Conrad Julian, Habs Maximilian, Ruehl Ria M, Bögle Rainer, Ertl Matthias, Kirsch Valerie, Eren Ozan E, Becker-Bense Sandra, Stephan Thomas, Wollenweber Frank A, Duering Marco, Zu Eulenburg Peter, Dieterich Marianne
Department of Neurology, University Hospital, LMU Munich, Germany; German Centre for Vertigo and Balance Disorders (DSGZ), University Hospital, LMU Munich, Germany.
Department of Neurology, University Hospital, LMU Munich, Germany; German Centre for Vertigo and Balance Disorders (DSGZ), University Hospital, LMU Munich, Germany.
Neuroimage Clin. 2022;33:102953. doi: 10.1016/j.nicl.2022.102953. Epub 2022 Feb 4.
The integration of somatosensory, ocular motor and vestibular signals is necessary for self-location in space and goal-directed action. We aimed to detect remote changes in the cerebral cortex after thalamic infarcts to reveal the thalamo-cortical connections necessary for multisensory processing and ocular motor control.
Thirteen patients with unilateral ischemic thalamic infarcts presenting with vestibular, somatosensory, and ocular motor symptoms were examined longitudinally in the acute phase and after six months. Voxel- and surface-based morphometry were used to detect changes in vestibular and multisensory cortical areas and known hubs of central ocular motor processing. The results were compared with functional connectivity data in 50 healthy volunteers.
Patients with paramedian infarcts showed impaired saccades and vestibular perception, i.e., tilts of the subjective visual vertical (SVV). The most common complaint in these patients was double vision or vertigo / dizziness. Posterolateral thalamic infarcts led to tilts of the SVV and somatosensory deficits without vertigo. Tilts of the SVV were higher in paramedian compared to posterolateral infarcts (median 11.2° vs 3.8°). Vestibular and ocular motor symptoms recovered within six months. Somatosensory deficits persisted. Structural longitudinal imaging showed significant volume reduction in subcortical structures connected to the infarcted thalamic nuclei (vestibular nuclei region, dentate nucleus region, trigeminal root entry zone, medial lemniscus, superior colliculi). Volume loss was evident in connections to the frontal, parietal and cingulate lobes. Changes were larger in the ipsilesional hemisphere but were also detected in homotopical regions contralesionally. The white matter volume reduction led to deformation of the cortical projection zones of the infarcted nuclei.
White matter volume loss after thalamic infarcts reflects sensory input from the brainstem as well the cortical projections of the main affected nuclei for sensory and ocular motor processing. Changes in the cortical geometry seem not to reflect gray matter atrophy but rather reshaping of the cortical surface due to the underlying white matter atrophy.
体感、眼球运动和前庭信号的整合对于空间自我定位和目标导向行动是必要的。我们旨在检测丘脑梗死后大脑皮层的远程变化，以揭示多感官处理和眼球运动控制所需的丘脑 - 皮质连接。
对13例出现前庭、体感和眼球运动症状的单侧缺血性丘脑梗死患者在急性期和6个月后进行纵向检查。采用基于体素和表面的形态测量法来检测前庭和多感官皮质区域以及中央眼球运动处理的已知枢纽的变化。将结果与50名健康志愿者的功能连接数据进行比较。
旁正中梗死患者表现出扫视和前庭感知受损，即主观垂直视觉（SVV）倾斜。这些患者最常见的主诉是复视或眩晕/头晕。丘脑后外侧梗死导致SVV倾斜和体感缺陷但无眩晕。与后外侧梗死相比，旁正中梗死的SVV倾斜度更高（中位数11.2°对3.8°）。前庭和眼球运动症状在6个月内恢复。体感缺陷持续存在。结构纵向成像显示与梗死丘脑核相连的皮质下结构（前庭核区域﹑齿状核区域﹑三叉神经根进入区﹑内侧丘系﹑上丘）有显著体积减小。与额叶﹑顶叶和扣带回的连接中体积损失明显。同侧半球的变化更大，但在对侧的同位区域也可检测到。白质体积减小导致梗死核的皮质投射区变形。
丘脑梗死后白质体积损失反映了来自脑干的感觉输入以及主要受影响核团在感觉和眼球运动处理方面的皮质投射。皮质几何形状的变化似乎并非反映灰质萎缩，而是由于潜在的白质萎缩导致的皮质表面重塑。
