Abstract
Objective
We investigated the interdependency between striatal activity and the electrophysiological dynamics of the cortical epileptogenic zone using intracerebral stereoelectroencephalographic recordings in patients with drug-resistant epilepsy. We performed both qualitative and quantitative analyses of ictal striatal activity and its synchronization with the cerebral cortex to gain deeper insight into the striatal contribution to seizure regulation.
Methods
Thirty-one patients were retrospectively included. The Epileptogenicity Index (EI) was computed, high EI values corresponded to structures in the epileptogenic zone (EZ), and brain regions with sustained discharge during the seizure were defined as the propagation zone network (PZN). To study the functional and directed connectivity between the striatum and the broader network, a nonlinear correlation coefficient (h
2) and an index Dᵪᵧ that provides quantitative information about the direction of couplings between neuronal populations were computed.
Results
We analyzed 31 subjects and 68 seizures. We found that 84% (n = 57) of seizures spread to the ipsilateral striatum. This spread was mainly late during seizure evolution (69.12%, n = 47) and was mostly present in seizures characterized by a focal slow spread pattern (33.82%, n = 23). Striatal epileptogenicity was overall low, with only 4.41% (n = 3) of seizures exhibiting a striatal EI ≥ .4. Interestingly, the positive correlation between striatal epileptogenicity and the PZN (r = .4193, p = .0004) indicates that higher striatal epileptogenicity is associated with the recruitment of a greater number of brain regions within the PZN. Moreover, striatal functional connectivity with the broader network was the lowest during the background period and progressively increased during ictal and postictal phases (p < .001), with directed connectivity shifting from the EZ to the striatum in the preictal and termination phases.
Significance
These findings provide a framework for future research investigating the potential of basal ganglia-targeted therapies in epilepsy management.
JUN