A Topodiagnostic Investigation on Lesions Causing Body Lateropulsion in the Absence of Clinical Signs of Vestibular Dysfunction

Abstract

Background: Body lateropulsion is often seen in patients with lateral medullary infarctions (LMI) and may occur with or without vestibular nucleus involvement. Whether body lateropulsion in LMI sparing the vestibular nucleus is due to a lesion of the lateral vestibulospinal tract (LVST) or the dorsal spinocerebellar tract (DSCT) is still unclear. Patients and Methods: We retrospectively analyzed the clinical files of a group of 258 consecutive patients presenting with clinical signs and symptoms of acute ischemia in the vertebrobasilar territory for body lateropulsion in the absence of clinical signs of vestibular dysfunction. All patients had magnetic resonance imaging (MRI) with biplane T2- and echo planar diffusion-weighted imaging (EPI-DWI) with slice orientation parallel and perpendicular to slices of the stereotactic anatomical atlas of Schaltenbrand and Wahren. Individual slices were normalized and projected into the corresponding slices of the anatomical atlas. Results: We only identified 10 patients, all with unilateral LMI, who had ipsilesional body lateropulsion as the predominant clinical sign. A comparison of the lesion sites in these patients with the lesion sites in a group of 14 patients with brainstem infarctions at the same level but without body lateropulsion revealed an area midway between the end of the DSCT and the beginning of the lower cerebellar peduncle as the crucial area for the occurrence body lateropulsion. Lesion sites of patients with body lateropulsion without limb ataxia were located more dorso-medial than those of patients with limb ataxia, that were more ventro-lateral. Conclusions: We attributed body lateropulsion without limb ataxia to an impairment of vestibulo-spinal postural control, as the dorso-medial sites of the responsible lesions involved the region of the LVST. Body lateropulsion with limb ataxia more likely reflects impaired or absent proprioceptive information, since lesions in these patients involved the DSCT.