微电极导向苍白球腹后部毁损术治疗帕金森病

目的　探讨苍白球腹后部毁损术 (PVP)治疗帕金森病 (PD)的手术方法及疗效。方法　采用坐标定位结合MRI图象定位 ,在微电极导向下 ,完成对 6例病人单侧苍白球腹后部 (Gpi)的定位 ,并实施毁损。结果　 6例病人的震颤、僵硬及运动迟缓均得到明显改善 ,UPDRS运动部分积分“开”状态下改善率 32 .2 % ,“关”状态下改善率 5 8.6 % ,无永久并发症。结论　坐标结合MRI图象法能准确定位Gpi,微电极记录是其必要的补充。PVP能全面改善PD病人的征象 ,是一种安全有效的方法     

微电极引导立体定向脑内核团毁损术治疗帕金森病

2003年5月至2007年3月，我们采用螺旋CT或MRI定位，微电极引导立体定向手术射频毁损丘脑腹后外侧核（Vim），苍白球内侧核（Gpi）和丘脑底核（STN）治疗帕金森病患者63例，取得明显疗效，报告如下。     

立体定向丘脑腹外侧核毁损治疗帕金森病

目的:评价立体定向丘脑腹外侧核毁损术的疗效及适应证选择。方法:对42例原发性帕金森病应用MRI行丘脑腹外侧核定位,以微电极进行功能定位后,应用射频毁损治疗。手术前后进行UPDRS计分并计算改善率。结果:42例均有显著近期疗效,术后2例出现轻微并发症。症状改善率:开状态(71.1±8.2)％,关状态(86.1±9.2)％(P<0.001)。平均随访34.8个月,7例于6～12个月后行对侧手术,疗效均稳定。结论:立体定向丘脑腹外侧核毁损术治疗帕金森病有显著疗效,严格掌握适应证的选择,应用微电极技术进行功能定位,适当的毁损容积是手术成功的保障。     

脑立体定向术治疗帕金森病12例

我院２００１－０１～２０００－０３对１２例帕金森病患者应用立体定向技术，行苍白球腹后部毁损术（PVP）和丘脑腹外侧核毁损术（VL）治疗。现总结报告如下。１临床资料１．１治疗对象１２例均为在我院神经外科住院，符合１９８４年全国体外系疾病讨论会提出的帕金森病诊断标准［１］，服用多巴胺类药物系统治疗，效果不满意的帕金森病患者。男７例，女５例。年龄４０～７２岁，平均５６岁。病程２～１２年，平均６年。１２例患者均有明显的震颤、僵直或运动迟缓等征象，其中４例服用多巴胺药物后出现严重的开关现象。１．２治疗方法用…     

微电极引导立体定向治疗133例帕金森病的疗效观察

目的　探讨微电极引导立体定向治疗帕金森病的疗效。方法　对 133例帕金森病患者分别行苍白球腹后外侧部 (PVP核 )毁损术和 /或丘脑腹中间核 (Vim核 )毁损术 ,观察术前、术后 1周病人临床症状的改变情况。结果　术前和术后 1周分别对病人行UPDRS评分 ,术前“开”状态评分为 4 7 82± 6 4 8分 ,术后 1周评分为 2 2 73± 4 6 4分 ,得分下降了 5 2 4 7% ;术前“关”状态评分为90 75± 17 5 2分 ,术后 1周为 36 4 1± 12 2 6分 ,得分下降了 5 9 88%。两种状态术前、后评分均有显著性差异 (P <0 0 1)。结论　微电极引导立体定向手术治疗帕金森病是一种疗效确切、并发症少、安全可靠的治疗方法     

螺旋CT结合术中电刺激立体定向射频治疗帕金森病

目的 研究CT扫描结合术中电生理刺激验证的方法精确定位射频治疗帕金森病。方法 对80例帕金森病患者进行CT扫描确定影像学位置后,再用术中电生理刺激的方法验证然后进行丘脑腹中间核(Vim)和(或)苍白球(VPIP)射频毁损术。观察术前术后对药物反应情况和症状改善程度。结果 立体定向射频毁损术对帕金森病患者的震颤、僵直、运动迟缓均有明显的改善,其中对震颤的缓解率为100％。Hoehn-Yahr分级显著改善。结论 CT定位结合术中电生理刺激立体定向射频毁损术对帕金森病有良好的治疗效果。     

