帕金森综合征30例临床分析

目的 探讨帕金森综合征的发病原因及头颅MRI的改变。方法 对30例帕金森综合征病人的临床资料及头颅MRI改变进行分析。结果 在所有帕金森综合征中以血管性帕金森综合征最多见，占80％。结论 预防脑血管病是减少血管性帕金森综合征的一个重要方面。     

血管性帕金森综合征53例临床分析

目的　探讨血管性帕金森综合征 (VP)的临床诊断。方法　对 5 3例 VP患者的临床特点、MMSE、HDS、FAQ、HIS量表及 MRI检查资料进行分析。结果　本组 VP患者中 2次以上脑卒中者 31例(5 8.5 % ) ;病程呈阶梯样进展 ,有局限性神经系统定位体征 ,多无静止性震颤 ,智能障碍 32例 (6 0 .4% ) ;MMSE、HDS2 4.6± 2 .1分 2 8例 (5 2 .8% ) ,MMSE、HDS15 .1± 1.7分 4例 (7.5 % ) ,FAQ≥ 7分 16例(30 .2 % ) ,HIS>6分 5 3例 (10 0 % ) ;MRI均可见局限性或普遍性脑萎缩 ,多发性脑梗死 (MCI) 36例 (6 7.9% ) ,脑白质疏松 9例 (17% )。结论　 VP的发生与脑血管病发生次数及 MCI有关 ,临床诊断应结合其临床特征、智能障碍及影像学改变进行综合分析。     

血管性帕金森综合征33例

目的：探讨血管性帕金森综合征（VP）的临床特点及MRI的改变。方法：对33例住院确诊的VP患者的临床资料及头颅MRI改变进行分析。结果：本组VP患者多发少动-强直为主,特别是双下肢明显,静止性震颤少见,其发病年龄较帕金森病（PD）晚,除有锥体外系症状和体征外,可伴有锥体束征、假性延髓麻痹及记忆、智能障碍。左旋多巴替代治疗效果不明显,给予改善微循环药物效果满意。头颅MRI改变主要表现为额叶白质损害及主要分布在分水岭、基底节区的单发或多发的腔隙性梗死。结论：VP的临床表现、MRI改变不同于PD,可作为一独立的临床综合征而存在。     

血管性帕金森综合征33例

目的 :探讨血管性帕金森综合征 (VP)的临床特点及MRI的改变。方法 :对 33例住院确诊的VP患者的临床资料及头颅MRI改变进行分析。结果 :本组VP患者多以少动 -强直为主 ,特别是双下肢明显 ,静止性震颤少见 ,其发病年龄较帕金森病 (PD)晚 ,除有锥体外系症状和体征外 ,可伴有锥体束征、假性延髓麻痹及记忆、智能障碍。左旋多巴替代治疗效果不明显 ,给予改善微循环药物效果满意。头颅MRI改变主要表现为额叶白质损害及主要分布在分水岭、基底节区的单发或多发的腔隙性梗死。结论 :VP的临床表现、MRI改变不同于PD ,可作为一独立的临床综合征而存在。     

药源性帕金森综合征53例临床分析

帕金森综合征(Parkinsonism,PDS)是指除特发性帕金森病以外的各种原因引起的类似帕金森病(Parkinson disease,PD)表现的运动障碍,常继发于某些神经系统的疾病,如脑血管病、脑外伤、化学物质中毒、颅内炎症、毒物、药物等。近年来随着新药的开发及应用,药源性帕金森综合征的发生率也逐渐升高。药源性帕金森综合征的临床症状和体     

