Functional connectivity evidence of cortico–cortico inhibition in temporal lobe epilepsy
Article first published online: 15 SEP 2012
Copyright © 2012 Wiley Periodicals, Inc.
Human Brain Mapping
Volume 35, Issue 1, pages 353–366, January 2014
How to Cite
Tracy, J. I., Osipowicz, K., Spechler, P., Sharan, A., Skidmore, C., Doucet, G. and Sperling, M. R. (2014), Functional connectivity evidence of cortico–cortico inhibition in temporal lobe epilepsy. Hum. Brain Mapp., 35: 353–366. doi: 10.1002/hbm.22181
- Issue published online: 9 DEC 2013
- Article first published online: 15 SEP 2012
- Manuscript Accepted: 22 JUL 2012
- Manuscript Revised: 3 JUL 2012
- Manuscript Received: 31 JAN 2012
- National Institute for Neurological Disorders and Stroke (NINDS). Grant Number: R21 NS056071-01A1
- unilateral versus bilateral epileptiform activity;
- cortical inhibition
Epileptic seizures can initiate a neural circuit and lead to aberrant neural communication with brain areas outside the epileptogenic region. We focus on interictal activity in focal temporal lobe epilepsy and evaluate functional connectivity (FC) differences that emerge as function of bilateral versus strictly unilateral epileptiform activity. We assess the strength of FC at rest between the ictal and non-ictal temporal lobes, in addition to whole brain connectivity with the ictal temporal lobe. Results revealed strong connectivity between the temporal lobes for both patient groups, but this did not vary as a function of unilateral versus bilateral interictal status. Both the left and right unilateral temporal lobe groups showed significant anti-correlated activity in regions outside the epileptogenic temporal lobe, primarily involving the contralateral (non-ictal/non-pathologic) hemisphere, with precuneus involvement prominent. The bilateral groups did not show this contralateral anti-correlated activity. This anti-correlated connectivity may represent a form of protective and adaptive inhibition, helping to constrain epileptiform activity to the pathologic temporal lobe. The absence of this activity in the bilateral groups may be indicative of flawed inhibitory mechanisms, helping to explain their more widespread epileptiform activity. Our data suggest that the location and build up of epilepsy networks in the brain are not truly random, and are not limited to the formation of strictly epileptogenic networks. Functional networks may develop to take advantage of the regulatory function of structures such as the precuneus to instantiate an anti-correlated network, generating protective cortico–cortico inhibition for the purpose of limiting seizure spread or epileptogenesis. Hum Brain Mapp 35:353–366, 2014. © 2012 Wiley Periodicals, Inc.