Motor Retardation Research Articles

Homocysteine in Schizophrenia: Independent Pathogenetic Factor with Prooxidant Activity or Integral Marker of Other Biochemical Disturbances?

A wide range of studies have demonstrated that hyperhomocysteinemia is associated with the risk of schizophrenia, but currently available assumptions about the direct involvement of homocysteine (Hcy) in the pathogenesis of schizophrenia are hypothetical. It is possible that in vivo Hcy is only a marker of folate metabolism disturbances (which are involved in methylation processes) and is not a pathogenetic factor per se. Only one study has been conducted in which associations of hyperhomocysteinemia with oxidative stress in schizophrenia (oxidative damage to protein and lipids) have been found, and it has been suggested that the oxidative stress may be induced by the elevated Hcy in schizophrenic patients. But the authors did not study the level of reduced glutathione (GSH), as well as possible causes of hyperhomocysteinemia—disturbances of folate metabolism. The aim of this work is to analyze the association of Hcy levels with the following: (1) redox markers in schizophrenia GSH, markers of oxidative damage of proteins and lipids, and the activity of antioxidant enzymes in blood serum; (2) with the level of folate and cobalamin (В12); and (3) with clinical features of schizophrenia measured using the Positive and Negative Syndrome Scale (PANSS). 50 patients with schizophrenia and 36 healthy volunteers, matched by sex and age, were examined. Hcy in patients is higher than in healthy subjects (p = 0.0041), and this may be due to the lower folate level in patients (p = 0.0072). In patients, negative correlation was found between the level of Hcy both with the level of folate (ρ = −0.38, p = 0.0063) and with the level of B12 (ρ = −0.36, p = 0.0082). At the same time, patients showed higher levels of oxidative modification of serum proteins (p = 0.00046) and lower catalase (CAT) activity (p = 0.014). However, Hcy is not associated with the studied markers of oxidative stress in patients. In the group of patients with an increased level of Hcy (>10 μmol/l, n = 42) compared with other patients (n = 8), some negative symptoms (PANSS) were statistically significantly more pronounced: difficulty in abstract thinking (N5, p = 0.019), lack of spontaneity and flow in conversation (N6, p = 0.022), stereotyped thinking (N7, p = 0.013), and motor retardation (G7, p = 0.050). Thus, in patients with schizophrenia, hyperhomocysteinemia caused by deficiency of folate and B12 is confirmed and can be considered a marker of disturbances of vitamin metabolism. The redox imbalance is probably not directly related to hyperhomocysteinemia and is hypothetically caused by other pathological processes or by an indirect effect of Hcy, for example, on the enzymatic antioxidant defence system (CAT activity), which requires further exploration. Further study of the role of Hcy in the pathogenesis of schizophrenia is relevant, since the proportion of patients with hyperhomocysteinemia is high and correlations of its level with negative symptoms of schizophrenia are noted.

Protective Effect of Butylphthalide on Neuronal Apoptosis in Parkinson Rats and Its Effect on miR-146a-5p Expression and Phosphatidylinositide 3-Kinases/Protein Kinase B Pathway

80 male Wistar rats were stochastically assigned to Sham + Vehicle group, Sham + BUT group, PD + Vehicle group and PD + BUT group. Rotenone PD model rats were prepared by subcutaneous injection of rotenone sunflower oil emulsion 2 mg/(kg · d) for 5 consecutive weeks. Butylphthalide 80 mg/(kg · d) were given to the rats in Sham + BUT group and PD + BUT group by gavage from the first day of rotenone injection for 5 weeks. Subsequently, the motor retardation ability and the morphological changes of the substantia nigra (SN) of each group were evaluated. Meanwhile, the levels of neuronal injury, apoptosis, inflammation and oxidative stress in each group of rats were assayed. The impact of BUT treatment on miR-146a-5p expression and PI3K/AKT signal pathway in rat brain tissue was assayed. Finally, by constructing a PD cell model of the neurotoxin 6-hydroxydopamine (6-OHDA)-treated human neuroblastoma cell line SH-SY5Y, the in vitro anti-PD pharmacological effect of BUT was further verified.

A Case of Pica with Motor-Mental Retardation and with Foreign Bodies in the Larynx and Gastrointestinal Tract: Autopsy Results and Current Literature Review

A Case of Pica with Motor-Mental Retardation and with Foreign Bodies in the Larynx and Gastrointestinal Tract: Autopsy Results and Current Literature Review

Clinical and genetic analysis of six Chinese children with Poirier-Bienvenu neurodevelopmental syndrome caused by CSNK2B mutation.

