立体定向下丘脑Vim核毁损术治疗特发性震颤的相关因素分析

目的探讨立体定向下丘脑腹中间核(Vim核)毁损术治疗特发性震颤(essentialtremor,ET)的疗效及相关因素。方法回顾性分析微电极导向下单侧丘脑毁损术治疗的55例ET患者。对患者术前术后肢体震颤、生活功能改善情况进行评估,对并发症、症状复发及手术适应证进行分析。结果手术对侧肢体震颤完全消失47例,遗留有轻微震颤8例,头颈、躯干部震颤及声音震颤有所改善,同侧肢体震颤无缓解,震颤的整体改善率54.1%,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,无永久性并发症。结论立体定向单侧Vim核毁损术治疗ET是一种安全、有效的方法,微电极引导准确定位是手术成功的保障,症状复发及并发症的出现与靶点定位不准及毁损灶大小有关。     

微刺激在选择性丘脑腹中间核毁损术中的定位作用

目的探讨微刺激在选择性丘脑腹中间核毁损术中的定位作用.方法在对23例震颤型帕金森病患者进行的微电极引导选择性丘脑腹中间核毁损术中,比较丘脑腹中间核(Vim)及其周围结构在微刺激时,对侧肢体震颤变化情况及异常感觉情况.结果靶点上方2-5mm不仅震颤遏止机率最大,为靶点上方7～10mm的3倍以上,而且阈值小于10mA,比靶点上方7～10mm的阈值小1倍以上.不同亚核刺激时感觉异常的发生机率不同.刺激腹尾侧核(VC)时患者感觉确切,部位局限,阈值较小,常常小于10μA.结论微刺激可以确定VC与Vim的边界、手术靶点的内外侧界和手术毁损区域,在选择性丘脑毁损术靶点定位中有重要意义.     

微电极导向VL核和PVP核联合毁损治疗帕金森病

目的：对震颤、僵硬及运动迟缓帕金森病（ＰＤ）患者的立体定向手术方法学进行探讨。方法：应用微电极导向技术,对４３例ＰＤ患者,同侧丘脑腹外侧核（Ｖim/Vop)及苍白球腹后部（PVP）进行联合毁损术。结果：43例PD患者的肢体震颤、僵硬及运动迟缓均得到明显改善。术前术后Motor UPDRS积分,开状态及关状态均显著改善（P＜0．01）,无永久并发症。结论：应用微电极导向立体定向技术对伴有肢体震颤、强直及运动迟缓的ＰＤ患者,行同侧Ｖim核和PVP核联合毁损手术,能全面改善PD患者的症状,是一种安全有效的手术方法。     

射频毁损电极直径对射频治疗疗效的影响

目的：比较使用直径1.1mm和1.8mm的射频毁损电极进行立体定向内侧苍白球腹后部毁损术或丘脑Vim核毁损术的疗效与并发症,分析探讨射频毁损电极直径是否影响手术疗效及并发症的发生。方法：通过比较28例接受1.8mm直径毁损电极与32例接受1.1mm直径毁损电极,进行立体定向内侧苍白球腹后部毁损术及丘脑vim核毁损术的帕金森病患者,术后近期情况的综合评估,进行方差分析,判断不同直径毁损电极的疗效与并发症是否存在统计学差异。结果：接受1.8mm直径毁损电极进行立体定向射频治疗的治疗组与1.1mm微电极治疗组比较,术后肢体僵硬、震颤、运动迟缓症状的缓解无显著差异;而1.8mm治疗组患者术后发生语言障碍,膈肌痉挛,吞咽困难、饮水呛咳、轻度偏竣,面瘫等并发症的发生率高,且发生的程度较重,二者有显著差异。结论;精电极（1.8mm)作为毁电极,由于其本身直径较粗,输出功率较大,热传导效应范围较广,毁损时热效应容易影响到靶点周围的脑深部重要结构。如下丘脑、内囊,视束等,造成短暂或永久并发症发生。     

