Trials

In the years after 1980, drug trials departed increasingly from the concept of treating real patients. Clinical trials accompanied psychopharmacology as a basic means of gathering evidence in the field, but they also served as the premier means of evasion and distortion used fraudulently and covertly to corrupt the evidence base of psychopharmacology. The fundamental problem in running clinical trials of depression treatments was that the “patients” were considered heterogeneous or “fantasy patients” who really had nothing. Leo Hollister recommended that depression trials be confined to patients with serious or “endogenous” depression, who were the minority of patients encountered in clinical practice.

Validation of the Wistar-kyoto Rat Kept in Solitary Housing as an Animal Model for Endogenous Depression Using Voxel-based Morphometry

Major depressive disorder is a common psychiatric condition that is often resistant to medication. The Wistar-Kyoto (WKY) rat has been suggested as an animal model of endogenous depression; however, it is challenging to translate results obtained in animal models into humans. Solitary housing is a mild stress paradigm that could simulate the environment of depressive patients with limited social activity due to symptoms. We used voxel-based morphometry to directly compare the solitary-housed WKY rat model with data from previous human studies, and validated our results with behavioural studies and correlation analyses. Atrophy in WKY rats was detected in the ventral hippocampus, caudate putamen, lateral septum, cerebellar vermis, and cerebellar nuclei (p < 0.05, corrected for family-wise error rate). Further, locomotor behaviour was negatively correlated with hippocampal atrophy and positively correlated with atrophy of the cerebellar vermis. The regions of brain atrophy validate WKY rats as an animal model for endogenous depression and can aid the translation of study results to humans. Our study also reveals the possibility of a cerebellar contribution to depression.

Serotonin, Sleep and Depression: A Hypothesis

For most cases of endogenous depression (major depression), the hypothesis of monoamine deficiency, despite a number of limitations it faces, is still considered the most acceptable explanation. The main difficulty faced by this hypothesis is the reason for the decrease in the level of cerebral monoamines (primarily serotonin) during depression. It is assumed either increased activity of the MAO enzyme, which metabolizes serotonin, or a mutation with the loss of function of the gene of the Tph-2 enzyme, which synthesizes serotonin, as possible causes. In this review, a third cause is proposed, which can explain a number of cases of «spontaneous» onset of depressive symptoms in apparently healthy people, as well as links the hypotheses of “monoamine deficiency” and “disturbances in circadian rhythms.” It is assumed that the formation of endogenous depression is due to a combination of two factors: a reduced “basal” level of cerebral serotonin and excessively long pre-morning periods of REM sleep, during which the release of cerebral monoamines stops altogether. As a possible way to of non-drug treatment of depression, not deprivation, but fragmentation of this phase of sleep is suggested, that is much easier for patients to tolerate.

Youth Chronic Endogenous Depression in Disorders of the Affective and Schizophrenic Spectrum

Background: chronic endogenous depression in youth has a number of features associated with their severe atypia, work and social maladjustment, deterioration in the quality of life, high risk of suicidal and self-injurious behavior, difficulties in choosing therapy, difficulty in diagnosis and nosological evaluation. Until now, no special research has been done on chronic endogenous depression among young people of this age.Purpose of research: to identify psychopathological features and dynamics of endogenous depression developed in youth, to work out a clinical typology. Patients: 62 young patients (16–25 years old) were clinically and psychopathologically examined, who were first admitted to FSBSI MHRC, within the period of 2017 to 2020 suffering from chronic endogenous depression state for more than two years. Clinically significant somatic, neurological, and mental pathology defined the criteria for exclusion.Methods: for the research the clinical-psychopathological and psychometric methods were used. The patients were examined by the psychometric method upon admission to the hospital and at the stage of reduction of psychopathological disorders upon discharge: the HDRS, SANS and SOPS scales included.Results and conclusion: the clinical picture of youth chronic endogenous depression is characterized by pronounced polymorphism, atypia, erosion of the thymic component, and the dominance of negative affectivity. Based on the analysis of psychopathological characteristics of endogenous depression in youth, two typological varieties were identified: unitary depressions (type I) and supplementary depressions (type II). Among the type II depressions, 2 subtypes were distinguished: with neurosis-like disorders and with psychopathic-like disorders.

