Regional increase of cerebral cortex thickness in juvenile myoclonic epilepsy *†Saud Alhusaini, *‡Lisa Ronan, *Cathy Scanlon, †Christopher D. Whelan, §Colin P. Doherty, †¶Norman Delanty, and *Mary Fitzsimons *Brain Morphometry Laboratory, Epilepsy Programme, Beaumont Hospital, Dublin, Ireland; †Molecular and Cellular Therapeutics Department, Royal College of Surgeons in Ireland, Dublin, Ireland; ‡Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom; §Neurology Department, St. James’s Hospital, Dublin, Ireland; and ¶Neurology Department, Beaumont Hospital, Dublin, Ireland SUMMARY The goal of this study was to characterize cerebral cortex thickness patterns in juvenile myoclonic epilepsy (JME). Surface-based morphometry (SBM) was applied to pro- cess brain magnetic resonance images acquired from 24 patients with JME and 40 healthy controls and quantify cerebral cortex thickness. Differences in cortical thick- ness between patients and controls were determined using generalized linear model (covariates: age and gen- der). In patients with JME, thickness increase was detected bilaterally within localized regions in the orbito- frontal and mesial frontal cortices. Such thickness pat- terns coexisted with significant bilateral reduction in thalamic volume. These findings confirm that the underly- ing mechanisms in JME are related to aberrant corticotha- lamic structure and indicate that frontal cortex abnormalities are possibly linked to regional increase in cerebral cortical thickness. KEY WORDS: Juvenile myoclonic epilepsy, Magnetic res- onance imaging, Cortical thickness. Juvenile myoclonic epilepsy (JME) is a well-defined idi- opathic generalized epilepsy (IGE) syndrome that is charac- terized by age-related onset of seizures manifesting as myoclonic jerks, generalized tonic–clonic seizures, and sometimes typical absence seizures (Pedersen & Petersen, 1998). Clinically, patients reveal no focal neurologic abnor- malities and standard electroencephalography (EEG) recordings often show bilaterally diffuse generalized spike- wave (GSW) or polyspike-wave activity, sometimes with frontocentral predominance (Pedersen & Petersen, 1998). Quantitative neuroimaging studies of patients have detected several subtle neuroanatomic abnormalities, including thalamic gray matter volume (GMV) reduction and increased ventromedial frontal cortex (Duncan, 2005). These observa- tions suggest that the underlying mechanisms in JME are related to aberrant frontothalamic structure (Duncan, 2005). Recently, we investigated cerebral cortex surface mor- phology in a group of JME patients and reported anomalies in a number of regions dispersed throughout the cerebral cortex (Ronan et al., 2012). These morphologic alterations spared the frontal cortex and were related predominantly to changes in cortical surface area. Such cortical surface area– based findings, which likely reflect relevant JME-related pathologic processes, did not relate to previously described frontal cortex GMV alterations (Woermann et al., 1999). Building on our previous investigation of cortical surface morphology, in this study, we examined cerebral cortex thickness patterns in the same patient cohort. Methods The medical research ethics committee at Beaumont Hospital Dublin approved this study. Written informed consent was obtained from all participants. Study participants In total, 24 patients with JME were recruited from the epi- lepsy clinic at Beaumont Hospital and considered for this study. This sample of patients was described in detail in our previous report (Ronan et al., 2012). All patients underwent comprehensive evaluation that confirmed the clinical fea- tures of JME as defined by the International League Against Epilepsy (ILAE). In addition, 40 control subjects with no known neurologic deficits were included. See Table 1 for a summarized description of study participants. MR image acquisition and processing Patients and controls underwent brain magnetic resonance imaging (MRI) using a 1.5 T scanner (Signa, Accepted June 24, 2013. Address correspondence to Mary Fitzsimons, Brain Morphometry Labo- ratory, Neurophysics Department, Beaumont Hospital, Dublin 9, Ireland. E-mail: maryfitzsimons@beaumont.ie Wiley Periodicals, Inc. © 2013 International League Against Epilepsy 1 Epilepsia, **(*):1–4, 2013 doi: 10.1111/epi.12330 BRIEF COMMUNICATION