46例血管性帕金森综合征临床分析

目的探讨血管性帕金森综合征(VP)的临床与影像学特点,并与原发性帕金森病(PD)相鉴别。方法对46例VP患者的临床表现及影像学结果进行回顾性分析,并与31例PD患者的临床资料进行对比。结果VP发病年龄大于PD;病前绝大多数患者有高血压、脑卒中及糖尿病病史;急性或亚急性起病多见;最早以步行困难、运动迟缓起病;临床表现以肌强直-运动迟缓为主、静止性震颤少见;多伴有锥体束损害、智能障碍及尿失禁等;影像学改变以皮质下白质、基底节多发腔隙性梗死为主。结论VP发病年龄较高;急性或亚急性起病多见;最早以步行困难、运动迟缓起病;临床表现以肌强直-运动迟缓为主,静止性震颤少见;影像学改变主要以皮质下白质、基底节多发腔隙性梗死为主。     

血管性帕金森综合征的临床与头部MRI研究

目的探讨血管性帕金森综合征(Vascular Parkinsonism,VP)患者的临床表现、MRI的特征及发病机制。方法对42例VP患者的临床表现及MRI结果进行回顾性分析。结果本研究中多数患者有脑血管病危险因素及卒中史;临床表现以细碎步态、运动减少、肌强直为主,无4~6Hz静止性震颤;多有局灶性神经定位体征,伴有智能障碍、假性球麻痹、尿失禁等;对左旋多巴制剂疗效欠佳。MRI以基底节区、脑室周围多发性腔隙性脑梗死为主,可伴脑白质疏松或脑萎缩。结论VP的临床诊断应结合病史、临床表现、影像学改变及对多巴胺制剂的疗效进行综合分析。     

早期帕金森综合征60例临床特征分析

目的 探讨帕金森综合征的早期临床特点,减少误诊率。方法 对60例帕金森氏综合征患者进行临床分析。结果 误诊为脊柱、风湿、关节疾患居多。结论 帕金森综合征早期发病以肌张力增高为主要表现,女性发病年龄轻,年老者以脑血 管病后多见。     

血管性帕金森综合征与原发性帕金森的临床与影像学

目的:探讨血管性帕金森综合征(VPS)与原发性帕金森病(PD)临床与影像学区别。方法:对15例VPS及27例PD临床及影像学检查进行综合分析和统计学处理,并用15例椎—基动脉供血不足者作对照。结果:发现VPS临床以四肢强直—行走困难为主(93%),多伴锥体束损害体征。PD以震颤或震颤—少动—强直为主(88%)。VPS影像学异常高于PD(P<0.01),主要表现为多发皮质下白质腔梗及基底节腔梗。PD多为脑萎缩部分为苍白球钙化。结论:VPS与PD病因与发病机理不同,临床表现与影像学亦有差别。     

Lisuride in the treatment of Parkinsonism

Lisuride 1.2–4.8 mg daily was given to 10 patients with severe Parkinsonism for up to 9 months. All had been taking bromocriptine and eight had been taking levodopa combined with carbidopa. Total replacement of bromocriptine by lisuride was achieved in every case, but partial or total levodopa replacement was possible only in five patients. Lisuride 1 mg has approximately the same antiparkinsonian activity as bromocriptine 15 mg or levodopa 250–500 mg combined with carbidopa, but the duration of action of each dose is short, and gastro-intestinal and neuropsychiatric side effects are common. However, lisuride i.v. may be of considerable value in the emergency treatment of severe Parkinsonism.     

Escitalopram-induced Parkinsonism

Objective

Since the early reports associating extrapyramidal side effects (EPS) to serotonin reuptake inhibitors (SSRI), SSRIs have been pointed as more common offenders among antidepressants in producing EPS. The induction of EPS by SSRIs has been thought to be a consequence of serotonergically mediated inhibition of the dopaminergic system. We would like to present a case of escitalopram-induced Parkinsonism to increase awareness of this clinical problem.

Method

A 29-year-old male patient complaining of anger outbursts was started on escitalopram 10 mg/day without titration for impulse control in an outpatient clinic. Personal and family history was not significant for any chronic disorder, including movement disorders.

