Epilepsy is related to theta band brain connectivity and network topology in brain tumor patients

Abstract

BackgroundBoth epilepsy patients and brain tumor patients show altered functional connectivity and less optimal brain network topology when compared to healthy controls, particularly in the theta band. Furthermore, the duration and characteristics of epilepsy may also influence functional interactions in brain networks. However, the specific features of connectivity and networks in tumor-related epilepsy have not been investigated yet. We hypothesize that epilepsy characteristics are related to (theta band) connectivity and network architecture in operated glioma patients suffering from epileptic seizures. Included patients participated in a clinical study investigating the effect of levetiracetam monotherapy on seizure frequency in glioma patients, and were assessed at two time points: directly after neurosurgery (t1), and six months later (t2). At these time points, magnetoencephalography (MEG) was recorded and information regarding clinical status and epilepsy history was collected. Functional connectivity was calculated in six frequency bands, as were a number of network measures such as normalized clustering coefficient and path length.ResultsAt the two time points, MEG registrations were performed in respectively 17 and 12 patients. No changes in connectivity or network topology occurred over time. Increased theta band connectivity at t1 and t2 was related to a higher total number of seizures. Furthermore, higher number of seizures was related to a less optimal, more random brain network topology. Other factors were not significantly related to functional connectivity or network topology.ConclusionsThese results indicate that (pathologically) increased theta band connectivity is related to a higher number of epileptic seizures in brain tumor patients, suggesting that theta band connectivity changes are a hallmark of tumor-related epilepsy. Furthermore, a more random brain network topology is related to greater vulnerability to seizures. Thus, functional connectivity and brain network architecture may prove to be important parameters of tumor-related epilepsy.

Neocortical pathological high-frequency oscillations are associated with frequency-dependent alterations in functional network topology

“…It has been found that seizure semiologies characterized by impaired consciousness demonstrate abnormal slow-wave activity (Yang et al 2012). Theta band connectivity has also been proposed as an early diagnostic test for epilepsy (Douw et al 2010a), and pathologically elevated theta connectivity has related to greater seizure frequency (Douw et al 2010b). Finally, a treatment of epilepsy, vagus nerve stimulation, has previously been shown to increase and decrease gamma and theta band connectivity, respectively, underscoring the potential relevance of our findings for seizure control (Marrosu et al 2005).…”

The relation between cortisol and functional connectivity in people with and without stress‐sensitive epilepsy

“…19,20,34,35 An increase in theta band functional connectivity was associated with seizure frequency in tumor-related epilepsy. 36 One could speculate that increased functional connectivity in epilepsy is somehow a protective mechanism against seizure generation, which fails in a stress-sensitive subset of subjects as cortisol increases. There is evidence for the hypothesis that desynchronization takes place accompanied by a reduction of IEDs prior to seizure onset.…”

Glioma-Associated Epilepsy

“…In essence, the strength of connections among network nodes and their directionality may define for us the extent of epileptogenic territory. An altered functional connectivity has been proposed in the case of both mesial temporal lobe epilepsy [14] and tumour-associated epilepsy [15] patients. A pathologically increased theta or low frequency band connectivity was found to be related to increased seizure activity in brain tumour patients raising some consideration as to whether such findings may shed light on peritumoural epileptogenesis.…”