Mutations in CSNK2B lead to Poirier-Bienvenu neurodevelopmental syndrome (POBINDS), a rare neurodevelopmental disorder. Only 14 cases of POBINDS have been reported worldwide. The main manifestations are seizures, often tonic-clonic, with or without intellectual disability, growth retardation, and developmental language retardation. We conducted a comprehensive phenotypic mining and trio-whole exome sequencing on six children with POBINDS for gene diagnosis and analyzed the different variants using bioinformatics analysis software and related experiments. This paper reviews previous literature and discusses two common missense variants that lead to structural changes. Among the six patients, four, one, and one had tonic-clonic, myoclonic, and febrile seizures, respectively. Language development disorder, motor development disorder, and developmental delay/intellectual disability (DD/ID) are the main clinical features. All children had de novo mutations in CSNK2B, including three missense variants (c.410G > T/p.(Cys137Phe), c.494A > G/p.(His165Arg), and c.3G > A/p.(Met1Ile)), two splice variants (c.292-2A > T, c.558-3T > G), and one frameshift variant (c.499delC/p.(Leu167Serfs*60)). Three missense variants were predicted to be harmful by various software programs, and two splicing variants were found to produce new exonic splicing enhancers by the minigene assay. Western blot analysis showed that the frameshift variant resulted in decreased protein expression. According to a literature review, c.3G > A/p.(Met1Ile), c.292-2A > T, c.558-3T > G, and c.499delC/p.(Leu167Serfs*60) are novel variants of CSNK2B. The decrease or loss of protein function caused by CSNK2B mutations may be a pathogenic factor in this cohort. The severity of the POBINDS phenotype differs, and refractory epilepsy may be accompanied by a more serious DD/ID, language disorder, and motor retardation. At present, there is no specific treatment, and antiepileptic therapy usually requires the combination of two or more anti-epileptic drugs.

A case of 15q11‐q13 duplication syndrome and literature review

BackgroundThe chromosomal 15q11‐q13 regions are structurally complex, and their abnormalities are associated with various neuropsychiatric disorders, including autism spectrum disorder (ASD), epilepsy, Angelman syndrome, and Prader–Willi syndrome.Case descriptionA 6‐year‐old child was admitted to the hospital as a result of an “epileptic status” showing ASD, intractable epilepsy, and total developmental retardation. Chromosome gene detection showed repetitive variation in the 15q11‐q13 regions, and the video electroencephalogram was abnormal. Although children are currently given antiepileptic treatment and rehabilitation training, intermittent seizures can still occur.ConclusionThe clinical phenotypes of 15q11‐q13 repetitive syndrome are complex, and vary in severity. Children with intractable epilepsy, ASD, and language and motor retardation should be considered to have this syndrome, which requires confirmation by multiplex ligation‐dependent probe amplification and gene detection. These approaches can enable early rehabilitation treatment and improve the patients’ quality of life.

Dosage escalation of antenatal steroids in preterm twin pregnancies does not improve long-term outcome.

To analyze long-term effects of antenatal betamethasone (≤16mg, =24mg and >24mg) in preterm twins on infant and childhood morbidity. Retrospective cohort study among 198 preterm twins. Three follow up time points, including a total of 84 outcomes, were evaluated: first neonatal examination after birth and in the neonatal period up to 10days after birth using data from the clinic charts; examination from the 21st to the 24th month of life and examination from the 60th to the 64th months, using data from copies of the children's examination booklets sent back by the parents. Dosage-dependent and sex-specific long-term effects of antenatal betamethasone treatment on neonatal, infant and early childhood development and morbidity up to 5.3 years of age were analyzed. Dosage escalation of >24mg was not associated with improved neonatal, infant or early child hood outcome, independent of twin pair structure. In contrast, higher doses >24mg were significantly linked to increased rates of congenital infections (OR 5.867, 95% CI 1.895-18.167). Male sex as a factor was obvious for lower rates of apnea-bradycardia-syndrome in neonates, higher rates ofno free steps after 15months in infancy and highest rates of motor clumsiness in early childhood. Betamethasone dosage escalation >24mg in twins born between 23+5 and 33+6 weeks of gestation did not improve neonatal, infant or early childhood morbidity. In contrast, higher doses >24mg total dose resulted in significantly higher rates of congenital infections and are not recommended. For males, 24mg betamethasone appears to be the preferable dose.