帕金森病核团毁损术疗效与并发症的关系

目的：进一步总结帕金森病的微电极导向苍白球腹后部毁损术和丘脑腹中间核毁损术疗效。方法：微电极导向立体定向核团毁损术治疗帕金森病患者300例。对近期进行的100例患者在手术靶点选择、手术方法、手术疗效和并发症等方面进行总结，并与早期进行的100例手术患者比较。结果：近期进行的100例患者手术效果较好，并发症发生率低。结论：根据患者症状选择合适的毁损术能提高手术疗效；对靶点采用磁共振成像（MRI）图像和座标相结合的定位方法,可减少个体差异引起的误差；适当减少微电极记录针道数，降低毁损温度，能减轻电极与脑组织粘连，减少脑出血等并发症。     

立体定向选择性Vim核和(或)PVP核毁损术治疗帕金森病疗效观察

目的观察应用立体定向脑内核团毁损术治疗帕金森病的临床疗效。方法 2012年7至2013年12月采用立体定向丘脑腹中间核(Vim核)和或苍白球腹后外侧部(PVP核)毁损术治疗帕金森病45例。术前、术后1个月进行UPDRS评分,比较手术前后评分的变化和症状改善情况。结果 45例帕金森病患者的肢体震颤、僵硬及运动迟缓均得到明显改善,术后1个月的UPDRS评分较术前明显减少(P0.01),术后无明显并发症。结论立体定向脑内核团毁损术治疗帕金森病疗效显著,靶点定位、毁损范围及程度与手术疗效及并发症密切相关。     

慢性丘脑刺激治疗帕金森病

近 50年来 ,利用立体定向外科方法治疗各种震颤和运动障碍性疾病取得了飞速的发展 ,经过对不同靶点的探索和研究 ,目前认为丘脑的腹中间核( Vim)核、苍白球腹后外侧部 ( PVP)以及丘脑底核( STN)是治疗帕金森病理想靶点。随着近年来神经影像学及微电极记录等电生理技术的快速发展 ,立体定向丘脑毁损术和苍白球毁损术的定位更加精确 ,毁损灶趋向更小 ,而控制震颤和肌僵直的效果更好。尽管如此 ,根据国内外大宗资料报道 ,其毁损手术后造成的暂时性或永久性神经功能缺损如偏瘫、感觉缺失、言语障碍、视野缺损等达 2 %～ 2 5% [1～ 7]。自从 1…     

帕金森病外科治疗的适应证及毁损部位的选择

目的介绍微电极导向立体定向毁损手术治疗帕金森病的适应证及毁损部位选择的经验.方法回顾607例帕金森病患者采用微电极导向立体定向毁损手术治疗经验,根据临床症状分型确定,单纯震颤型,选择丘脑腹外侧核(Vim,Vop)为靶点;僵直少动型选择苍白球腹后内侧部为靶点;混合型首先选择苍白球腹后内侧部为靶点,术中如肢体震颤改善不理想时,再加丘脑腹外侧核(Vim)毁损.结果手术有效率97.3%,术后患者Hoehn和Yah分级及UPDRS评分及药物所致运动障碍均有显著改善.术后1周开状态改善率62.3%±11.3%,关状态改善率76.1%±8.7%.总并发症的发生率为5.5%,永久性并发症为1.3%.结论微电极记录技术能显著提高手术定位准确率及成功率.合适的病例选择对于良好的手术疗效是第一位的,手术适应证的选择应该遵循一个基本原则,即诊断明确,手术操作有助于改善患者目前的生活质量.毁损靶点的选择,取决于患者的临床症状分型,根据病人的临床症状,灵活地选择毁损靶点.     

