Parkinsonian syndromes associated with basal ganglia pathology have very rarely been reported in patients with end-stage renal failure. The nature and pathophysiology of the basal ganglia lesion responsible for parkinsonism were unknown. A 48-year-old man who had advanced renal failure developed disturbance of balance and gait and decreased spontaneity. Brain magnetic resonance (MR) imaging disclosed bilateral basal ganglia lesions. By the finding of diffusion-weighted image, the apparent diffusion coefficient map, MR angiography, and SPECT, we suggest that the basal ganglia lesions may be the result of vasogenic edema attributable to focal hyperemia secondary to abnormal dilatation of small vessels.
Movement disorders seen in uremic patients typically consist of asterixis and myoclonus, which may be related to cortical dysfunction, namely uremic encephalopathy [1]. Akinetic, parkinsonian syndromes associated with basal ganglia pathology have very rarely been reported in patients with end-stage renal failure [2] and [3]. However, the nature and pathophysiology of the basal ganglia lesion responsible for parkinsonism in uremic patients are unknown. Here, we describe a patient with end-stage renal failure who showed parkinsonian features, and we present the results of imaging studies that provide a clue to understanding the underlying pathogenesis.