Marx Juergen J, Iannetti Gian D, Thömke Frank, Fitzek Sabine, Galeotti Francesca, Truini Andrea, Stoeter Peter, Dieterich Marianne, Hopf Hanns C, Cruccu Giorgio
Department of Neurology, Johannes Gutenberg-University Mainz, Langenbeckstr 1, Mainz, Germany.
Neuroimage. 2008 Feb 15;39(4):1625-32. doi: 10.1016/j.neuroimage.2007.10.006. Epub 2007 Oct 16.
The topodiagnostic implications of hemiataxia following lesions of the human brainstem are only incompletely understood. We performed a voxel-based statistical analysis of lesions documented on standardised MRI in 49 prospectively recruited patients with acute hemiataxia due to isolated unilateral brainstem infarction. For statistical analysis individual MRI lesions were normalised and imported in a three-dimensional voxel-based anatomical model of the human brainstem. Statistical analysis revealed hemiataxia to be associated with lesions of three distinct brainstem areas. The strongest correlation referred to ipsilateral rostral and dorsolateral medullary infarcts affecting the inferior cerebellar peduncle, and the dorsal and ventral spinocerebellar tracts. Secondly, lesions of the ventral pontine base resulted in contralateral limb ataxia, especially when ataxia was accompanied by motor hemiparesis. In patients with bilateral hemiataxia, lesions were located in a paramedian region between the upper pons and lower midbrain, involving the decussation of dentato-rubro-thalamic tracts. We conclude that ataxia following brainstem infarction may reflect three different pathophysiological mechanisms. (1) Ipsilateral hemiataxia following dorsolateral medullary infarctions results from a lesion of the dorsal spinocerebellar tract and the inferior cerebellar peduncle conveying afferent information from the ipsilateral arm and leg. (2) Pontine lesions cause contralateral and not bilateral ataxia presumably due to major damage to the descending corticopontine projections and pontine base nuclei, while already crossed pontocerebellar fibres are not completely interrupted. (3) Finally, bilateral ataxia probably reflects a lesion of cerebellar outflow on a central, rostral pontomesencephalic level.
人脑干病变后偏侧共济失调的拓扑诊断意义目前仅得到部分理解。我们对49例因孤立性单侧脑干梗死导致急性偏侧共济失调的前瞻性招募患者的标准化MRI记录病变进行了基于体素的统计分析。为了进行统计分析，将个体MRI病变进行归一化处理，并导入人脑干的三维基于体素的解剖模型中。统计分析显示，偏侧共济失调与脑干三个不同区域的病变相关。最强的相关性是指同侧延髓嘴侧和背外侧梗死，影响小脑下脚以及背侧和腹侧脊髓小脑束。其次，脑桥基底部的病变导致对侧肢体共济失调，尤其是当共济失调伴有运动性偏瘫时。在双侧偏侧共济失调患者中，病变位于脑桥上段和中脑下段之间的旁正中区域，累及齿状核 - 红核 - 丘脑束的交叉。我们得出结论，脑干梗死后的共济失调可能反映三种不同的病理生理机制。（1）延髓背外侧梗死导致的同侧偏侧共济失调是由于背侧脊髓小脑束和小脑下脚病变，这些结构传递来自同侧上肢和下肢的传入信息。（2）脑桥病变导致对侧而非双侧共济失调，可能是由于皮质脑桥投射和脑桥基底部核团受到严重损害，而已经交叉的脑桥小脑纤维并未完全中断。（3）最后，双侧共济失调可能反映了中脑桥脑中央嘴侧水平的小脑传出通路病变。