Features of the Interaction of Cognitive Functions with the Work of the Magnocellular and Parvocellular Systems in Patients with Schizophrenia and Endogenous Depression.

The article presents a study devoted to the study of cognitive dysfunctions in patients with schizophrenia and endogenous depression in their relationship with the functioning of the magnocellular and parvocellular systems. Mismatch in the work of neural systems leads to violations of the integrity of visual perception and to a violation of the selectivity of thinking in endogenous patients, which makes it difficult to assess and select meaningful, essential information in the formation of judgments. 60 patients with schizophrenia (43 (75%) male and 17 (25%) female; mean age ― 34.0±12.0 years) and 25 patients with endogenous depression (11 (44%) male and 14 (56%) female, mean age ― 38.0±13.6 years) with the use of psychophysiological (the method of visocontrastometry with an assessment of the contrast sensitivity of the visual system, the method of assessing the noise immunity of the visual system) and experimental psychological methods (Trial-Making test by Reitan, Memorizing 10 words, Poppelreiter's figures, Incomplete images, Excluding the 4th superfluous). The established features of cognitive dysfunctions in endogenous depression and schizophrenia are associated with the features of the functional state of the magnocellular and parvocellular neuronal systems and the nature of the interaction of these systems. The specificity of impairments in cognitive functions in patients with endogenous depression is due to changes in the dynamic component of cognitive activity, while the specificity of impairments in cognitive functions in patients with schizophrenia is associated with changes in the selectivity of information and early sensory defects. The data obtained make it possible to develop an idea of the profiles of sensory-cognitive impairments in endogenous depression and schizophrenia, which is of particular importance for differential diagnosis.

Contemporary approaches to correction of cognitive impairment in endogenous depression

Cognitive dysfunction is one of the basic symptoms of endogenous depression, gaining much of the researchers’ interest lately. It is observed at the initial stage, at the peak intensity of depressive symptoms and even after their reduction, which leads to the persistence of residual depressive state. Cognitive impairment during the depressive episode can be detected by objective methods (clinical and neuropsychological), and their subjective importance is being revealed by standardized questionnaires. Depressed patients show lower results in executive functions, working memory, reaction speed, verbal learning, immediate and delayed recall subtests of neuropsychological batteries. There are few pharmacological agents (mostly antidepressants) with well-proven procognitive activity in depression. Besides, some new pharmacological and non-pharmacological approaches for treatment of cognitive impairment in depression have appeared lately and are described in literature as promising.

Neuropsychological Profile of Endogenous Depressions with Overvalued Ideas

Objective: the article presents the results of a study of the neuropsychological profile of cognitive functions in patients with endogenous depression, in the structure of which overvalued formations are revealed. The study of cognitive processes in patients with such disorders will help determine prognostic criteria and contribute to the development of optimal recommendations for personalized therapy of these conditions.The aim of the study was to determine the characteristics of cognitive functioning and its dynamics in patients with endogenous depression with overvalued formations.Patients and methods: using clinical-psychometric, neuropsychological, pathopsychological methods, 45 patients were examined. 26 men (average age 28.7 ± 7.3) and 19 women (average age 34 ± 8.6) had a manifest or repeated depressive state within the framework of an affective disease (F31-34 according to ICD-10) with the phenomenon of overvalued formations. The control group was represented by a similar in number, comparable in terms of sex and age group of patients (45 patients) with a depressive state that forms within the affective phase (F31-34 according to ICD-10), without overvalued formations.Results: in the course of the work, differences were found in the structure of the neurocognitive deficit of endogenous depression with overvalued formations from that of depressions without the phenomenon of overvalued formations. As a result of neuropsychological screening of patients in the group of endogenous depressions with overvalued formations, data were obtained on dysfunction of the anterior sections of the predominantly left hemisphere and related regulatory deficiency. Conclusions: patients with endogenous depressions occurring with a predominance of overvalued formations in the clinical, a neurocognitive deficiency of the regulatory domain is characteristic, which is different from that in depressions without the phenomenon of overvalued formations.