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Influence of somatosensory input on motor function in patients with chronic stroke

Challenging established mythology can provoke strong reaction and, although we appreciate the interest of Bali and colleagues in our work, they have missed the actual interpretation and emphasis of our article. Our literature review was of twins with the clinical syndrome of benign rolandic epilepsy (BRE), and the other twins mentioned in the article by Doose did not fulfill criteria for the diagnosis of BRE. As described in our article, we agree that concordant twins with BRE exist in the literature, and that there is an elevated sibling risk, but we showed in this twin sample, and in a subsequent validation study with twins from Scandinavia and the United States (L. Vadlamudi, et al, unpublished data) that the concordance for BRE is very low, particularly when referral bias is minimized. This suggests that the genetic influence in BRE is far less than has been traditionally considered. Importantly, we were not examining the genetics of centrostemporal spikes (CTSs) in this study. CTSs do have a familial component (prevalence in siblings of cases 11% according to Doose and in healthy children 1.6%; relative risk, 7). As discussed in our article, we may have underestimated the concordance of this trait, but this is not of relevance to the main argument of the genetics of the clinical epileptic syndrome of BRE. The issue of aggregation of language impairment with CTSs and rolandic epilepsy syndromes is complex. On one extreme is the autosomal dominant syndrome described by us of rolandic epilepsy and speech dyspraxia; on another are the apparently sporadic cases with severe language impairment and focal spikes (Landau–Kleffner syndrome), and then there are more subtle language disorders in “typical” BRE cases as confirmed by Bali and colleagues. Whether familial factors associated with language impairment are related to CTSs or BRE per se remains unexplored. The putative locus by Neubauer and colleagues for CTSs (not for the clinical syndrome of BRE) has not been replicated; hence the significance is uncertain. The confusion from previous literature is that the genetics of CTSs are mis-interpreted as the genetics of BRE. CTSs are seen in many clinical settings, with and without seizures, have a genetic component, are a necessary prerequisite for BRE, but only explain a small portion of the risk for BRE (L. Vadlamudi et al, unpublished data). The epidemiologically derived twin data clearly show that there are major nonfamilial factors in BRE, and that genetic factors are far less important than previously perceived. Epilepsy Research Centre, Department of Medicine (Neurology), University of Melbourne, Austin Health; Children’s Epilepsy Program, Department of Neurology, RCH; and Centre for Genetic Epidemiology, University of Melbourne, Melbourne, Australia