书写痉挛的外科治疗

目的：回顾书写痉挛的立体定向丘脑腹外侧核毁损术治疗方法及疗效。探讨书写痉挛的发生和治疗的机理。方法：运用微电极导向立体定向技术，对8例书写痉挛患者实施了丘脑腹外侧核毁损术，进行疗效分析。结果：8例患者术后书写功能即刻恢复正常，无手术并发症，1－2年的随访疗效稳定。结论：立体定向丘脑膜外侧核毁损术是治疗书写痉挛有效，安全的治疗手段，可能的治疗机制是阻断了基底节的异常爆发性电活动。     

丘脑Vim核毁损术中的微电极定位技术

目的 探讨丘脑Ｖｉｍ核毁损术中的微电极定位方法，实施靶点调查。方法 术中采用微电极技术，确定Ｖｉｍ的位置后，进行毁损治疗，术后进行靶点调查。结果 全部患者震颤完全消除，无一例永久并发症发生，靶点调查显示一定的分布规律。结论 精确的微电极引导丘脑Ｖｉｍ核毁损术可以获得良好的手术效果，并降低并发症的发生。     

A follow-up study of very low field MRI findings and clinical course in multiple sclerosis

Seventy-three consecutive patients with definite multiple sclerosis (MS) were examined with very low field (0.17 and 0.02 tesla) magnetic resonance imaging (MRI) of the brain. Fifty-seven patients were examined a second time after 6 months, 41 patients a third time after 1 year, and 25 patients a fourth time after 2 years. The initial finding was abnormal in 57/73 patients (78%). The number of lesions increased with age, duration of disease, and increasing disability. Plaques were more numerous in progressive than in remitting MS. Of the patients with abnormal MRI 65% had more than 3 lesions, and in 82% lesions were smaller than 2.5 cm in diameter. After follow-ups of 1 year and 2 years the size of MRI lesions remained unchanged in 55% and 64%, respectively. Unchanged plaque numbers were found in 72% and 60%. Unchanged MRI was most common among patients with remitting MS who were in a stable phase. Decrease in size and disappearance of plaques correlated well with clinical remissions. Increase in size was rare even during relapses. New plaques could appear during all phases of clinical course although they reflected better a relapse of remitting or progressive disease.     

The prognostic significance of abnormalities seen on magnetic resonance imaging in late life depression: clinical outcome, mortality and progression to dementia at three years

OBJECTIVE. To study the course of depressive symptoms over 3 years, rate of dementia and mortality in relation to baseline neuroradiological abnormalities. DESIGN. Retrospective casenote analysis of 38 patients (of 44) who had a Magnetic Resonance Imaging (MRI) scan 3 years earlier. Twenty-two patients also received a detailed interview. RESULTS. Overall outcome was good for around two-thirds of the sample. Poorer clinical course was associated with lesions in pons and more than five Virchow Robins spaces in the corona radiata. Pontine raphe lesions and confluent periventricular lesions were associated with later dementia and with reduced survival from cardiovascular death. Males had more recurrences and a reduced survival. CONCLUSIONS. MRI lesions influence outcome, mortality and the onset of dementia. However, because they are quite common in elderly depressed patients they have limited utility on their own as predictors of outcome. The association of periventricular lesions with dementia is a new finding, and suggests that the site and type of lesions may be as important than the quality of them.     

Non-neoplastic brain abnormalities on MRI in children and adolescents with neurofibromatosis type 1.

The occurrence, localization and longitudinal course of non-neoplastic MRI abnormalities in children and adolescents with neurofibromatosis type 1 (NF 1) were studied. Thirty-five patients who satisfied the criteria for NF 1 underwent 114 MRI examinations. They were 9 months to 18 years old at their first examination, and 23 were examined more than once (2 - 11 times). The follow-up time varied from 3 months to 10 years (mean 4 years). Thirty-one patients (89%) showed focal high signal intensities on T2-weighted images in the cerebellum, brain stem, deep cerebral gray matter and, less frequently, in the cerebral white matter. Changes were also seen in 80% and 50% of the proton density-weighted and T1-weighted images, respectively. Newly appearing, growing, decreasing and disappearing lesions occurred contemporaneously and in all ages. New lesions still developed in the late teens. Three lesions showed temporary contrast enhancement. Five expansive lesions were found in four individuals without related clinical symptoms. Four of them receded during follow-up. These cases indicate that the differential diagnosis between neoplastic and non-neoplastic lesions is not clear. The results support the view that high T2-signal lesions are so common in NF 1 that they should be included as another criterion for the diagnosis.     

