We appreciate the comments of Pohlmann-Eden and colleagues regarding our article on poststroke seizures. We agree that there are significant problems with most published studies in this area. Thus, we emphasized the large prospective study by Bladin et al1 throughout our review.
Their second point argues that the role of cortical involvement in stroke was overemphasized in our review, but we acknowledged that a smaller percentage of subcortical strokes are associated with seizures. It is difficult, however, to determine whether an individual seizure actually originates from subcortical regions. Patients with lesions that appear exclusively subcortical on neuroimaging studies may also have an undetected cortical component. Furthermore, the mechanism of seizures associated with subcortical lesions is unknown. In the absence of additional published findings, we are skeptical of the observation that combined cortical-subcortical lesions are more epileptogenic than exclusively cortical ones. In the future, imaging and EEG seizure localization techniques will likely better explain the relationship between lesion localization and the site of epileptogenesis. The role of positron emission tomography is not established at this time.
Silverman IE, Restrepo L, Mathews GC. In reply. Arch Neurol. 2002;59(11):1831–1832. doi:
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