微电极引导立体定向下丘脑腹中间核毁损术治疗特发性震颤

目的探讨微电极引导立体定向下丘脑腹中间核(Vim核)毁损术治疗特发性震颤(ET)的临床疗效和并发症。方法对55例ET患者采用微电极导向技术确定Vim核的位置,进行单侧丘脑毁损术。对患者术前术后肢体震颤、生活功能改善情况及并发症进行定性评估和分析。结果手术对侧肢体震颤完全消失47例,在精神紧张时仍遗留有轻微震颤8例,头颈、躯干部震颤及声音震颤亦有所改善,同侧肢体震颤无缓解。术后复发3例,同侧二次手术后震颤完全控制。长期随访疗效稳定,患者生活质量明显提高。一过性并发症15例,均在1～3周后消失,无永久性并发症。结论微电极引导立体定向下单侧Vim核毁损术治疗ET是一种安全、高效、微创的方法,准确定位是手术成功的保障。     

腹侧苍白球向基底外侧杏仁核的投射参与可卡因复吸简

腹侧苍白球是中脑边缘奖赏系统中的重要位点,它向伏隔核、泛杏仁体、边缘丘脑、黑质和腹侧被盖区（VTA）均有密集的纤维投射,参与VTA调节的奖赏行为。近日,来自南卡罗来医科大学Gary AstonJones研究小组的Mahler博士研究发现腹侧苍白球向VTA的投射在可卡因觅药行为中发挥重要作用。以往研究表明,腹侧苍白球是非均一质的结构,分为腹内侧（吻端,RVP）和背外侧（尾端,     

CT引导立体定向苍白球腹后内侧部切开术治疗帕金森病

目的 研究立体定向苍白球腹后内侧部切开术(posteroventral pallidotomty,PVP)治疗帕金森病的方法、疗效、并发症及其对策。方法 应用CT引导立体定向技术进行PVP治疗32例帕金森病患者,分析其术后临床症状的改善情况及其并发症,平均随访时间9个月。结果 PVP对帕金森病患者僵直改善率为93．0％,运动迟缓改善率为85．0％,震颤改善率为82.3％,步态改善率73．5％,平衡改善率70．2％,“关”状态改善率73．0％,Hoehn-Yahr分级显著改善,术前术后UPDRS评分“开”状态下降47．0％,“关”状态下降58．2％。左旋多巴引起的并发症基本消除,无严重及永久并发症。结论 CT引导立体定向苍白球腹后内侧部切开术治疗帕金森病比丘脑切开术治疗效果更加全面,尤其对僵直、运动迟缓和左旋多巴引起的并发症具有治疗优势,副作用少。选择适宜病例、精确定位生理靶点是手术成功的关键,严密的术前准备可以减少手术并发症,远期疗效有待进一步观察。     

脑细胞刀治疗帕金森氏病和癫痫临床应用

195 4年 ,美国 Hassler和 Riechert应用立体定向神经外科技术首创丘脑腹外核切开术治疗帕金森氏病 (PD)。195 6年 ,瑞典 L ars L esell创立外侧苍白球腹后部切开术 ,以上两者的靶点定位都是建立在神经影像学基础上的解剖定位 ,由于其个体差异 ,术前的 MRI或 CT定位系统误差 ,术中脑脊液流失造成脑移位性偏差等原因 ,即靶点的理论位置与实际定位常有误差 ,从而造成临床疗效欠佳及引起一些并发症。到 196 2年Albe- Fessard等首次将微电极记录技术应用于临床 ,196 6年Bertran和 Jasper首次作了脑电单细胞记录 ,直到 1973年Freidman等将…     

Emerging drugs for Parkinson's disease

Parkinson's disease (PD) afflicts millions of people worldwide. There are numerous drugs available for PD; however, levodopa remains the gold standard of pharmacotherapy to which all other therapies are compared. Levodopa is quite effective for many motor symptoms (bradykinesia, tremor, rigidity) of PD; however, non-levodopa-responsive motor symptoms (postural instability) and nonmotor symptoms are frequently the most troublesome in middle and later stages of disease. Although motor symptoms remain an important focus for emerging drugs, current research is largely geared to identify and develop disease-slowing therapies. Another important area of focus has become treatment of the nonmotor symptoms of PD (especially depression and dementia). This review discusses emerging drugs in the management of the motor and nonmotor symptoms of PD and drugs under study as disease-slowing/neuroprotective agents.     

