Migraine Comorbidities.

Novel knowledge about the interrelationships and reciprocal effects of migraine and epilepsy, migraine and mood disorders, or migraine and irritable bowel syndrome has emerged in recent decades. Over time, comorbid pathologies associated with migraine that share common physiopathological mechanisms were studied. Among these studied pathologies is epilepsy, a disorder with common ion channel dysfunctions as well as dysfunctions in glutamatergic transmission. A high degree of neuronal excitement and ion channel abnormalities are associated with epilepsy and migraine and antiepileptic drugs are useful in treating both disorders. The coexistence of epilepsy and migraine may occur independently in the same individual or the two may be causally connected. The relationship between cortical spreading depression (CSD) and epileptic foci has been suggested by basic and clinical neuroscience research. The most relevant psychiatric comorbidities associated with migraine are anxiety and mood disorders, which influence its clinical course, treatment response, and clinical outcome. The association between migraine and major depressive disorder can be explained by a robust molecular genetic background. In addition to its role as a potent vasodilator, CGRP is also involved in the transmission of nociception, a phenomenon inevitably linked with the stress and anxiety caused by frequent migraine attacks. Another aspect is the role of gut microbiome in migraine's pathology and the gut-brain axis involvement. Irritable bowel syndrome patients are more likely to suffer migraines, according to other studies. There is no precise explanation for how the gut microbiota contributes to neurological disorders in general and migraines in particular. This study aims to show that migraines and comorbid conditions, such as epilepsy, microbiota, or mood disorders, can be connected from the bench to the bedside. It is likely that these comorbid migraine conditions with common pathophysiological mechanisms will have a significant impact on best treatment choices and may provide clues for future treatment options.

Default mode function in patients with generalised epilepsy syndromes: from generalised to focal findings.

INTRODUCTION: Many recent studies have suggested that generalised epilepsy is associated with cortical epileptogenic focus, and therefore distinguishing between focal and generalised often becomes difficult. AIM OF STUDY: We aimed to detect differences between default mode function in patients with idiopathic generalised epilepsy who have discharges on EEG, and healthy persons. MATERIAL AND METHODS: This was a case-control study; we performed EEG analysis with LORETA in 17 patients with a type of generalised epilepsy and a control group represented by 17 healthy age-matched persons. We performed statistical non- -parametric tests for current density electrical distribution for our two groups ('t-statistic on Log transformed data') and we defined regions of interest (ROIs) from the default mode network. In the second part, we compared the average activation for each ROI for each timeframe in the epoch for the group with epilepsy, and for controls (we performed a Wilcoxon rank-sum test for two means). RESULTS: In the first part, we obtained that in the medial frontal gyrus (BA 9) delta oscillations significantly differed in patients with epilepsy who had electrical discharges on EEG in resting state conditions compared to healthy controls (medial frontal gyrus in this group had a greater number of synchronously oscillating neurons than did the controls). In the second part, we ran statistics on our localised activity from the default mode network (defined ROIs) and we obtained statistically significant differences in the left medial frontal gyrus (the values were higher for the group with epilepsy, p-value = 0.0066). CONCLUSIONS AND CLINICAL IMPLICATIONS: It may be possible to move from a 'generalised theory' about epilepsy to a 'focused theory' by understanding how various areas of interest are activated within default mode networks. Insights into the pathophysiology of generalised epilepsy may lead to new treatment options.

Cortical connectivity in stroke using signals from resting-state EEG: a review of current literature.

INTRODUCTION: Stroke is considered a substantial cause of disability worldwide and many researches are focused on rehabilitative interventions. Functional magnetic resonance imaging studies centered on brain networks after stroke describe affected functional connectivity between areas within the default mode, sensorimotor, visual, fronto-parietal and executive networks. Recent studies renewed the perspective of utilizing electroencephalography to describe markers of cortical activity in stroke and recovery neurophysiological processes. METHODS: We included in our research studies realized on patients that had an ischemic or hemorrhagic stroke that performed electroencephalography and had an analysis of connectivity indices. Resting-state electroencephalography has the advantage of including patients with any neurological deficit and it is easier to perform than the task-based variant. The changes in resting-state EEG networks after stroke are important to determine a relationship between frequency cortical activity and spatial conformation of a network. From conventional to quantitative EEG analysis in stroke, these techniques are improved with additional brain connectivity tools that lead to a better characterization between injured areas and other intra- and inter-hemispheric areas. RESULTS: There are studies that underline the disruptions in local networks in a frequency-dependent modality after stroke, while other results are focused on bilateral changes in resting-state cortical networks, independent of the side of the lesions. CONCLUSIONS: Many studies found alterations in various connectivity measures after stroke with the help of EEG, but the clinical significance of these findings is a field of increasing interest in research area.