Parkinsonism in corticobasal syndrome may not be primarily due to presynaptic dopaminergic deficiency
- Author:
Ji Young Yun
;
Jong-Min Kim
;
Han-Joon Kim
;
Jee-Young Lee
;
Hee Jin Kim
;
Ji Seon Kim
;
Yu Kyeong Kim
;
Sang Eun Kim
;
Tae-Beom Ahn
;
Beom S Jeon
- Publication Type:Review
- MeSH:
Parkinsonian Disorders
- From:Neurology Asia
2015;20(1):23-27
- CountryMalaysia
- Language:English
-
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.
- Full text:P020150623393870402887.pdf
