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Impaired benzodiazepine receptor binding in peri-lesional cortex of patients with symptomatic epilepsies studied by [C- 11]-flumazenil PET

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Sobesky,  Jan
Klinisches PET, Neurologische Abteilung, Max-Planck-Institut für neurologische Forschung, Managing Director: D. Yves von Cramon, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Bauer,  Bernd
Radiochemistry, Scientific Services and Development, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Herholz,  Karl
Wolf-Dieter Heiss, Emeriti, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Heiss,  Wolf-Dieter
Wolf-Dieter Heiss, Emeriti, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Citation

Szelies, B., Sobesky, J., Pawlik, G., Mielke, R., Bauer, B., Herholz, K., et al. (2002). Impaired benzodiazepine receptor binding in peri-lesional cortex of patients with symptomatic epilepsies studied by [C- 11]-flumazenil PET. European Journal of Neurology, 9(2), 137-142.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0026-D5C5-1
Abstract
Copyright 2002 BLACKWELL SCIENCE LTD
Individual benzodiazepine receptor (BZR) binding of peri- lesional cortex was investigated in symptomatic epilepsies. Eleven patients aged 19-44 years were studied whose diagnosis was established by medical history, clinical, electroencephalographic, and magnetic resonance imaging (MRI) findings. Three-dimensional [C-11]-flumazenil (FMZ) positron emission tomography and MRI scans were obtained and coregistered. Lesions (five low-grade brain tumours, one AV malformation, one cavernoma, one cystic lesion of unknown aetiology, one traumatic brain injury, one post-operative and one post-haemorrhagic defect) were outlined on individual MRI scans. Adjacent to those lesions, and in homologous contralateral structures, FMZ binding was analysed in four pairs of cortical 9 x 9-mm regions of interest (ROIs) placed on transaxial and coronal slices, respectively, as well as in the lesion volume and its mirror region. Percentage asymmetry ratios were calculated and those at or outside the 90-110% range were operationally defined significant. Peri-lesional FMZ binding asymmetries ranged from 70 to 125%, lesional asymmetries from 38 to 82%. Only one patient showed no significant change, whilst nine exhibited significant reductions of FMZ binding in at least one ROI (3 x 1, 4 x 2, 1 x 3, 1 x 4), and significant increases were observed in two ROIs of another patient. Therefore, peri-lesional disturbances of BZR binding are common but variable in location. Because a close correlation between regional decreases in FMZ binding and spiking activity was recently demonstrated in neocortical epilepsies, abnormal peri-lesional FMZ binding may bear some relation to the mechanisms of epileptogenesis in symptomatic epilepsies.