帕金森非运动症状表现特点及对生活质量的影响

目的探讨帕金森非运动症状特点及对患者生活质量的影响。方法观察132例帕金森病患者,评估不同临床分期帕金森病患者非运动症状的临床表现及对生活质量的影响。结果帕金森病患者在不同临床阶段均可伴发多种复杂的非运动症状,其中自主神经功能障碍的发生率最高,达81.8%,采用多重回归分析得知自主神经功能障碍、抑郁和睡眠障碍是影响患者生活质量的主要因素,差异有统计学意义(P<0.01)。结论帕金森病患者普遍存在非运动性症状,其中自主神经功能障碍、抑郁和睡眠障碍是导致生活质量恶化的主要原因,对患者的生活质量有明显影响。     

帕金森病生活质量量表应用及评价

帕金森病是中老年人常见的神经变性疾病,临床表现包括运动症状和非运动症状,缓慢进展,严重影响患者生活质量。目前对帕金森病患者生活质量的评价主要依靠量表。本文拟就帕金森病生活质量问卷之通用量表和专用量表,以及显著影响生活质量的帕金森病非运动症状如抑郁和焦虑、认知功能障碍、睡眠障碍和疲劳相关量表进行概述,并对其进行简要评价。     

经颅超声评价帕金森病伴发抑郁的研究进展

正帕金森病(Parkinson’s disease,PD)是一种以静止性震颤、肌强直、运动迟缓、姿势平衡障碍等运动症状以及以包括抑郁、焦虑、睡眠障碍、精神症状等非运动症状为主要特征的神经系统变性疾病,目前帕金森病诊断主要依据是患者的临床症状、体征以及对左旋多巴等治疗的反应性,尤其在发病早期尚缺乏特异的生物学诊断指标。相对于运动症状而言,目前认为非运动症状对帕金森病患者的生活质量影响更大,其中抑郁是帕金森病的常见的非运动症状之一,约40%～     

帕金森病睡眠障碍的治疗进展

正帕金森病(Parkinson’s disease,PD)是一种中老年人常见的神经系统变性疾病,除静止性震颤、运动迟缓、肌强直、姿势步态异常等典型运动症状外,睡眠障碍、感觉障碍、神经精神障碍和自主神经功能障碍等非运动症状也日益引起人们的重视。其中睡眠障碍的发生率高达60%~98%[1-4],严重影响患者的生活质量,是导致患者丧失生活能力最常见的非运动症状。PD患者睡眠障碍可发生在疾病的任何阶段,     

帕金森病所致精神障碍

帕金森所致精神障碍一直在诊断与治疗过程中难度较大,成为影响帕金森病患者生存质量的重要原因,其表现多种多样,包括抑郁、焦虑、精神病性症状、认知功能障碍、睡眠障碍等,本文就帕金森病所致精神障碍有关的研究进展进行综述。     

脑深部电刺激术对帕金森病睡眠觉醒障碍的影响

正睡眠觉醒障碍是帕金森病(Parkinson disease, PD)常见的非运动症状,对PD患者生活质量影响较大~([1])。PD患者睡眠觉醒障碍的发生与多巴胺能和非多巴胺能系统病变导致睡眠网络异常相关,而肌张力障碍、开关现象、异动症等运动并发症和常见的夜间幻觉、夜尿增多、焦虑、抑郁、疼痛等非运动症状都会影响患者的睡眠质量~([1])。此外,抗帕金森病药物如多巴胺能受体激动剂、金刚烷胺等也可导致睡眠结构改变、加重失眠及日间嗜睡症状~([2-3])。脑深部电刺激术(deep brain stimulation, DBS)是治疗中晚期PD的有效方法。DBS对PD患者运动症状的改善是确切的~([4]),然而对非运动症状睡眠觉醒障碍的改善作用尚不明确。用于PD治     

帕金森病抑郁的研究进展

<正>帕金森病主要的运动症状包括静止性震颤、僵直、运动迟缓和姿势平衡障碍,严重影响患者的运动功能。近年来的临床研究得出结论,与运动症状相比,帕金森病伴发的非运动症状是降低患者生活质量更为主要的原因。抑郁是帕金森病非常常见的非运动症状之一,严重影响患者情绪和生活。但是在临床工作中,帕金森病患者的抑郁却很少被诊断,更难以做到规范有效地治疗。本文综述了帕金森病并发抑郁的可能机制,临床特点和评估以及综合治疗等内容。     

早期帕金森病非运动症状对患者生活质量的影响

目的探讨早期帕金森病(PD)患者非运动症状(NMS)的发病情况及其对患者生活质量的影响。方法选择我院门诊及住院160例早期PD患者为观察组;选取同期门诊就诊的非PD患者100例为对照组。采用帕金森病非运动症状筛查量表对2组的NMS发病情况进行调查;采用帕金森病生活质量问卷(PDQ-39)评估患者生活质量;分析PD患者的NMS的发病情况及其对帕金森病患者生活质量的影响。结果观察组NMS平均(8.1±4.2)分,显著高于对照组(4.9±3.1)分(P0.01);焦虑、抑郁、大便排空不完全感、注意力障碍、失眠、记忆力下降对日常生活有显著的负面影响(P0.05)。结论神经精神症状、自主神经功能障碍、睡眠障碍是PD患者最常见的非运动症状,对帕金森病患者生活质量有显著的负面影响,早期评估和干预非运动症状对提高患者生活质量有重要意义。     

伴有认知障碍帕金森病患者的楔前叶影像学研究进展

正帕金森病(PD)是仅次于Alzheimer's病(AD)的第二大常见的神经系统变性疾病。PD主要表现在运动症状,表现为静止性震颤、运动迟缓、肌强直和姿势步态障碍。近年来人们越来越多的注意到痴呆、抑郁和睡眠障碍等非运动症状,也是PD患者常见的主诉,它们对患者生活质量的影响甚至超过运动症状。PD患者以每年10%的速度进展为PD痴呆(PDD)[1],PD认知下降作为常见的非运动症状,给患者本人     

帕金森病患者便秘的研究进展

帕金森病(Parkinson disease,PD)是一种中老年常见的神经变性病,慢性致残率高。疾病早期除了典型运动症状,患者还诉嗅觉减退、睡眠障碍、抑郁和便秘等非运动症状(non-motor symptoms,NMS)。临床中随着抗帕金森药物的应用,NMS成为影响患者生活质量的主要因素[1],而便秘是临床常见、发生率很高的     

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.     

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.     

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.     

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.