FUNCTIONAL MRI ANALYSIS OF EPILEPTIFORM DISCHARGES AND SLOWING IN JUVENILE MYOCLONIC EPILEPSY
Abstract number :
1.243
Submission category :
Year :
2003
Submission ID :
3974
Source :
www.aesnet.org
Presentation date :
12/6/2003 12:00:00 AM
Published date :
Dec 1, 2003, 06:00 AM
Authors :
Graeme D. Jackson, Tony B. Waites, Angelo Labate, Paolo Federico Brain Research Institute, University of Melbourne, Victoria, Australia; Department of Clincial Neurosciences, Univeristy of Calgary, AB, Canada
We have previously shown that the posterior cingulate may have a role in the generation of spike and wave discharges (SWD) in persistent childhood absence epilepsy. Using event-related fMRI, we sought to document regional changes in blood oxygen level dependent (BOLD) activity associated with spontaneous generalized SWD as well as slow waves in a patient with juvenile myoclonic epilepsy.
A 29 year old male with a clinical diagnosis of juvenile myoclonic epilepsy and frequent SWD was studied. EEG was recorded continuously inside a 3 T MR scanner for 30 minutes, and the timing of occurrence of SWD and slow wave events were noted. These events were considered separately for analysis. An event-related analysis of the two groups of events was carried out using SMP99. The statistical threshold for activation was set at [italic]p[/italic] [lt] 0.005 with a minimum affected cluster size of 10 pixels.
During the study, the subject had 30 SWD (4.5 Hz spike and polyspike and wave) as well as five bursts of 2-3 Hz semi-rhythmic generalized slowing. Significant SWD-related BOLD signal decreases were seen in the posterior cingulate. Some SWD-related BOLD increases were seen in the depths of the pre-central sulci. No thalamic BOLD signal changes were seen with SWDs. In contrast, generalized slowing was associated with significant BOLD signal increases in the thalamus and brainstem reticular formation bilaterally. No significant BOLD signal decreases were seen with generalized slowing.
We have confirmed our previous observation that the posterior cingulate may have a role in the generation of SWD in generalized epilepsies. We have also shown that the thalamus and brainstem reticular formation activation is seen with generalized slowing but not with SWD. These results suggest that posterior cingulate deactivation and brainstem/thalamic activation may have different, but complementary roles in the electro-clinical phenomena of SWD and generalized slowing.
[Supported by: National Health and Medical Research Council of Australia, Canadian Institutes of Health Research, Alberta Heritage Foundation for Medical Research.]