Parkinsonism in corticobasal syndrome may not be primarily due to presynaptic dopaminergic deficiency

Abstract

The clinical features of corticobasal degeneration (CBD) are quite asymmetric. The severity of clinical symptoms and dopamine transporter (DAT) bindings were less correlated compared to other parkinsonisms, suggesting that presynaptic nigrostriatal dopaminergic dysfunction may not explain extrapyramidal manifestations in CBD. Therefore we wanted to reexamine asymmetry and severity between DAT imaging and clinical findings. We studied patients meeting the diagnostic criteria for CBD based on clinical features. We collected their clinical information and imaging retrospectively. Seven patients were enrolled and all had asymmetric rigidity, bradykinesia and unilateral limb dystonia. These symptoms did not improve with levodopa. All patients showed symptoms bilaterally in the last visit, but asymmetry of clinical symptoms was remarkable at the time of DAT imaging. The DAT bindings were decreased in six subjects. However, one patient showed normal DAT binding. Four patients had a more evident DAT reduction on the side contralateral to the more clinically affected side, however, two patients had a more prominent reduction on the ipsilateral side. The symptoms that we regard as parkinsonian features in CBD are not only explained by presynaptic dopaminergic dysfunction. Our findings suggest that postsynaptic dopaminergic or nondopaminergic systems may play a major role in parkinsonian symptoms in corticobasal syndrome.