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
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Publikationsverlauf

received 27. Juli 2011

accepted 24. Oktober 2011

Publikationsdatum:
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.

 
  • References

  • 1 Demirkiran M, Jankovic J. Paroxysmal dyskinesias: clinical features and classification. Ann Neurol 1995; 38: 571-579
  • 2 Kertesz A. Paroxysmal kinesigenic choreoathetosis. An entity within the paroxysmal choreoathetosis syndrome. Description of 10 cases, including 1 autopsied. Neurology 1967; 17: 680-690
  • 3 Guerrini R. Idiopathic epilepsy and paroxysmal dyskinesia. Epilepsia 2001; 42: S36-S41
  • 4 Hayashi R, Hanyu N, Yahikozawa H et al. Ictal muscle discharge pattern and SPECT in paroxysmal kinesigenic choreoathetosis. Electromyogr Clin Neurophysiol 1997; 37: 89-94
  • 5 Ko CH, Kong CK, Ngai WT et al. Ictal 99mTc ECD SPECT in paroxysmal kinesigenic choreoathetosis. Pediatr Neurol 2001; 24: 225-227
  • 6 Houser MK, Soland VL, Bhatia KP et al. Paroxysmal kinesigenic choreoathetosis: A report of 26 patients. J Neurol 1999; 246: 120-126
  • 7 Shirane S, Sasaki M, Kogure D et al. Increased ictal perfusion of the thalamus in paroxysmal kinesigenic dyskinesia. J Neurol Neurosurg Psychiatry 2001; 71: 408-410
  • 8 Joo EY, Hong SB, Tae WS et al. Perfusion abnormality of the caudate nucleus in patients with paroxysmal kinesigenic choreoathetosis. Eur J Nucl Med Mol Imaging 2005; 32: 1205-1209
  • 9 Mir P, Huang YZ, Gilio F et al. Abnormal cortical and spinal inhibition in paroxysmal kinesigenic dyskinesia. Brain 2005; 128: 291-299
  • 10 Van Paesschen W. Ictal SPECT. Epilepsia 2004; 45: S35-S40