Decreased dopamine transporter and receptor ligand binding in Parkinsonism with diabetic uremic syndrome.

Here, we describe the case of a 47-year-old man with bilateral striatal lesions with diabetic uremia. Following 4 years of hemodialysis, the patient experienced sudden onset of rigidity, bradykinesia, gait disorder, and postural instability. Symptoms were remediated 2 months later, and were no longer responsive to levodopa approximately 1 year after the onset. Brain magnetic resonance imaging (MRI) during the acute phase showed T 2-weighted high signal edematous lesions in the bilateral striatum, subsequently developing into vacuolated lesions. A positron emission tomography (PET) scan using ((11)C)-labeled 2-carbomethoxy-3-(4-fluorophenyl) tropane [((11)C) CFT] and ((11)C)-labeled raclopride [((11)C) RAC] revealed significant decreases bilaterally in pre- and postsynaptic functions of the dopaminergic neurons. When we experience a case with bilateral putaminal destruction resulting in Parkinsonism, examination of the function of doperminergic neurons and dopamine receptors using molecular imaging is useful to predict levodopa response and prognosis.