Cerebral perfusion pressure--targeted approach in children with central nervous system infections and raised intracranial pressure: is it feasible?

This study was conducted to evaluate the feasibility of cerebral perfusion pressure-targeted therapy in children with raised intracranial pressure caused by central nervous system infection. A prospective observational pilot study was conducted in the pediatric intensive care unit of a tertiary care teaching hospital. Twenty children (ages 6 months to 12 years) with a clinical diagnosis of meningitis or meningoencephalitis were included. Intracranial pressure and blood pressure monitoring were initiated soon after enrollment. Interventions to reduce intracranial pressure and elevate blood pressure were used to achieve a target cerebral perfusion pressure of greater than 70 mm Hg in children 2 years of age or older and greater than 60 mm Hg in children less than 2 years. Therapies used to achieve target cerebral perfusion pressure were initial fluid boluses (in 14 patients), vasopressors (in 8), and mannitol (in 10). The target cerebral perfusion pressure was achieved in 6 patients, whereas a cerebral perfusion pressure greater than 50 mm Hg was achieved in 16 patients. All 4 patients with mean cerebral perfusion pressure less than 50 mm Hg died of intractable, raised intracranial pressure. In contrast, only 3 of 16 patients with mean cerebral perfusion pressure more than 50 mm Hg died. In children with raised intracranial pressure caused by central nervous system infection, it was feasible to achieve a cerebral perfusion pressure greater than 50 mm Hg, mainly by increasing the blood pressure within the first 24 hours and by reducing intracranial pressure after the first 24 hours.     

Demyelinating lesions in the cervical cord in multiple sclerosis 10 years after onset of the disease. Correlation between MRI parameters and clinical course

BACKGROUND AND PURPOSE: Demyelinating lesions in spinal cord in multiple sclerosis (MS) are found in magnetic resonance imaging (MRI) in 47-90% of patients; spinal cord atrophy, however, which is a measure of axonal loss and correlates with disability, is found in 13-41% of patients. Presence and character of lesions depend on the duration and progression of the disease. The aim of this study was to estimate the presence, character and location of lesions and cervical cord atrophy in MRI performed 10 years after the onset of MS in relation to the clinical course. MATERIAL AND METHODS: 60 patients (41 females and 19 males) with definite MS according to McDonald's criteria were studied. The age of patients ranged from 29 to 62 years and disease duration ranged from 11 to 40 years. The MS group comprised 20 patients with secondary progressive MS (SPMS), 20 patients with primary progressive MS (PPMS) and 20 patients with benign form of MS (BMS). Spinal cord MRI was performed in conventional T1 and T2-weighted sequences. RESULTS: Demyelinating lesions were found in 62% of patients (50% of patients with BMS, 60% with PPMS and 75% with SPMS). 42 intrinsic focal lesions were identified in 18 patients and diffuse lesions of spinal cord were noted in 19 patients. Focal lesions were seen in patients with BMS, whereas SPMS patients had diffuse cervical cord abnormalities, and PPMS patients exhibited both forms of changes. 60% of intrinsic focal lesions were located at C3-C5 levels. Medium-sized lesions prevailed in BMS form; in PPMS form small and medium-size lesions, and in SPMS form large lesions (>10 mm) were more frequent. The spinal cord was atrophic in 8% of patients (10% of patients with PPMS and 15% with SPMS). In BMS no atrophy of the cervical cord was observed. We did not find focal demyelinating lesions in the cervical segment of patients with spinal cord atrophy. CONCLUSIONS: Presence and character of demyelinating lesions in cervical cord ten years after onset of MS is significantly related to the clinical form of the disease. The mid-cervical region of the spinal cord appeared to be the commonest location of the focal lesions. Cervical cord atrophy was more frequent in patients with PPMS and SPMS, but it was not accompanied with intrinsic focal cord lesions.     

