Prefrontal thickening in PD with levodopa-induced dyskinesias: New evidence from cortical thickness measurement
Prefrontal thickening in PD with levodopa-induced dyskinesias: New evidence from cortical thickness measurement
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DOI：
10.1016/j.parkreldis.2012.06.003
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发表时间：
2013-01-01
影响因子：
4.1
通讯作者：
Quattrone, Aldo
中科院分区：
文献类型：
--
作者：
Cerasa, Antonio;Morelli, Maurizio;Quattrone, Aldo
目的：帕金森病（PD）患者左旋多巴诱导的运动障碍（LID）的神经退行性过程仍然是一个有争议的问题。最近，我们证明，这种临床表型与前额叶皮质灰质异常增加相比，PD没有LID。这一证据是通过使用基于体素的形态测量（VBM）发现的。然而，VBM可能不是评估皮质病理的最合适的程序，因为其标准化/平滑步骤降低了解剖学表征脑沟和脑回的能力。本研究的目的是通过使用先进的神经影像学方法更好地描述LID相关的解剖学异常，该方法提供了对皮质形态的直接和客观测量。皮质外套膜的表面研究通过使用Freesurfer在两组治疗的患有LID（no 29）和没有LID（no 30）的PD患者中进行皮质厚度（cortex thickness），结果：皮质厚度分析显示，与无LID的PD患者相比，有LID的PD患者右额下沟的厚度明显增加。目前的研究证实了我们以前关于前额叶皮层在LID病理生理学中的作用的形态学发现，并更精确地描绘了解剖学异常。表征这种临床表型。(C)2012爱思唯尔有限公司保留所有权利。
Purpose: Neurodegenerative processes in Parkinson's disease (PD) patients with levodopa-induced dyskinesias (LID) are still a matter of debate. Recently, we demonstrated that this clinical phenotype is associated with an abnormal gray matter increase in the prefrontal cortex when compared to PD without LID. This evidence was found by using voxel-based morphometry (VBM). However, VBM may not be the most appropriate procedure to assess cortical pathology, since its normalization/smoothing steps reduce the ability to anatomically characterize sulci and gyri. The aim of this study is to better delineate the LID-related anatomical abnormalities by using an advanced neuroimaging method that provides a direct and objective measure of the cortical morphology.Methods: Surface-based investigation of cortical mantle (cortical thickness) was carried out by using Freesurfer in two groups of treated PD patients with LID (no 29) and without LID (no 30), and one group of age- and sex-matched controls (no 24).Results: Cortical thickness analysis revealed a pronounced increase of thickness in the right inferior frontal sulcus in PD patients with LID with respect to PD patients without LID.Discussion: The current study confirms our previous morphological findings on the role of the prefrontal cortex in the pathophysiology of LID and delineates with more precision the anatomical abnormalities characterizing this clinical phenotype. (C) 2012 Elsevier Ltd. All rights reserved.