Is Rolandic epilepsy associated with abnormal findings on cranial MRI?
Introduction
Benign epilepsy of childhood with centrotemporal spikes (BECTS), also known as Rolandic epilepsy (RE), is an idiopathic epilepsy syndrome and its etiology is presumed to be complex genetic (Bali et al., 2005). The designation “idiopathic” implies absence of structural, inflammatory or metabolic brain lesions (Commission, 1989). However, several reports have demonstrated a relatively high frequency of routine brain MRI abnormalities in RE patients (Lundberg et al., 1999, Eeg-Olofsson et al., 2000, Gelisse et al., 2003). These include both specific parenchymal abnormalities, such as hippocampal asymmetry, possibly ipsilateral to the Rolandic seizure focus (Lundberg et al., 1999, Eeg-Olofsson et al., 2000) and focal brain lesions (Shevell et al., 1996), as well as apparently incidental abnormalities such as ventricular dilatation, dilated perivascular spaces, non-specific white matter signal hyperintensities, Arnold–Chiari malformations, and congenital cysts (Lundberg et al., 1999, Gelisse et al., 2003).
The etiological significance of such findings is not entirely clear because the incidence of these types of abnormalities in the general pediatric population is not well known, although they are probably fairly common (Kim et al., 2002). Moreover, because routine MRIs are evaluated by visual inspection, the possible role of observer bias in concluding that an association exists between Rolandic epilepsy and MRI abnormalities is also unknown. Image quality and other technical factors may further confound a potential association. Hence to test the hypothesis that RE patients exhibit excess imaging abnormalities on brain MRI, we compared the prevalence of MRI abnormalities in Rolandic epilepsy patients against controls. If the hypothesis were true, then we would predict (i) the prevalence of abnormalities in RE cases to exceed that in controls; (ii) that there would be some specificity to the types of imaging abnormality in RE; and (iii) that these abnormalities would tend to be ipsilateral to the hemisphere from which RE discharges emanate.
Section snippets
Design
This was an unmatched case-control study with one-to-one ratio of cases and controls. Observer bias was controlled by blinding the neuroradiologists to the study hypothesis and to the identity of case and control MRI exams. We measured potential confounding variables including age and sex of subjects, and technical factors relating to the imaging quality, quantity and MR pulse sequences.
Materials
We obtained the brain MRI examinations of 25 RE patients and 25 pediatric control patients of similar age and
Results
The imaging quality and quantity of exams did not differ significantly between groups (Table 2). RE cases were slightly older at time of examination than controls, and there were also more males in the case group. Inter-rater agreement was excellent for most classes of abnormality, ranging from kappa of 0.79–0.98 (Table 3). There was more disagreement about the classification of dilated perivascular spaces, a normal variation, than other “true” abnormalities (kappa 0.79). All discrepancies were
Discussion
This is the first controlled study to test the hypothesis that RE cases exhibit an excess of abnormalities on routine cranial MRI. There was a high frequency of abnormalities (52% overall) with no excess of abnormalities in RE cases compared to controls. We found no evidence that existing MRI abnormalities lateralized to the hemisphere from which Rolandic discharges predominantly emanated. Our results do not support an association between any particular type of abnormality and RE. We also
Acknowledgements
This study was sponsored by the Partnership for Pediatric Epilepsy Research, Epilepsy Foundation; and through the generous support of the Charles L. Shor Foundation for Epilepsy Research, Inc.; and the National Institutes for Neurological Disorders and Stroke NS047530-R01. Our thanks to the physicians who referred cases to the Multicenter Genetic Study of Rolandic Epilepsy: Steven L. Kugler MD, Steven M. Wolf MD, William D. Brown MD, David E. Mandelbaum MD Ph.D., Murray Engel MD, and John
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