Outcome prediction in severe head injury: analyses of clinical prognostic factors.

Retrospective analysis of 272 patients with severe head injury was performed. Patient age, Glasgow Coma Scale (GCS) score, pupillary abnormalities, impaired oculocephalic response, presence of subarachnoid haemorrhage, and multiplicity of parenchymal lesions on computerised tomography (CT) were examined. The CT findings were divided into 2 groups, diffuse brain injury (DBI) and mass lesion, according to the classification of the Traumatic Coma Data Bank. The DBI, basically, has no high or mixed density lesion more than 25 ml on CT, and was classified into 4 subgroups: DBI I includes injuries where there is no visible pathology; DBI II includes all injuries in which the cisterns are present with a midline shift of less than 5 mm; DBI III includes injuries with swelling where the cisterns are compressed or absent and the midline shift is less than 5 mm; DBI IV includes injuries with a midline shift of more than 5 mm. The mass lesions were categorised into 3 subgroups: epidural haematoma; acute subdural haematoma; and intracerebral haematoma. Outcomes were determined at 6 months following trauma using the Glasgow Outcome Scale. All DBI I patients recovered well. In the DBI II group, age, GCS score and detection of multiple parenchymal lesions on CT were significantly correlated with outcome. For the DBI III and IV groups, the only significant prognostic factor was the GCS score. In patients with a mass lesion, the GCS score was the only significant prognostic factor in the epidural haematoma group, but the GCS score and the presence of subarachnoid haemorrhage were predictive factors in the acute subdural haematoma group. Outcomes were unfavourable in the majority of patients with intracerebral haematoma. GCS score could predict outcome in all groups. The confidence of the outcome prediction ranged from 75.8 to 92.1%, depending on logistic regression analysis.     

Multiple sclerosis: Remyelination of nascent lesions: Remyelination of nascent lesions

The relationship between plaque pathology and disease duration was examined in 15 patients with multiple sclerosis who died early in the course of their illness. Myelin-stained sections revealed that most plaques examined in patients who died during the first month of their illness showed evidence of ongoing myelin destruction accompanied by a loss of oligodendrocytes. Plaques containing large numbers of oligodendrocytes were not observed in these patients, but were relatively common in patients who died more than 1 month after clinical onset. Remyelination affecting more than 10% of the plaque area was observed in 3 of 82 plaques in 5 patients who died within 10 weeks of clinical onset, in 38 of 105 plaques in 5 patients who died 3 to 10 months after clinical onset, and in 19 of 92 plaques in 5 patients who died 18 months or longer after clinical onset. The study provides new evidence that both oligodendrocytes and myelin are destroyed in new lesions, that this activity ceases completely in many lesions within a few weeks, and that remyelination frequently ensues following repopulation of the plaque by oligodendrocytes. The findings suggest that new lesions normally remyelinate unless interrupted by recurrent activity and that remyelinated shadow plaques are the outcome of a single previous episode of focal demyelination.     

A longitudinal study of T1 hypointense lesions in relapsing MS: MSCRG trial of interferon beta-1a. Multiple Sclerosis Collaborative Research Group

