Background: the clinical polymorphism of depressive disorders, together with the available data on the different responses of patients to treatment, motivate modern neuroscience to search for models that can explain such heterogeneity.Objective: to identify neurophysiological subtypes of depressive disorders.Patients and methods: 189 patients with moderate depression in the structure of a depressive episode (n = 42), recurrent depressive (n = 102) and bipolar affective disorders (n = 45); 56 healthy subjects. Clinical-psychopathological, psychometric, neurophysiological and statistical research methods were used in the work.The results: with the help of coherent EEG analysis, it is possible to identify at least 6 subtypes of the disorder, which characterize various branches of the pathogenesis of affective pathology, which go beyond the currently accepted nomenclature. The selected subtypes were determined by the profi les of dysfunctional interaction of various cortical zones in the alpha, beta and gamma ranges of the EEG. Subtype 1 was characterized by a decrease relative to the norm of imaginary alpha-coherence between the right parietal and left central, right parietal and left anterior temporal, as well as the right parietal and right anterior temporal EEG leads (P4-C3, P4-F7, P4-F8) and explained part of depressions, in the pathogenesis of which the leading role was played by violations of the promotion of positive and suppression of negative affect. Subtype 2 — an increase in beta-2-imaginary-coherence between the frontal leads of the left and right hemispheres, between the left frontal and right central cortex (F3-F4; F3-C4) and its decrease between the central cortical zones (C4-C3), in clinical terms this subtype was characterized by a persistent hedonic response and was associated with the clinical picture of atypical depression. Subtype 3 — an increase in imaginary alpha-coherence between the frontal (F4-F3) and its decrease between the central leads of the left and right hemisphere (C4-C3), correlated with the severity of depressive rumination. Subtype 4 — a decrease in imaginary alpha-coherence between the anterior temporal and frontal, as well as the anterior temporal and central cortex of the right hemisphere (F8-F4 and F8-C4), explained part of the depressions that developed against the background of avoidance personality disorder. Subtype 5 — a decrease in imaginary gamma coherence between the frontal and parietal, as well as the central and occipital cortical zones of the left hemisphere (F3-P3 and C3-O1), was associated with an outwardly oriented utilitarian style of thinking (alexithymia). Subtype 6 — a decrease in imaginary beta-1 coherence between the left central and right anterior temporal cortex (C3-F8), explained part of the depression with phobic and hypochondriacal disorders in the structure of recurrent depressive disorder. Such a clinical and biological typology seems new and promising in terms of searching for specifi c neurophysiological disorders in different types of depression and, accordingly, reaching differentiated therapeutic recommendations.
Background: The neuronal correlates of depression with mixed traits (according to DSM-5) at rest have not been studied. Objective: to determine the indicators of imaginary coherence of EEG-rest, which distinguish patients with depression with mixed features (according to DSM-5) from patients with depression without mixed features and healthy subjects, and also to trace the dependence of the identified neurophysiological characteristics on the diagnostic belonging of the symptom complex to bipolar II type or recurrent depressive disorder. Patients and methods: on a background free from drug therapy, 80 patients with depression with mixed features (XD; n = 40 — with bipolar II disorder (XB) and n = 40 — with recurrent depressive disorder (XR)), 80 patients with depression without mixed traits (TD; n = 40 — for bipolar II type (TB) and n = 40 — for recurrent depressive disorder (TR), as well as 80 healthy subjects (N). The study groups were matched by sex and age. The study used clinical-psychopathological, psychometric, neurophysiological and statistical research methods. According to the Kruskal–Wallis criterion for independent samples the parameters of imaginary coherence (modulo) of standard frequency ranges (delta (δ) — 0.5–4 Hz, theta (θ) — 4–8 Hz, alpha (α) — 8–13 Hz, beta-1 (β1) — 13–20 Hz, beta-2 (β2) — 20–30 Hz, gamma (γ) — 30–45 Hz) between pairs of 14 cutaneous standard EEG derivations (according to the “10–20” system) in three (XD, TD and N), and then in five (XB, XR, TB, TR and N) comparison groups. Post-hoc analysis was performed using the U-test. The significance level was adjusted according to the Bonferroni correction. Results: three indicators were identified: α-ICoh(C3–P4), β1-ICoh(C3–P3) and β2-ICoh(F3–C4). For all three parameters, the H-test values for the “Group” factor (n = 3 and n = 5) were highly significant. In this case, α-ICoh(C3– P4) — XD = TD, XD < N, TD < N; β1-ICoh(C3–P3) — XD < TD, XD < N; TD < N; β2-ICoh(F3–C4) — XD > TD; XD > N, TD > N. The groups of patients with XD within the framework of recurrent depressive and bipolar II disorders significantly differed in terms of β1- ICoh(C3–P3) — XR > XB. At the level of statistical trends, in type II bipolar disorder — XB > TB according to α-ICoh(C3–P4), and in recurrent depressive disorder — XR > TR according to β2-ICoh(F3–C4). Conclusion. Thus, depression with mixed features can be considered in terms of dysfunctional interactions of the left frontal, bilateral central and parietal cortical zones, depending on the diagnostic affiliation of the depressive symptom complex and reflecting violations of automatic and voluntary regulation of affect, cognitive and behavioral changes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.