Spinal cord infarction is a relatively rare condition, with the most common type being anterior spinal artery syndrome, presenting with acute bilateral weakness/paraparesis, impaired spinothalamic sensation and usually preserved deep sensation with or without respiratory dysfunction [1]. Common aetiologies include atherosclerosis, aortic aneurysm, surgery or dissection, and hypercoagulability states. Hence, spinal cord infarction arising from an atherosclerotic pathogenesis has a propensity to occur in elderly and vasculopath patients [1–3]. The classical MRI features of spinal cord infarction are central T2 hyperintensity without significant cord expansion or contrast enhancement. Although usually technically difficult to image, if possible, diffusion-weighted imaging demonstrates corresponding abnormal restricted diffusion, as in acute cerebral infarction [2]. These MRI changes were evident in our patient with H-shaped T2 hyperintensity demonstrated on the axial image (Fig. 1A of Images in Neuroscience: Question) which was confined to the grey matter of the cord, consistent with the known particular sensitivity of the neuronal perikaryon to hypoxia. The striking diffuse apparent diffusion coefficient hypointensity along the cord which was congruent with increased signal intensity demonstrated on diffusion weighted imaging, is also consistent with abnormal restricted diffusion indicative of an acute ischaemic process (Fig. 1B, Fig. 1C from Images in Neuroscience: Question). The CT aortogram (Fig. 1A) demonstrates severe calcific atherosclerosis throughout the aorta and its major abdominal branches, which is a common underlying cause of cord infarction in this age group [4]. Our patient had clinical and radiological findings consistent with diffuse cord infarction which is an unfortunate condition with little prospect of recovery, as occurred in this patient [1,5].