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书写痉挛患者的脑激活模式:一项功能磁共振成像研究。

Cerebral activation patterns in patients with writer's cramp: a functional magnetic resonance imaging study.

作者信息

Preibisch C, Berg D, Hofmann E, Solymosi L, Naumann M

机构信息

Bayerische Julius-Maximilians-Universität, Würzburg, Germany.

出版信息

J Neurol. 2001 Jan;248(1):10-7. doi: 10.1007/s004150170263.

DOI:10.1007/s004150170263
PMID:11266013
Abstract

Functional MRI (fMRI), visualizing changes in cerebral blood oxygenation, has to date not been performed either in patients with writer's cramp or in healthy subjects during writing. We compared the cerebral and cerebellar activation pattern of 12 patients with writer's cramp during writing with a group of 10 healthy subjects performing the same tasks over 30-s periods of rest or writing. Sixty echo planar imaging multislice datasets were analysed using SPM96 software. Data were analysed for each subject individually and groupwise for patients vs. controls. Healthy subjects showed a significant activation of the ipsilateral dentate nucleus, contralateral cerebellar hemisphere, contralateral primary sensorimotor cortex, and contralateral precentral gyrus during writing. Patients with writer's cramp showed significantly greater activation of the ipsilateral cerebellar hemisphere than controls. Also the activation in the primary sensorimotor cortex extended further caudally and anteriorly towards the premotor association area. Activation was observed in the thalamus during writing only among the patients. Our results indicate an increased basal ganglia output via the thalamus to the motor and premotor cortical areas in dystonia patients and support the notion of disinhibition of the motor cortex leading to cocontractions and dystonic postures.

摘要

功能磁共振成像(fMRI)可显示脑血氧合的变化,迄今为止,尚未对书写痉挛患者或健康受试者在书写过程中进行过此项检查。我们比较了12例书写痉挛患者在书写时的大脑和小脑激活模式,以及10名健康受试者在30秒的休息或书写期间执行相同任务时的激活模式。使用SPM96软件分析了60个回波平面成像多层数据集。对每个受试者的数据进行单独分析,并对患者与对照组进行组间分析。健康受试者在书写过程中,同侧齿状核、对侧小脑半球、对侧初级感觉运动皮层和对侧中央前回均有明显激活。书写痉挛患者同侧小脑半球的激活明显高于对照组。此外,初级感觉运动皮层的激活向尾侧和前方进一步延伸至运动前联合区。仅在患者书写过程中观察到丘脑有激活。我们的结果表明,肌张力障碍患者通过丘脑向运动和运动前皮层区域的基底神经节输出增加,并支持运动皮层去抑制导致共同收缩和肌张力障碍姿势的观点。

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