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Ann Clin Transl Neurol. 2015 May;2(5):456-64. doi: 10.1002/acn3.178. Epub 2015 Apr 11.

Abnormal cortical thickness connectivity persists in childhood absence epilepsy.

Annals of clinical and translational neurology

Evan K Curwood, Mangor Pedersen, Patrick W Carney, Anne T Berg, David F Abbott, Graeme D Jackson

Affiliations

  1. The Florey Institute of Neuroscience and Mental Health Austin Campus, Heidelberg, Victoria, Australia.
  2. Florey Department of Neuroscience and Mental Health, The University of Melbourne Heidelberg, Victoria, Australia.
  3. The Florey Institute of Neuroscience and Mental Health Austin Campus, Heidelberg, Victoria, Australia ; Department of Medicine, The University of Melbourne Parkville, Victoria, Australia.
  4. Epilepsy Center, Ann and Robert H. Lurie Children's Hospital of Chicago Chicago, Illinois.
  5. The Florey Institute of Neuroscience and Mental Health Austin Campus, Heidelberg, Victoria, Australia ; Florey Department of Neuroscience and Mental Health, The University of Melbourne Heidelberg, Victoria, Australia ; Department of Medicine, The University of Melbourne Parkville, Victoria, Australia.

PMID: 26000319 PMCID: PMC4435701 DOI: 10.1002/acn3.178

Abstract

OBJECTIVE: Childhood absence epilepsy (CAE) is a childhood-onset generalized epilepsy. Recent fMRI studies have suggested that frontal cortex activity occurs before thalamic involvement in epileptic discharges suggesting that frontal cortex may play an important role in childhood absence seizures. Neurocognitive deficits can persist after resolution of the epilepsy. We investigate whether structural connectivity changes are present in the brains of CAE patients in young adulthood.

METHODS: Cortical thickness measurements were obtained for 30 subjects with CAE (mean age 21 ± 2 years) and 56 healthy controls (mean age 24 ± 4) and regressed for age, sex, and total intracranial volume (TIV). Structural connectivity was evaluated by measuring the correlation between average cortical thicknesses in 915 regions over the brain. Maps of connectivity strength were then obtained for both groups.

RESULTS: When compared to controls, the CAE group shows overall increased "connectivity" with focal increased connection strength in anterior regions including; the anterior cingulate and the insula and superior temporal gyrus bilaterally; the right orbito-frontal and supramarginal regions; and the left entorhinal cortex. Decreased connection strength in the CAE group was found in the left occipital lobe, with a similar trend in right occipital lobe.

INTERPRETATION: Brains in young adults whose CAE was resolved had abnormal structural connectivity. Our findings suggest that frontal regions correlate most with cortical thickness throughout the brain in CAE patients, whereas occipital regions correlate most in well matched normal controls. We interpret this as evidence of a developmental difference in CAE that emphasizes these frontal lobe regions, perhaps driven by frontal lobe epileptiform activity.

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