Results

Two weeks after the initiation of escitalopram, the patient started complaining of tremor, rigidity, slowness of movement, use of small steps when walking difficulty to rise when seated, disturbance of speech and along with the development of a mask-like facial expression. An MRI of the brain revealed normal findings. With a diagnosis of drug-induced Parkinsonism, he was started on 4-mg/day biperiden leading to full resolution of symptoms in 4 weeks, with no further complaints at follow up for 1.5 years.

Conclusion

As described, drug-induced Parkinsonism may persist or remit slowly despite prompt discontinuation of the offending drug. Some patients may require medications temporarily to relieve symptoms.     

Juvenile Parkinsonism: a heterogeneous entity

We studied the clinical features, laboratory investigation, management and natural history of a cohort of patients with Juvenile Parkinsonism (JP), seen at a tertiary referral centre. JP was defined as Parkinsonism with onset at age 20 years or less. Six patients (five male, one female) entered the study. The mean age at onset of Parkinsonism was 12.5 years (range 7-19) and the mean follow-up time was 49.3 months (range 40-57). Bradykinesia, rigidity, and postural instability were observed in all patients and five subjects had tremor. Dystonia was present in four subjects. Other clinical features were dementia (five subjects), supranuclear ophthalmoparesis (five subjects), seizures (three subjects), multifocal myoclonus (one subject), decreased deep reflexes (one subject), pyramidal signs (one subject). Family history of Parkinson's disease (PD) was positive in one subject. Work-up for Wilson's disease was negative in all patients. Neuroimaging studies showed cortical atrophy in two subjects and mild brainstem atrophy in two others. Sea-blue histiocytes were found in one subject. L-dopa improved the Parkinsonism in all subjects but four rapidly developed fluctuations and dyskinesias, requiring, in one, stereotaxic surgery. After a mean disease duration of 6.5 years, five subjects require assistance for performance of all daily activities. JP is a heterogeneous clinical entity. In the majority of patients, no underlying cause is identified. The unusual clinical features suggest most subjects have a CNS degenerative disease distinct from PD. There is, however, evidence suggesting that PD may rarely cause JP. Gangliosidosis is another cause of L-dopa-responsive JP. Regardless of the cause, in the present study JP displays an aggressive and rapidly progressive course in most patients.     

Valproate-induced Parkinsonism in epilepsy patients.

We systematically examined 226 epilepsy patients in a tertiary-referral center and found 6 (5.04%) to have valproate-induced Parkinsonism. There was a significantly higher prevalence of patients with Parkinsonism in the group of patients treated with valproate compared to those who were on other antiepileptic drugs (6 [5.04%] of 119 vs. 0 [0%] of 107; chi2 = 5.54; P = 0.025). These six patients had been on valproate for more than 3 years (mean, 75.67 +/- 25.32 months) at an average dose of 750 +/- 273.86 mg/day. The valproate doses were decreased or discontinued with supplementation from another antiepileptic medication. The mean UPDRS motor score significantly improved from 10.67 +/- 5.1 to 4.75 +/- 2.75 (P < 0.05). There was no relapse of seizures. Clinicians working in tertiary-referral centers should have a high index of suspicion for valproate-induced Parkinsonism. Early recognition and switching into another antiepileptic medication may help reduce unnecessary suffering in these patients.     

Smoking-responsive juvenile-onset Parkinsonism.

We describe a patient with juvenile levodopa-responsive Parkinsonism who reported a dramatic response to cigarette smoking with transient but marked improvement of motor symptoms associated with oculogyric crises and psychotic behavior. His beta-CIT single-photon emission computed tomography scan showed a complete absence of presynaptic dopaminergic nerve terminals.     

Parkinsonism after acute cadmium poisoning

A 64-year-old man suffered from acute exposure to cadmium, followed by multiple organ failure. Three months after exposure, the patient developed parkinsonian features. The case suggests that cadmium intoxication may damage the basal ganglia, resulting in parkinsonism.