LAUSR

Our case is an exceptional illustration of the proposed flexion-induced pathophysiology of Hirayama disease. Evidence, privileging a mechanical pathophysiology, is growing and diagnostic inclusion criteria are involving MRI-confirmed evidence of the mechanical pathophysiology. The forward displacement of the posterior wall during neck flexion is considered to be the hallmark and primary pathophysiologic mechanism of this disease [1]. In our case, the subacute onset and short disease course with contrasting extensiveness of the myelopathy could be explained by a more important contribution of secondary ischemic myelopathy with subsequent extensive T2-hyperintensity and clinical pyramidal signs. We support that the technical diagnostic working-out of Hirayama disease primarily includes dynamic MRI imaging of the cervical spine next to MRI imaging in neutral position, as suggested by Huang and Chen [2].