University of Twente Student Theses
Source Reconstruction and Parameter Estimation of Generalized Periodic Discharges
Slingerland, T.P. (2023) Source Reconstruction and Parameter Estimation of Generalized Periodic Discharges.
|
PDF
2MB |
| Abstract: | Generalized Periodic Discharges (GPDs) occur in 20% of postanoxic comatose patients. The underlying pathophysiology of GPDs is far from understood. In a previous study, a cortical meanfield model has been used to explain the pathophysiology of GPDs. In another study, source reconstruction revealed that GPDs originate in subcortical structures, mainly the thalamus. However in both cases, no distinction was made between GPDs on a continuous background and GPDs on a suppressed background. GPDs on a continuous background are associated with a good outcome, whilst GPDs on a suppressed background are associated with a poor outcome. Why this difference in outcome occurs remains unclear. In this study, we used source reconstruction, and parameter estimation on a corticothalamic meanfield model to investigate whether a difference in anatomical source and/or pathophysiological mechanisms could explain the difference in outcome between the two types of GPDs, and in the process elucidate the underlying pathophysiology of GPDs. From an existing dataset of continuous electroencephalograms (EEGs) of 47 patients with GPDs, we identified 26 patients with GPDs on a continuous background and 19 patients with GPDs on a suppressed background. We also included 50 EEGs from healthy controls for the estimation of reference values for the parameters of the corticothalamic meanfield model. Source reconstruction results revealed that the anatomical source of both types of GPDs was located predominantly in the subcortical regions. We found no significant difference between the two types of GPDs. Parameter estimation revealed significant differences in the cortical and corticothalamic loop variables between both GPD groups and healthy controls. Both GPD groups exhibited significantly lower cortical loop values and predominantly negative corticothalamic loop values compared to mostly positive values in healthy controls. The corticothalamic delay was also significantly higher in the GPD groups. There were no significant differences between the two types of GPDs, except for the decay rate. We concluded that the difference in prognosis between the two types of GPDs could not be explained by a difference in anatomical source or pathophysiological variables of the corticothalamic meanfield model, despite the significant difference in decay rate. We hypothesize that the difference in prognosis could be attributed to the continuous background, yet further research is needed. Next, our results indicate that both the cortical and corticothalamic loop are involved in the spread or generation of GPDs. In both cases the strength of the inhibitory neurons increased relative to the strength of the excitatory neurons. |
| Item Type: | Essay (Master) |
| Faculty: | TNW: Science and Technology |
| Subject: | 44 medicine |
| Programme: | Biomedical Engineering MSc (66226) |
| Link to this item: | https://purl.utwente.nl/essays/95262 |
| Export this item as: | BibTeX EndNote HTML Citation Reference Manager |
Show download statistics for this publication
Show download statistics for this publicationRepository Staff Only: item control page