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Updated: Jul 13, 2026

A Multimodal Imaging- and Stimulation-based Method of Evaluating Connectivity-related Brain Excitability in Patients with Epilepsy
Published on: November 13, 2016
Motor cortical excitability in patients with poststroke epilepsy
Jee Hyun Kim1, Hyang Woon Lee, Leonardo G Cohen
1Department of Neurology, Ewha Womans University, Seoul, Korea.
Poststroke epilepsy (PSE) may stem from increased cortical excitability in the affected hemisphere, potentially due to heightened glutamatergic activity. This study compared motor cortical function in patients with and without PSE.
Area of Science:
- Neuroscience
- Neurology
- Epileptology
Background:
- Poststroke epilepsy (PSE) is a common complication following ischemic or hemorrhagic stroke.
- Understanding the neurophysiological mechanisms of PSE is crucial for developing targeted treatments.
- Cortical excitability changes are implicated in the development of epilepsy after brain injury.
Purpose of the Study:
- To investigate the differences in motor cortical function between chronic stroke patients with and without poststroke epilepsy (PSE).
- To identify potential neurophysiological mechanisms contributing to the development of PSE.
Main Methods:
- Transcranial magnetic stimulation (TMS) was used to assess motor cortical function.
- Measurements included resting motor threshold (RMT), motor evoked potential (MEP) amplitudes, cortical silent period (CSP), intracortical inhibition (ICI), and intracortical facilitation (ICF).
- GABAergic and glutamatergic neurotransmission influences were examined via ICI and ICF, respectively.
Main Results:
- Patients with PSE exhibited larger MEP amplitudes and increased ICF in the affected hemisphere compared to the unaffected hemisphere.
- These findings were not observed in stroke patients without epilepsy.
- Both groups showed higher RMT and longer CSP in the affected hemisphere, with no differences in ICI, H-reflexes, or F-waves.
Conclusions:
- Enhanced cortical excitability in the affected hemisphere, potentially linked to increased glutamatergic activity, may be a key mechanism in the pathogenesis of PSE.
- These findings provide insights into the neurophysiological basis of epilepsy after stroke.
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