Case report demonstrates ipsilateral hemiparesis following acute left hemispheric stroke in an older adult, suggesting unilateral non-decussation of the corticospinal tract.
Most corticospinal tract (CST) fibres decussate at the medullary pyramids, such that supratentorial infarction typically causes contralateral weakness. Markedly asymmetric or absent CST decussation is uncommon and may create unexpected lesion-deficit laterality. We report a patient with an acute left hemispheric infarct and left-sided hemiparesis in whom diffusion tensor imaging (DTI) tractography demonstrated a markedly asymmetric CST configuration consistent with unilateral non-decussation of the left CST. A 65-year-old right-handed man with a 15-year history of hypertension presented 2.5 h after sudden-onset dysarthria and left-sided limb weakness (National Institutes of Health Stroke Scale [NIHSS] score 4). Intravenous tenecteplase (0.25 mg/kg) was administered within 4.5 h of symptom onset on the basis of the clinical diagnosis of acute ischaemic stroke and after exclusion of intracranial haemorrhage on acute neuroimaging. Subsequent MRI showed an acute left periventricular infarct. Because the acute infarct and motor deficit were ipsilateral, DTI tractography was performed after thrombolysis for anatomical clarification. The right CST showed the expected crossing pattern at the medullary pyramids, whereas no identifiable crossing fibres were demonstrated for the left CST, which descended predominantly ipsilaterally; the infarct lay along the reconstructed left CST. The NIHSS score decreased to 2 at discharge (modified Rankin Scale [mRS] score 2). A markedly asymmetric CST configuration consistent with unilateral non-decussation may provide an anatomical explanation for ipsilateral hemiparesis in selected patients with hemispheric stroke. When clinical and imaging laterality are discordant, DTI tractography may be useful for subsequent anatomical clarification but should not delay reperfusion therapy. Tractography findings should be interpreted cautiously and in the context of alternative mechanisms, including prior stroke-related motor reorganisation.
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