- Poster presentation
- Open Access
A potential role for the cerebellar nuclei in absence seizures
© Alva et al; licensee BioMed Central Ltd. 2013
Published: 8 July 2013
Absence seizures are characterized by a temporary lapse of consciousness, which typically lasts up to ten seconds, and they are accompanied by spike-wave discharges (SWDs) in cerebral electroencephalogram (EEG) recordings. The oscillatory activity that underlies cortical SWDs has been shown to often originate from a specific focus that can be located in various brain regions, such as the cerebral cortex, thalamus or hippocampus . Yet, the role of the cerebellum, which is anatomically connected to each of these potential foci, is unknown. Here, we used Cacna1a tottering (tg) mice, an established model for absence epilepsy characterized by a loss-of-function of calcium channels , to study how the cerebellar activity changes during absence seizures. Given that recent evidence shows that cerebellar Purkinje cells in tottering mice exhibit an altered expression of calcium channels  and structurally abnormal synapses in the cerebellar nuclei (CN), it is our hypothesis that the cerebellar output, which is dominated by neurons in the CN, changes during absence seizures.
The result, shown in Figure 1, depicts two distinct clusters for ictal and inter-ictal data. The confusion matrix for this data denotes true positive where predicted ictal data match actual ictal data (95.7%), true negative where predicted inter-ictal data match actual inter-ictal data (70%), false positive for actual ictal data incorrectly predicted as inter-ictal data (4.3%), and false negatives for actual inter-ictal data incorrectly predicted as ictal data (30%). The F-score achieved by this classification was 0.84. The separation between the ictal and inter-ictal data could further be improved by the application of Support Vector Machines (SVMs). We are currently using a conductance based model of a CN neuron to study which conditions can result in spike patterns associated with seizures.
- Danober L, Deransart C, Depaulis A, Vergnes M, Marescaux C: Pathophysiological mechanisms of genetic absence epilepsy in the rat. Progress in Neurobiology. 1998, 55 (127): 57-Google Scholar
- Hoebeek FE, Khosrovani S, Witter L, De Zeeuw CI: Purkinje cell input to cerebellar nuclei in tottering: ultrastructure and physiology. Cerebellum. 2008, 7 (4): 547-558. 10.1007/s12311-008-0086-0.View ArticlePubMedGoogle Scholar
- Noebels JL, Sidman RL: Inherited epilepsy: spike-wave and focal motor seizures in the mutant mouse tottering. Science. 1979, 204 (4399): 1334-1336. 10.1126/science.572084.View ArticlePubMedGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.