Epilepsia · 2007
Neuroimaging and neurophysiology of periodic lateralized epileptiform discharges: observations and hypotheses.
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Kalamangalam Giridhar P, Diehl Beate, Burgess Richard C
Аннотация
PURPOSE: We assessed neuroimaging lesion type and distribution in patients with periodic lateralized epileptiform discharges (PLEDs), with a view to identifying electrographic differences between PLEDs associated with differing lesion locations. Our observations led us to consider a conceptual synthesis between PLEDs and periodic complexes (PCs).
METHODS: Retrospective review of acute neuroimaging results (CT/MRI) on patients identified to have EEG PLEDs, for the period 1999-2003 (n=106). Blinded classification of original EEG recordings.
RESULTS: Neuroimaging abnormalities were classified as acute or chronic cortical, or acute or chronic subcortical. Seven out of 106 scans were classified nonlesional. Overall approximately 70% of scans had cortical abnormalities, whether acute or chronic; approximately 23% had subcortical abnormalities. "Cortical" PLEDs were significantly longer in duration (p<0.05) and more variable in morphology (p<0.01) than "subcortical" PLEDs.
CONCLUSIONS: Structural brain disease commonly, but not invariably, underlies PLEDs; lesion type is spatiotemporally variable. Cortical and subcortical PLEDs have distinct EEG signatures. There is evidence that these may relate to mechanisms for other pathological large-scale oscillatory brain synchronies (e.g., PCs).
METHODS: Retrospective review of acute neuroimaging results (CT/MRI) on patients identified to have EEG PLEDs, for the period 1999-2003 (n=106). Blinded classification of original EEG recordings.
RESULTS: Neuroimaging abnormalities were classified as acute or chronic cortical, or acute or chronic subcortical. Seven out of 106 scans were classified nonlesional. Overall approximately 70% of scans had cortical abnormalities, whether acute or chronic; approximately 23% had subcortical abnormalities. "Cortical" PLEDs were significantly longer in duration (p<0.05) and more variable in morphology (p<0.01) than "subcortical" PLEDs.
CONCLUSIONS: Structural brain disease commonly, but not invariably, underlies PLEDs; lesion type is spatiotemporally variable. Cortical and subcortical PLEDs have distinct EEG signatures. There is evidence that these may relate to mechanisms for other pathological large-scale oscillatory brain synchronies (e.g., PCs).