Human Motor Control Section, NINDS, NIH, Bethesda, MD, United States; Institut du Cerveau et de la Moelle (ICM-CRICM), Centre de Neuroimagerie de Recherche (UPMC/INSERM, UMR_975, CNRS 7225), Hôpital de la Pitié Salpétrière, Paris, France.
Human Motor Control Section, NINDS, NIH, Bethesda, MD, United States.
Neuroimage Clin. 2017 Oct 13;17:90-97. doi: 10.1016/j.nicl.2017.10.011. eCollection 2018.
To investigate GABA-ergic receptor density and associated brain functional and grey matter changes in focal hand dystonia (FHD).
18 patients with FHD of the right hand and 18 age and gender matched healthy volunteers (HV) participated in this study. We measured the density of GABA-A receptors using [C] Flumazenil and perfusion using [O] HO. Anatomical images were also used to measure grey matter volume with voxel-based morphometry (VBM).
In FHD patients compared to HV, the vermis VI of the right cerebellum and the left sensorimotor cortex had a decrease of Flumazenil binding potential (FMZ-BP), whereas the striatum and the lateral cerebellum did not show significant change. Bilateral inferior prefrontal cortex had increased FMZ-BP and an increase of perfusion, which correlated negatively with disease duration. Only the left sensorimotor cortex showed a decrease of grey matter volume.
Impairments of GABAergic neurotransmission in the cerebellum and the sensorimotor cortical areas could explain different aspects of loss of inhibitory control in FHD, the former being involved in maladaptive plasticity, the latter in surround inhibition. Reorganization of the inferior prefrontal cortices, part of the associative network, might be compensatory for the loss of inhibitory control in sensorimotor circuits. These findings suggest that cerebellar and cerebral GABAergic abnormalities could play a role in the functional imbalance of striato-cerebello-cortical loops in dystonia.
研究局灶性手部肌张力障碍（FHD）中 GABA 能受体密度及相关脑功能和灰质变化。
18 例右侧 FHD 患者和 18 名年龄和性别匹配的健康志愿者（HV）参与了这项研究。我们使用 [C]氟马西尼和 [O] HO 测量 GABA-A 受体的密度。还使用解剖图像通过体素形态计量学（VBM）测量灰质体积。
与 HV 相比，FHD 患者右侧小脑蚓部 VI 区和左侧感觉运动皮层的氟马西尼结合潜能（FMZ-BP）降低，而纹状体和外侧小脑没有显示出明显的变化。双侧下前额叶皮层的 FMZ-BP 增加，灌注增加，与疾病持续时间呈负相关。只有左侧感觉运动皮层的灰质体积减少。
小脑和感觉运动皮层区域 GABA 能神经传递的损伤可以解释 FHD 中抑制控制丧失的不同方面，前者涉及适应性可塑性，后者涉及周围抑制。下前额叶皮层的重组，作为联想网络的一部分，可能是对感觉运动回路中抑制控制丧失的代偿。这些发现表明，小脑和大脑 GABA 能异常可能在肌张力障碍的纹状体-小脑-皮质环路的功能失衡中起作用。
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