Motor Abnormalities, Depression Risk, and Clinical Course in Adolescence

BackgroundMotor abnormalities, such as psychomotor agitation and retardation, are widely recognized as core features of depression. However, it is not currently known whether motor abnormalities connote risk for depression. MethodsUsing data from the Adolescent Brain Cognitive Development (ABCD) Study, a nationally representative sample of youth (N = 10,835, 9–11 years old), the present paper examines whether motor abnormalities are associated with 1) depression symptoms in early adolescence, 2) familial risk for depression (familial risk loading), and 3) future depression symptoms. Motor abnormality measures included traditional (DSM) motor signs such as psychomotor agitation and retardation as well as other motor domains such as developmental motor delays and dyscoordination. ResultsTraditional motor abnormalities were less prevalent (agitation = 3.2%, retardation = 0.3%) than nontraditional domains (delays = 13.79%, coordination = 35.5%) among adolescents. Motor dysfunction was associated with depression symptoms (Cohen’s d = 0.02 to 0.12). Familial risk for depression was related to motor abnormalities (Cohen’s d = 0.08 to 0.27), with the exception of motor retardation. Family vulnerability varied in sensitivity to depression risk (e.g., retardation: 0.53%; dyscoordination: 32.05%). Baseline endorsement of motor abnormalities predicted future depression symptoms at 1-year follow-up. ConclusionsThese findings suggest that motor signs reflect a novel, promising future direction for examining vulnerability to depression risk in early adolescence.

Toxoplasmosis Is More Frequent in Schizophrenia Patients Than in the General Population in Mexico and Is Not Associated with More Severe Course of Schizophrenia Measured with the Brief Psychiatric Rating Scale.

Toxoplasmosis is a disease, which was discovered in 1908, caused by the intracellular parasite Toxoplasma gondii. T. gondii infects neuronal, glial, and muscle cells, and chronic infections are characterized by the presence of cysts, in the brain and muscle cells, formed by bradyzoites. T. gondii is capable of synthesizing L-DOPA, a precursor of dopamine. Dopamine is a neurotransmitter that is key in the etiology of neuropsychological disorders such as schizophrenia. Previous studies have shown high levels of IgG Toxoplasma antibodies in schizophrenia patients. Many published studies show that the prevalence of toxoplasmosis is higher in schizophrenia patients. In this study, we aimed to identify the prevalence of Toxoplasma infection in patients with schizophrenia and the relationships between, sociodemographic factors and the Brief Psychiatric Rating Scale. A total of 27 schizophrenic patients were included and IgG anti-T. gondii was determined in serum samples by ELISA. The Brief Psychiatric Rating Scale, sociodemographic factors were associated with seropositivity. We found that the prevalence of Toxoplasma antibodies was 51.7%. In the Brief Psychiatric Rating Scale, statistical significant association (p = 0.024) was found in Item 13 which is related to motor retardation, however, the association turned non-significant after of correction for multiple tests or after of analyzed with a logistic regression p = 0.059, odds ratio (OR) = 2.316 with a 95% confidence interval [0.970 to 5.532]. Other association was not found between toxoplasmosis and others factors. The prevalence of toxoplasmosis on our population under study was significantly higher than that reported by general population or other group of Mexican schizophrenia patients.

Clinical and molecular findings in 37 Turkish patients with isolated methylmalonic acidemia

Background/aim Isolated methylmalonic acidemia (MMA) is caused by complete or partial deficiency of the enzyme methylmalonyl-CoA mutase (mut0 or mut– enzymatic subtype), a defect of its cofactor adenosyl-cobalamin (cblA, cblB, or cblD-MMA), or deficiency of the enzyme methylmalonyl-CoA epimerase. While onset of the disease ranges from the neonatal period to adulthood, most cases present with lethargy, vomiting and ketoacidosis in the early infancy. Major secondary complications are; growth failure, developmental delay, interstitial nephritis with progressive renal failure, basal ganglia injury and cardiomyopathy. We aimed to demonstrate clinical and molecular findings based on long-term follow up in our patient cohort. Materials and methods The study includes 37 Turkish patients with isolated MMA who were followed up for long term complications 1 to 14 years. All patients were followed up regularly with clinical, biochemical and dietary monitoring to determine long term complications. Next Generation Sequencing technique was used for mutation screening in five disease-causing genes including; MUT , MMAA , MMAB , MMADHC , MCEE genes. Mutation screening identified 30 different types of mutations. Results While 28 of these mutations were previously reported, one novel MMAA mutation p.H382Pfs*24 (c.1145delA) and one novel MUT mutation IVS3+1G>T(c.752+1G>T) has been reported. The most common clinical complications were growth retardation, renal involvement, mental motor retardation and developmental delay. Furthermore, one of our patients developed cardiomyopathy, another one died because of hepatic failure and one presented with lactic acidosis after linezolid exposure. Conclusion We have detected two novel mutations, including one splice-site mutation in the MUT gene and one frame shift mutation in the MMAA gene in 37 Turkish patients. We confirm the genotype-phenotype correlation in the study population according to the long-term complications.