Emerging drugs for Parkinson’s disease

Parkinson’s disease (PD) afflicts millions of people worldwide. There are numerous drugs available for PD; however, levodopa remains the gold standard of pharmacotherapy to which all other therapies are compared. Levodopa is quite effective for many motor symptoms (bradykinesia, tremor, rigidity) of PD; however, non-levodopa-responsive motor symptoms (postural instability) and nonmotor symptoms are frequently the most troublesome in middle and later stages of disease. Although motor symptoms remain an important focus for emerging drugs, current research is largely geared to identify and develop disease-slowing therapies. Another important area of focus has become treatment of the nonmotor symptoms of PD (especially depression and dementia). This review discusses emerging drugs in the management of the motor and nonmotor symptoms of PD and drugs under study as disease-slowing/neuroprotective agents.     

Parkinson’s disease: the most common diagnostic mistakes in Lithuania

Parkinson’s disease (PD) belongs to group of neurodegenerative diseases. PD diagnosis is clinical, based on these signs: tremor, rigidity, bradykinesia, akinesia or hypokinesia. The aim of the work was to determine the frequency of separate clinical forms of Parkinson’s disease and difficulties at this disease diagnosis. After examining 267 patients, foreseen clinical criterion of Parkinson’s disease correspond 202 (44.0% persons) ? 115 women and 87 men and for 65 patients diagnosis of PD was not confirmed, because they did not correspond with accepted criteria of Parkinson’s disease. While analyzing clinical peculiarities of disease we ascertained that rigidity-tremor form of disease prevailed for 152 (75.2%, 86 women and 66 men) patients. The rigidity form was more rare ? 28 (13.9%, 13 women and 15 men). Not very frequent was a tremor form of disease -? 22 (10.9%, 16 women and 6 men) patients. According to data of our research, for almost one fourth of patients (65, 24.3%) the diagnosis of Parkinson’s disease was not confirmed after clinical examination. These patients did not correspond with clinical criteria of PD. The data of our research maintain that for almost one fourth (one fourth of what?) (24.3%) the diagnosis was incorrect. Although these patients did not correspond with accepted criteria of PD, they had been treated with antiparkinsonic medications. The PD diagnosis for them was determined only according to separate symptoms: tremor, gait alterations or memory deterioration and behaviour alternations. It must be noted, that symptoms of Wilson’s disease, MSA or brain infarction were estimated as PD. Examining patients at home, we ascertained that not all patients use prescribed L-dopa preparations. A part of patients or their relatives stopped using of this drug independently. We also made note of the fact that urinary incontinence manifested using dopamine agonist ropinirole. This side effect became significant problem for patient himself and for his relatives.     

Effects of rivastigmine on tremor and other motor symptoms in patients with Parkinson's disease dementia: a retrospective analysis of a double-blind trial and an open-label extension.

BACKGROUND AND AIM: Rivastigmine is now widely approved for the treatment of mild to moderately severe dementia in Parkinson's disease (PDD). However, since anticholinergic drugs have a role in the management of tremor in patients with Parkinson's disease (PD), concerns have been raised that the use of cholinergic drugs might worsen PD. The current analyses were performed to examine the potential of rivastigmine to affect tremor and other motor symptoms in patients with PDD. METHODS: The safety profile of rivastigmine was evaluated using a database from a 24-week, randomized, double-blind, placebo-controlled trial in 541 PDD patients (362 randomized to rivastigmine, 179 to placebo), and 334 PDD patients who subsequently entered an open-label 24-week extension on rivastigmine. RESULTS: During the double-blind trial, the adverse event (AE) of emerging or worsening tremor was reported in 10.2% of patients in the rivastigmine group, compared with 3.9% in the placebo group (p = 0.012). Tremor was most frequently reported during the titration phase of rivastigmine treatment, although this was not reflected in total motor Unified Parkinson's Disease Rating Scale (UPDRS) part III scores. Dose dependence of this AE was not observed. At the end of the double-blind phase, six (1.7%) rivastigmine-treated patients had discontinued the study because of tremor. In the open-label extension in which all patients received rivastigmine, tremor was reported by 6.9% of patients: 3.8% and 12.2% of whom had previously received double-blind rivastigmine and placebo, respectively (p = 0.006), suggesting that first exposure to rivastigmine leads to a transient increase in tremor. Three (0.9%) of the 334 patients who entered the open-label extension phase discontinued because of tremor. Incidences of worsening parkinsonism, bradykinesia and rigidity were all <5% in both treatment groups (all p-values not statistically significant, rivastigmine vs placebo). In the 48-week observation of rivastigmine treatment, there was no evidence of adverse long-term motor outcomes. Post-hoc analysis showed that similar improvements in the symptoms of dementia, including the ability to perform activities of daily living, were seen regardless of whether exacerbation of tremor was reported during the study. CONCLUSION: Rivastigmine did not induce clinically significant exacerbation of motor dysfunction in patients with PDD. Rest tremor incidence as an AE was a transient phenomenon during dose titration of rivastigmine. There was no indication that exposure to long-term rivastigmine was associated with a worsening of PD.     

