Neuropediatrics 2011; 42(06): 245-248
DOI: 10.1055/s-0031-1295406
Short Communication
© Georg Thieme Verlag KG Stuttgart · New York

Alteration of Ictal and Interictal Perfusion in Patients with Paroxysmal Kinesigenic Dyskinesia

Y.-D Kim
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
J.-S Kim
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
Y.-A Chung
2  Department of Nuclear Medicine, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
I.-U Song
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
Y.-S Oh
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
S.-W Chung
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
H.-T Kim
3  Department of Neurology, Hanyang University School of Medicine, Seoul, South Korea
,
Y.-I Kim
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
,
K.-S Lee
1  Department of Neurology, College of Medicine, The Catholic University of Korea, Seoul, South Korea
› Author Affiliations
Further Information

Publication History

received 27 July 2011

accepted 24 October 2011

Publication Date:
14 November 2011 (online)

Abstract

Although previous cerebral blood flow studies have suggested that the basal ganglia or thalamus are involved in the pathogenesis of paroxysmal kinesigenic dyskinesia (PKD), the precise anatomic substrate or pathophysiological networks associated with PKD remain unclear. Here, ictal and interictal single photon emission computed tomography (SPECT) in 2 patients with idiopathic PKD compared to 6 age-matched normal controls and the perfusion findings of subtraction ictal SPECT co-registered to MRI (SISCOM) in 1 patient are reported. The interictal and ictal perfusion changes were different in each of the patients and there were no consistent anatomic substrates observed. 2 patients had significant perfusion changes in the left frontal/temporal cortices compared to controls, whereas the others showed an increased uptake of 99mTc-ethyl cysteinate dimer (ECD) in the left occipital area on subtraction SPECT imaging. The results of this study suggest that the pathophysiology of PKD cannot be simply explained by lesions of the basal ganglia or thalamus, and that other associated areas of the cortex are likely involved in these movement disorders.