THE BURST SUPPRESSION PATTERN OF SECONDARY GENERALIZED SEIZURES
Abstract number :
1.045
Submission category :
3. Clinical Neurophysiology
Year :
2009
Submission ID :
9391
Source :
www.aesnet.org
Presentation date :
12/4/2009 12:00:00 AM
Published date :
Aug 26, 2009, 08:12 AM
Authors :
Atul Maheshwari and S. Cash
Rationale: Characterization of termination of secondary generalized seizures may give insight into the basic pathophysiology of the natural mechanism of seizure cessation Methods: In this study we examined the offset patterns of seizures from 25 patients with secondary generalized epilepsy. We analyzed 20 records from scalp recordings and, to gain even greater insight, 5 seizures from invasive monitoring. Patients were selected from a database of epilepsy monitoring unit patients at the Massachusetts General Hospital. Inclusion criteria included any seizure that was classified as secondary generalized. We first classified termination patterns based on visual inspection determining whether or not seizures ended synchronously or simultaneously. We then used a more quantitative approach in which the end of the seizure was broken into epochs divided by tandem bursts and suppressions. Bursts were defined as relative high frequency, large amplitude periods and suppressions defined as relatively low frequency, small amplitude periods. Results: Most of the seizures ended synchronously and simultaneously. As the seizures terminate the average suppression length significantly increased from a mean of 321 ms at 10 epochs prior to seizure end to 906 ms in the epoch prior to seizure end (standard deviation of 168 and 293 ms, respectively, and p<0.001). The average burst length had no significant change from a mean of 303 ms at 10 epochs prior to seizure end to 266 ms in the epoch prior to seizure end (standard deviation of 89 and 92 ms, respectively, and p=0.175). Conclusions: These results suggest that the mechanisms of seizure termination involve either a large scale network phenomenon, decreased drive from a central “pacemaker” or increased drive from a central inhibitory driver. It is unlikely that metabolic, extracellular, ephaptic or other similar mechanisms could account for such rapid and synchronous changes in state.
Neurophysiology