Extent of EEG epileptiform pattern distribution in "focal" cortical dysplasia.
To assess the pathophysiological complexity of cortical dysplasia-related intractable focal epilepsy among surgical candidates, using our data-based EEG classification system, we reviewed preresection scalp awake and sleep EEGs (median, 8) in 46 consecutive patients whose resected pathology disclosed cortical dysplasia. Epileptiform phenomena occurred on at least one EEG in 42 (91%) patients. Twenty-three (50%) of the 46 patients displayed at least one type of independently occurring abnormality (spikes, excess delta, or theta) in each hemisphere. Nineteen of these 23 (83%), thus 41% of all 46 patients, showed independently occurring epileptiform abnormalities (spikes) in each hemisphere, i.e., the multiple independent spike foci phenomenon. In an additional 13 of the 46 (28%) patients, spike foci involving more than one lobe appeared within a single hemisphere. Thus, spike foci involving more than one lobe appeared in 32 of the 46 (70%) patients. Generalized bilaterally synchronous epileptiform features (spike waves, slow spike waves, or fast rhythmic waves) appeared in 10 (22%) of the 46 patients. Two findings suggest more widespread dysfunction among extratemporal patients than temporal patients: (1) a significantly higher number of lobes containing focal interictal epileptiform activity in extra temporal patients (mean = 3.14) than among temporal patients (mean = 2.14) (P = 0.02), (2) a higher percentage of bisynchronous epileptiform abnormalities: 8 of 23 (35%) versus 2 of 23 (9%). Among 34 patients with a Principal Spike Lobe (more active spiking over more EEGs), those of 32 (94%) arose from the ultimately resected lobe. Of the 30 patients with scalp-recorded seizures, relationship between seizure origin and ultimately resected lobe were same lobe (16 patients), same and adjacent lobes (12), adjacent lobe only (1), and distant lobe (1). Thus, despite the multifocality of several EEG features, Principal Spike Lobe and scalp-recorded seizure origin correlate well with epileptogenesis.
Jiang
Yun Jenny
YJ
From the Epilepsy Program, Department of Clinical Neurosciences, University of Western Ontario, University Hospital, London, Ontario, Canada. jjiang27@uwo.ca
Ang
Lee-Cyn
LC
Blume
Warren Thomas
WT
D000293:Adolescent; D000328:Adult; D000368:Aged; D002648:Child; D004569:Electroencephalography; D004828:Epilepsies, Partial / Q000503:physiopathology* / Q000601:surgery; D006801:Humans; D054220:Malformations of Cortical Development / Q000503:physiopathology* / Q000601:surgery; D012640:Seizures / Q000503:physiopathology / Q000601:surgery; D016896:Treatment Outcome; D055815:Young Adult