Project

Advanced brain network analysis for a better understanding of functional and structural brain network changes in post-stroke epilepsy.

Code
3G027422
Duration
01 January 2022 → 31 December 2025
Funding
Research Foundation - Flanders (FWO)
Promotor-spokesperson
Research disciplines
  • Medical and health sciences
    • Neurological and neuromuscular diseases
    • Neurophysiology
    • Neurological and neuromuscular diseases
  • Engineering and technology
    • Biomedical image processing
    • Biomedical signal processing
Keywords
structure-function connectome Intracranial haemorrhage metabolism epilepsy
 
Project description

Spontaneous non-traumatic intracerebral haemorrhage (ICH) is the second most common type of stroke, after ischemic stroke, and occurs in 15% of all stroke patients. It is a devastating acute cerebrovascular disorder with high mortality and morbidity. When surviving, only 20% of patients achieve functional independence. ICH is also a known risk factor for the development of epileptic seizures, further reducing quality of life. Data regarding seizures after ICH are scarce, and the frequency and predictors of seizures in patients with ICH are poorly understood. Early seizures after stroke are likely to be differentiated from late seizures regarding pathophysiology. We aim to investigate how the organisation of brain changes after ICH using a multimodal imaging approach in order to better understand the pathophysiology of acute and late seizures. Therefore, we will combine and correlate functional magnetic resonance imaging, structural diffusion-weighted magnetic resonance imaging, positron emission tomography, video-EEG monitoring and histological analysis, using a rat model for ICH. Our hypothesis is that this multimodal imaging approach will provide us with a strong dataset that can identify brain regions/connections that might play a crucial role in seizure generation after ICH. We also aim to apply chemogenetics for selective inhibition of these brain regions/connections to prove their causal role in the generation of seizures after ICH.