Koenigkam-Santos M, Santos A C, Borduqui T, Versiani B R, Hallak J E C, Crippa J A S, Castro M
Division of Radiology, School of Medicine of Ribeirao Preto-University of Sao Paulo, Ribeirao Preto, SP, Brazil.
AJNR Am J Neuroradiol. 2008 Oct;29(9):1799-804. doi: 10.3174/ajnr.A1202. Epub 2008 Sep 3.
There are 2 main hypotheses concerning the cause of mirror movements (MM) in Kallmann syndrome (KS): abnormal development of the primary motor system, involving the ipsilateral corticospinal tract; and lack of contralateral motor cortex inhibitory mechanisms, mainly through the corpus callosum. The purpose of our study was to determine white and gray matter volume changes in a KS population by using optimized voxel-based morphometry (VBM) and to investigate the relationship between the abnormalities and the presence of MM, addressing the 2 mentioned hypotheses.
T1-weighted volumetric images from 21 patients with KS and 16 matched control subjects were analyzed with optimized VBM. Images were segmented and spatially normalized, and these deformation parameters were then applied to the original images before the second segmentation. Patients were divided into groups with and without MM, and a t test statistic was then applied on a voxel-by-voxel basis between the groups and controls to evaluate significant differences.
When considering our hypothesis a priori, we found that 2 areas of increased gray matter volume, in the left primary motor and sensorimotor cortex, were demonstrated only in patients with MM, when compared with healthy controls. Regarding white matter alterations, no areas of altered volume involving the corpus callosum or the projection of the corticospinal tract were demonstrated.
The VBM study did not show significant white matter changes in patients with KS but showed gray matter alterations in keeping with a hypertrophic response to a deficient pyramidal decussation in patients with MM. In addition, gray matter alterations were observed in patients without MM, which can represent more complex mechanisms determining the presence or absence of this symptom.
关于卡尔曼综合征(KS)中镜像运动(MM)的病因,主要有两种假说:一是主要运动系统发育异常,累及同侧皮质脊髓束;二是缺乏对侧运动皮质抑制机制,主要通过胼胝体。我们研究的目的是通过使用优化的基于体素的形态测量法(VBM)来确定KS患者群体中的白质和灰质体积变化,并研究这些异常与MM存在之间的关系,以探讨上述两种假说。
对21例KS患者和16例匹配的对照受试者的T1加权容积图像进行优化VBM分析。对图像进行分割和空间归一化,然后将这些变形参数应用于原始图像,再进行第二次分割。将患者分为有MM组和无MM组,然后在组与对照组之间逐体素应用t检验统计量,以评估显著差异。
在预先考虑我们的假说时,我们发现与健康对照相比,仅在有MM的患者中,左侧初级运动和感觉运动皮质的灰质体积增加了两个区域。关于白质改变,未发现涉及胼胝体或皮质脊髓束投射的体积改变区域。
VBM研究未显示KS患者有显著的白质变化,但显示灰质改变与MM患者锥体交叉不足的肥厚反应一致。此外,在无MM的患者中也观察到灰质改变,这可能代表了决定该症状有无的更复杂机制。