Parkinson's disease: emerging pharmacotherapy

Parkinson's disease (PD) is the second most common neurodegenerative disease. The prevalence is increasing with age and averages approximately 0.3% in the entire population. The clinical picture is dominated by the cardinal motor symptoms such as tremor at rest, bradykinesia, muscular rigidity, stooped posture and postural instability. Psychiatric comorbidity is common, comprising dementia, depression, anxiety and psychosis. Although many drugs have been developed and introduced into the market to provide symptomatic treatment, there is still no cure for PD and not even solid evidence for disease-modifying strategies. In addition, motor complications in advanced stages of the disease, side effects of the dopaminergic therapy, and non-motor symptoms remain huge challenges during long-term therapy. Thus, new therapeutic agents are desperately needed. Here, we describe current therapies and possible future developments that we hope will contribute to sustaining quality of life in patients suffering from Parkinson's disease for many years.     

Tremor-predominant Parkinson's disease. Approaches to treatment

Parkinson's disease is a neurodegenerative disorder that manifests clinically with variable degrees of tremor, muscle rigidity, bradykinesia and postural instability. Tremor-predominant Parkinson's disease is characterised by prominent tremor of one or more limbs with a relative lack of significant rigidity and bradykinesia. Despite the lack of other disabling motor symptoms, the tremor of tremor-predominant Parkinson's disease can be very disabling, especially if a postural and kinetic component exists. A wide variety of treatments for Parkinson's disease tremor are currently available and include use of oral medications, injections with botulinum toxin and neurosurgical procedures. Some of the first line medications (levodopa, dopamine agonists, anticholinergics) are very effective in controlling tremor. However, some patients with Parkinson's disease tremors are unresponsive to first line drugs and treatment with second line medications (clozapine, amantadine, clonazepam, propranolol, neurontin) should be attempted. In the small number of patients with disabling tremor that is refractory to all medications, neurosurgical intervention should be considered. Both thermocoagulation and deep brain stimulation at several different neuroanatomical sites (thalamus, globus pallidus, subthalamic nucleus) offer good to excellent tremor control with relatively low risk to the patient.     

Psychotic symptoms in Parkinson's disease: pathophysiology and management

Parkinson's disease (PD) is a chronic neurodegenerative disease, in which mainly dopaminergic neurons in the substantia nigra in the brain degenerate, leading to a depletion of dopamine (DA) in the striatum. The most important motor disturbances of the disease are bradykinesia (slowing down of movement), hypokinesia (poverty of movement), rigidity (muscle stiffness), tremor and postural instability. Besides these well-known motor symptoms, non-motor symptoms may develop, such as depression, cognitive impairment and psychosis. Psychotic symptoms constitute a relatively common but nevertheless serious complication, with visual hallucinations and paranoid delusions often being most prominent. These symptoms are important contributors to patient and caregiver distress and are often important risk factors for nursing home placement. Exogenous (related to therapeutic interventions) factors are of major importance but endogenous (related to the disease process itself) factors might also contribute to the development of psychotic symptoms in PD. Therapeutic strategies comprise reduction of antiparkinsonian treatment, cholinesterase inhibitors and atypical antipsychotics. As psychotic symptoms in PD are often influenced by both endogenous and exogenous factors, a combination of strategies may be chosen.     

Psychotic symptoms in Parkinson’s disease: pathophysiology and management

Parkinson’s disease (PD) is a chronic neurodegenerative disease, in which mainly dopaminergic neurons in the substantia nigra in the brain degenerate, leading to a depletion of dopamine (DA) in the striatum. The most important motor disturbances of the disease are bradykinesia (slowing down of movement), hypokinesia (poverty of movement), rigidity (muscle stiffness), tremor and postural instability. Besides these well-known motor symptoms, non-motor symptoms may develop, such as depression, cognitive impairment and psychosis. Psychotic symptoms constitute a relatively common but nevertheless serious complication, with visual hallucinations and paranoid delusions often being most prominent. These symptoms are important contributors to patient and caregiver distress and are often important risk factors for nursing home placement. Exogenous (related to therapeutic interventions) factors are of major importance but endogenous (related to the disease process itself) factors might also contribute to the development of psychotic symptoms in PD. Therapeutic strategies comprise reduction of antiparkinsonian treatment, cholinesterase inhibitors and atypical antipsychotics. As psychotic symptoms in PD are often influenced by both endogenous and exogenous factors, a combination of strategies may be chosen.