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.
Key words
paroxysmal kinesigenic dyskinesia (PKD) - cerebral blood flow - SPECT
