Abstract
Aim: The main objective of this work was to study the impact of repetitive Transcranial Magnetic Stimulation (rTMS) treatment on brain activity in 8 patients with major depressive disorder (MDD) and 10 patients with bipolar disorder (BP). Changes due to rTMS stimulation of the left dorsolateral prefrontal cortex (DLPFC) were investigated considering separately responders and non-responders to therapy in each of both groups. The aim of the research is to determine whether non-responders differ from responders suffered from both diseases, as well as if any change occurred due to rTMS across consecutive rTMS sessions.Methods: The graph-theory-based connectivity analysis of non-linearity measure of phase interdependencies—Phase Locking Value (PLV)—was examined from EEG data. The approximately 15-min EEG recordings from each of participants were recorded before and after 1st, 10th, and 20th session, respectively. PLV calculated from data was analyzed using principal graph theory indices (strength and degree) within five physiological frequency bands and in individual channels separately. The impact of rTMS on the EEG connectivity in every group of patients evaluated by PLV was assessed.Results: Each of four groups reacted differently to rTMS treatment. The strength and degree of PLV increased in gamma band in both groups of responders. Moreover, an increase of indices in beta band for BP-responders was observed. While, in MDD-non-responders the indices decreased in gamma band and increased in beta band. Moreover, the index strength was lower in alpha band for BP- non-responders. The rTMS stimulation caused topographically specific changes, i.e., the increase of the activity in the left DLPFC as well as in other brain regions such as right parieto-occipital areas.Conclusions: The analysis of PLV allowed for evaluation of the rTMS impact on the EEG activity in each group of patients. The changes of PLV under stimulation might be a good indicator of response to depression treatment permitting to improve the effectiveness of therapy.
Highlights
Major depressive disorder (MDD) is one of the most common mental disorders in the world and leads to a variety of emotional and physical problems such us overwhelming feeling of sadness and isolation, frequent anxiety and irritation, diminished selfesteem and reduction in attention or concentration (American Psychiatric Association (APA), 2013)
The repetitive Transcranial Magnetic Stimulation (rTMS) stimulation was targeted to the left dorsolateral prefrontal cortex (DLPFC), which is functionally connected to the limbic areas of the brain that is highly involved in regulation of mood (Kito et al, 2016)
The impact of rTMS on the EEG connectivity evaluated by Phase Locking Value (PLV) was studied for the first time
Summary
Major depressive disorder (MDD) is one of the most common mental disorders in the world and leads to a variety of emotional and physical problems such us overwhelming feeling of sadness and isolation, frequent anxiety and irritation, diminished selfesteem and reduction in attention or concentration (American Psychiatric Association (APA), 2013). According to recent estimation about 300 million people suffer from depression episodes, and, as a result, about 800,000 patients commit suicide (World Health Organization (WHO), 1992, 2017; National Institutes of Health (NIH), 2007). Depression classification includes the disease entity termed bipolar affective disorder. It is marked by depressive and manic episodes which occur in repeated periods. The origin of MDD is associated with functional deficits, abnormal structures of brain and defective activity of neurotransmitters. Numerous researches have demonstrated the differences in physiologic brain mechanisms between healthy people and patients with depression. The pathophysiology is observed in abnormal changes in structures in brain and in bioelectrical activity of neurons. The EEG-based methods show various atypical patterns in electroencephalogram of depressed people, such as frontal alpha EEG asymmetry and left frontal hypoactivation (Koo et al, 2017)
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