)、H-Y分级量表调查,检测患者血尿酸、血浆同型半胱氨酸的水平。分析引起认知功能障碍发生的危险因素。结果 MoCA调查显示帕金森病患者认知功能障碍发生率69.07%;无认知功能障碍组受教育年限、血尿酸高于认知功能障碍组(P0.05),病程、MAMD评分、H-Y分级、PUDRSⅡ评分、PUDRSⅢ评分、血浆同型半胱氨酸均低于认知功能障碍组(P0.05或P0.01);多因素Logistic回归分析显示,受教育年限、病程、MAMD评分、H-Y分级、PUDRSⅢ评分与患者发生认知功能障碍关系密切,是独立危险因素(P0.05或P0.01)。结论受教育年限、病程、MAMD评分、H-Y分级、PUDRSⅢ评分是帕金森病患者出现认知功能障碍的相关危险因素,应加以关注。     

帕金森病患者神经精神症状及其影响因素研究

目的调查帕金森病(PD)患者的神经精神症状的发生、分布情况,并分析各神经精神症状间的相互关系及影响因素。方法应用简明精神病量表(BPRS)调查209例PD患者的20项神经精神症状发生率和分布情况,并分析各神经精神症状间的相关性以及与临床特征包括年龄、受教育时间、病程、认知水平、运动功能、抑郁、焦虑、睡眠、生活质量、左旋多巴等效剂量等的相关性。结果 PD神经精神症状发生率较高的前3位分别为动作迟缓(84.21%)、关心身体健康(66.51%)和焦虑(54.55%),发生率较低的症状为不合作、定向障碍和自知力障碍(均为5.26%)。BPRS的5个分量表即焦虑抑郁、缺乏活力、思维障碍、激活性和敌对猜疑两两之间均具有相关性(均P0.01),其中思维障碍与敌对猜疑(r=0.477)、缺乏活力与思维障碍(r=0.441)、缺乏活力与敌对猜疑(r=0.429)之间呈中度相关。BPRS总分与受教育时间、帕金森病睡眠量表(PDSS)评分和简易精神状态检查量表(MMSE)评分呈负相关,与年龄、统一帕金森病评定量表(UPDRS)第3部分评分、修订Hoehn-Yahr(H-Y)分期、汉密尔顿抑郁量表(HAMD)评分、汉密尔顿焦虑量表(HAMA)评分、帕金森病生活质量问卷(PDQ-39)评分呈正相关(均P0.05),与病程和左旋多巴等效剂量无相关性(均P0.05)。BPRS高分组(35分)PD与BPRS低分组(≤35分)PD患者在年龄、起病年龄、UPDRSⅢ、PDQ-39、HAMA、HAMD和MMSE评分间比较存在统计学差异(均P0.05)。逐步多元线性回归分析结果示HAMA和MMSE评分对BPRS总分影响最大(r2分别为0.196和0.270)。结论 PD患者的神经精神症状发生率高且具多样性。MMSE评分越低,PD患者精神症状越严重。     

Hepatic Considerations in the Use of Antiepileptic Drugs

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.     

Vascular Malformations and Epilepsy: Clinical Considerations and Basic Mechanisms

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.     

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 and Utilization in Children

Summary: Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmacokinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.     

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.     

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.     

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.     

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.