BACKGROUND: T1 hypointense lesions (T1 black holes) are focal areas of relatively severe CNS tissue damage detected by MRI in patients with MS. OBJECTIVE: To determine the natural history of T1 hypointense lesions in relapsing MS and the utility of T1 hypointense lesions as outcome measures in MS clinical trials. METHODS: MR studies were from the Multiple Sclerosis Collaborative Research Group trial. Longitudinal results are reported in 80 placebo- and 80 interferon beta-1a (IFNbeta-1a)-treated patients with mild to moderate disability relapsing-remitting MS. RESULTS: There was a small but significant correlation between T1 hypointense lesion volume and disability at baseline and on trial (r = 0.22, r = 0.28). In placebo patients there was a 29.2% increase in the mean volume of T1 hypointense lesions (median 124.5 mm3) over 2 years (p < 0.001 for change from baseline), as compared to an 11.8% increase (median 40 mm3) in the IFNbeta-1a-treated patients (change from baseline not significant). These treatment group comparisons did not quite reach significance. The most significant contributor to change in T1 hypointense lesions was the baseline number of enhancing lesions (model r2 = 0.554). Placebo patients with more active disease, defined by enhancing lesions at baseline, were the only group to show a significant increase in T1 hypointense lesion volume from baseline. CONCLUSION: The development of T1 hypointense lesions is strongly influenced by prior inflammatory disease activity, as indicated by enhancing lesions. These results suggest that treatment with once weekly IM IFNbeta-1a (30 mcg) slows the 2-year accumulation of these lesions in the brain.     

The diagnostic value of erythrocyte sedimentation rate in management of brain tumors

Abstract

Objective: Erythrocyte sedimentation rate (ESR) is considered as an indicator of inflammatory processes, and it has a prognostic value in the management of specific neoplastic diseases. It also responds to surgical intervention. There is very little data about the alteration of ESR in patients with brain tumors and information on its course after intracranial tumor surgery is completely lacking.

Methods: ESR was measured for 10 days in 46 patients (19 women and 27 men; mean age: 49.7 years; range: 13–70 years) who underwent elective craniotomy for tumor microsurgery (70–425 minutes with a mean of 230 minutes) under general anaesthesia. Blood samples were taken on the day before surgery and on each consecutive day after surgery for 10 days. The standard method of measuring ESR was based on the technique first described by Westergren.

Results: The mean ESR level on the day before surgery was 8.26 ± 7.27 mm/h after 1 hour and 14.80 ± 10.36 mm/h after 2 hours. After tumor surgery, ESR increased stepwise. The mean peak value of 22.89 ± 13.41 mm/h after the first hour was reached on the third post-operative day. Whereas mean values varied over time, ESR remained increased and did not decline to normal values until the tenth post-operative day. The mean ESR peak value was higher in patients having undergone surgery for intra-axial lesions (31.36 ± 30.43 mm/h on the post-operative day 6) as compared to patients with extra-axial lesions (21.31 ± 12.20 mm/h on the post-operative day 3).

Conclusion: ESR is not relevantly increased in patients harboring brain tumors. Because it remains elevated until the tenth post-operative day after uneventful craniotomy and generally responds more slowly than other indicators like C-reactive protein, it is also not suitable for the detection of post-operative infective complications.     

Relationship between the extent of T2 lesions and the onset of secondary progression in multiple sclerosis

Patients with relapsing–remitting multiple sclerosis (MS) are at risk of converting to a secondary progressive disease course. To assess the relationship between brain magnetic resonance imaging (MRI) findings and onset of secondary progression, we reanalysed the initial brain MRI scans of 90 relapsing–remitting MS patients, who were clinically followed up for at least 10 years (median 14 years) after their scan, for the number and volume of T2 lesions, and for two measures of brain atrophy (bicaudate ratio and third ventricle width). The relationship to development of secondary progression was studied with Cox regression models and Kaplan–Meier survival analyses. At the end of follow-up, 36 patients had become progressive. The presence of more than 10 T2 lesions more than doubled the risk of becoming secondary progressive (hazards ratio 2.36; 95% CI 1.19–4.66). When at least one of the 10 lesions was confluent the risk increased to 3.51 (1.64–7.50). The hazards ratio for an estimated T2 lesion load of more than 800 mm³ was 2.11 (1.07–4.16). Linear brain atrophy measures were not predictive. Our data show a relationship between the extent of brain T2 lesions and the onset of secondary progression in MS.