[Structural brain changes in patients with temporal lobe epilepsy and comorbid depression]. / Strukturnye izmeneniya golovnogo mozga u patsientov s visochnoi epilepsiei i komorbidnoi depressiei.

OBJECTIVE: To assess the morphological features of the brain structures in patients with temporal lobe epilepsy and comorbid depression. MATERIAL AND METHODS: From 1 January 2017 to 31 December 2020, we studied 80 patients with temporal lobe epilepsy (aged 18-60 years, 38 of whom had comorbid depression) and 48 healthy subjects of comparable age. Magnetic resonance imaging (MRI) of the brain was performed using the epilepsy protocol in a scanner with a magnetic field strength of 1.5 T. Focal temporal lobe epilepsy was diagnosed by neurologists (epileptologists) specialising in epilepsy according to the International League Against Epilepsy (ILAE) classification of epilepsy. Psychiatrists assessed the presence and severity of depressive disorders by clinical interview and by participants' scores on the Beck Depression Inventory (BDI-II). MRI data were processed using FreeSurfer 6.0 software to determine volumes of subcortical structures and thicknesses of cortical structures. At the group level, analysis of covariance with Holm-Bonferroni correction was used as the statistical method. RESULTS: Morphometric analysis revealed a significant decrease in the volume of the thalamus bilaterally and the brain stem and an increase in the volume of the choroid plexus in the left hemisphere, as well as a significant decrease in the thickness of the entorhinal cortex, temporal pole and isthmus of the cingulate gyrus in the left hemisphere and middle temporal gyrus and inferior temporal gyrus in the right hemisphere in patients with epilepsy compared to healthy controls. No association was found between the presence of depression and significant structural changes on MRI. CONCLUSION: The data obtained suggest an effect of temporal lobe epilepsy, but not comorbid depression, on the morphology of brain structures.

[Apathy in depression: a morphometric analysis]. / Apaticheskaia depressiia: morfimetricheskii analiz.

AIM: To study structural correlates of apathy in patients with late-life depression. MATERIAL AND METHODS: Thirty-five patients (≥60 y.o.) with late-onset depression and 22 age-matched healthy volunteers underwent high resolution brain MRI-scanning, and a comprehensive neuropsychiatric examination including HAM-D and the Apathy Scale. RESULTS AND CONCLUSION: A morphometric analysis showed that apathy was associated with atrophy of the lateral prefrontal cortex and reduced grey matter volume of the caudate nucleus on the right, and the nucleus accumbens on the left. Depression correlated with reduced thickness of the medial orbitofrontal cortex bilaterally, rostral anterior cingulate gyrus on the left, isthmus cingulate gyrus on the right, and larger surface area of the entorhinal cortex. Total grey matter volume, grey/white matter volumes of the cerebellum, and cortical thickness in temporal and occipital regions were negatively correlated with both apathy and depression severity. Thus, atrophy of basal ganglia and lateral prefrontal cortex, well known neuroanatomical correlates of apathy in different psychiatric and neurological conditions, characterized it in late-life depression too. This supports the idea of independent pathophysiology of apathetic syndrome.

[Patterns of brain functional connectivity in frontal and temporal lobe epilepsies]. / Patterny funktsional'noi konnektivnosti mozga pri visochnoi i lobnoi épilepsii.

AIM: To examine alterations of functional connectivity (FC) of the brain in patients with frontal and temporal lobe epilepsies. MATERIAL AND METHODS: Forty-three patients, aged 18-55 years, including 32 with temporal lobe epilepsy (TLE) and 11 with frontal lobe epilepsy (FLE), and 32 age/gender-matched healthy controls (HC) underwent structural and functional MRI on 1,5 T scanner. Imaging data were further analysed for functional connectivity characteristics by seed-based and ICA analyses. RESULTS: Most prominent in the TLE group, was a decrease in FC of insula and peri-insular cortical regions compared to HC. These alterations of FC in left-side TLE were significant on the left. An increase of FC between dorsal part of attention resting network and regions of temporal and parietal cortices characterized right-side TLE. In addition, TLE group had decreased FC between anterior cingulate and basal ganglia. All the significant alterations of FC in FLE related to increased FC in patients compared to HC. FC of temporal regions was altered to a greater extent. CONCLUSION: Localization and lateralization of seizure focus determines the alterations of brain FC in patients with focal epilepsy.

[Neuronet restructuring in focal and generalized epilepsy according to resting state fMRI]. / Neirosetevye perestroiki pri fokal'noi i generalizovannoi épilepsii po dannym fMRT pokoia.

AIM: To compare neuronet restructuring in focal and generalized epilepsy. MATERIAL AND METHODS: Seventy-seven patients, aged from 18 to 65 years, with the diagnosis of epilepsy, including 63 patients with focal epilepsy and 14 with generalized epilepsy, were examined. A control group included 23 healthy people. Neuronet restructuring was studied using fMRI. RESULTS AND CONCLUSION: According to resting state fMRI, there were between-group differences in spatial organization (activity map) of the brain structures as well as in the results of cross-correlation analysis of interaction maps of resting-state networks. It has been concluded that functional restructuring in connectomes in focal and generalized epilepsy have the opposite patterns of disorganization (toward increase or decrease) in most structures studied though there are structures with the same direction of connectivity changes.

[Clinical and neurovisualization characteristics of apathetic depression]. / Klinicheskie i neirovizualizatsionnye kharakteristiki apaticheskoi depressii.

AIM: To study apathetic depression first diagnosed at late age and identify its relation to cognitive and social dysfunction as well as to morphological and functional changes in the brain. MATERIAL AND METHODS: Thirty-two patients at the age above 60 years with newly diagnosed depressive episode and 15 healthy age-matched volunteers were included in the study. All patients were divided into two groups by the score on the Apathy scale (AS): >14 - depression with apathy (n=21), <14 - depression without apathy (n=11). Patients were examined using psychometric methods (HAMD, GDS, AS, SHAPS, SF-36, MoCA-test), neuroimaging (MRI scanner with a magnetic field strength of 1.5 Tesla - EXCEL ART Vantage Atlas-X, Toshiba, Japan) and statistical data analysis. RESULTS AND CONCLUSION: Apathy component in clinical depression reflects a tendency towards the increase in depression severity and cognitive deterioration that results in the substantial lowering of quality of life and correlates with cerebrovascular changes, decrease in gray and white matter volume and mean cortical thickness of large hemispheres.

Intracortical microinjections may cause spreading depression and suppress absence seizures.

Intracerebral microinjection is a commonly used technique for local delivery of biologically active agents. However, it is known that mechanical injury of the cortex can induce spreading depression (SD), a wave of transient cellular depolarization. We examined the effects of intracortical microinjections of a new selective I(h) channel antagonist ORG 34167 and of different control treatments (saline and sham microinjections) on spontaneously occurring spike-wave discharges (SWDs) in WAG/Rij rats, a valid genetic model of absence epilepsy. Electroencephalographic (EEG) recording in awake rats has shown that both the drug and control microinjections are followed by long-term (for more than an hour) suppression of SWDs. dc-EEG recording in WAG/Rij rats has revealed that sham microinjections induce SD in 65% (31/48) cases. Number of SWDs decreased substantially for at least 90 min after the sham injections which induced cortical SD but remained unchanged if SD was not triggered by microinjection. These findings suggest that SD induced by intracortical microinjection may contribute to long-term suppression of non-convulsive epileptic activity after this experimental procedure.