Lack of appropriate controls leads to mistaking absence seizures for post-traumatic epilepsy

Introductory points. We have read the comments by D’Ambrosio and colleagues, including their supplemental material; these comments have not changed our interpretation of our data (or theirs) or our conclusions. We stand fully behind our paper, as published. (1) We believe all aspects of our experimental design were completely appropriate for studying epileptogenesis; the experimental techniques for fluid percussion injury (FPI) have been used by us and others to study traumatic brain injury (TBI), and our experimental design has been used in other animal models to reveal genuine bona fide acquired epilepsy; (2) We agree that the data from the FPI-treated and control animals in our study were essentially identical, and by extension, we did not induce post-traumatic epilepsy; this was in fact a very important point of our paper; (3) The criteria for separating different types of epileptic seizures that we used is standard and well-accepted across the clinical and experimental literature. The claims of D’Ambrosio and colleagues refer to their prior attempts to re-define the features of different types of seizures to retroactively fit their data from their FPI experiments into a clinical context; integral to our concerns about their work is how they studied their control animals; and, (4) Although we did not cite some publications by D’Ambrosio and colleagues, we have cited extensive antecedent literature that is directly relevant to our data (and theirs); their experiments with anti-epileptic drugs and cooling are only indirectly relevant, and we believe these experiments also are questionable if not potentially flawed. Although SWDs appear to have been useful as models for the study of absence seizures, the idiosyncrasies of the sensitivity (or not) of EEEs to various AEDs is peripheral to the core issue. Reports that EEEs are pharmacoresistant to traditional AEDs and convenient models for testing possible new AEDs could reflect that EEEs are simply normal oscillations and not models of the complex partial seizures characteristic of PTE. In spite of the criticisms by D’Ambrosio and colleagues, we see no reason to change anything in our paper; our data directly contradict the hypotheses and conclusions of D’Ambrosio and colleagues, which we believe are fundamentally flawed for several reasons, particularly the widespread and consistent occurrence of epileptiform electrographic events (EEEs) in control animals.