A COMPARATIVE STUDY OF PHENOMENOLOGY BETWEEN EARLY ONSET AND LATE ONSET PSYCHOSIS

Introduction: Phenomenology is the study of subjective experience. Psychiatric diagnoses are based on cross-sectional psychopathological features, for example, the presence of rst-rank symptoms in the case of schizophrenia. Phenomenological investigation focuses on the form of experience, i.e. the way in which the content is experienced, while the content itself is of secondary importance. This study was conducted to investigate the subtle differences between early-onset group (onset before 18 years of age) and late onset (onset after age of 40 years). Aim And Objectives: To study the socio-demographic prole and phenomenology of early onset psychosis and late onset psychosis compare them based on the variables studied. It is a cross sectional observational Materials And Methods: study carried out in the Department of Psychiatry, Gauhati Medical College and Hospital during the period of June 2018- May 2019. A semi structured, self designed proforma has been used to collect the socio-demographic data and personal details of the patients and their treatment history. The ICD-10 Classication of Mental and Behavioural Disorders, WHO, 1992, Brief Psychiatric Rating Scale (BPRS) Version 4.0, Modied Kuppuswamy Socio-economic status scale were used along with. All the data that was derived from the study were analyzed by using the software IBM SPSS 21.0. Observations And Results: Mean age of presentation in early onset psychosis is 19.22 years with Standard Deviation ±5.69. Mean age of presentation in early onset psychosis is 54.5 years with Standard Deviation ±11.9. Signicantly higher ratio of male was noted in early onset group and higher ratio of female was noted in that of the late onset group. Somatic concern, anxiety, depression and suspiciousness was signicantly more in late onset psychosis. In comparison to the group of late onset psychosis, self-neglect, blunted affect, emotional withdrawn, motor retardation, motor hyperactivity, mannerisms and posturing were signicantly more in early-onset psychosis. Major distinction was noted in the Conclusion: distribution of delusional disorders and acute and transient psychotic disorders. Age of onset was skewed to late adolescence with more number of male patients. Late onset psychosis group had more uneducated patients with considerable proportion of adults left unmarried in the late onset group. Late onset psychosis group shows predominance of somatic concern, anxiety, depression and suspiciousness in contrast to early onset psychosis group which shows predominance of motor hyperactivity, self-neglect, blunted affect, motor retardation, mannerisms and posturing

Preliminary Evaluation of Phenotypic Features from Clinical Interactions

Clinical interactions are not commonly scored and most result in a clinical progress note. Interactions quantified by instrument scores are liable to training biases, lack of granularity, and enforced phenotypic dimensionality. Measurements derived from speech and facial features have been previously demonstrated to correlate with clinical assessment. Here we evaluate face, gaze, head, and speech features recorded during routine clinical interactions for useful disease state phenotypic information. Clinical interactions were voluntarily recorded from eight inpatient participants over 48 sessions as they progressed from admission to discharge. We used a Zoom Q8 camera and two channel audio. Face action units, head pose, and gaze features were calculated using the OpenFace library1,. Acoustic, prosodic, and linguistic features were extracted using common software tools (e.g. Praat, Opensmile, GloVe, LIWC). We evaluated the results of four algorithms (Support vector, Lasso, Ridge, and Linear regression) to infer several Brief Psychiatric Rating Scale (BPRS) sub-scores using a 10-fold cross-validation approach. In addition, we visually explored the feature space for phenotypic subtypes and potential response to treatment. From face, gaze, and head movement features we predicted non-zero BPRS depressive mood scores with accuracy of .93 and inferred BPRS depressive mood, blunted affect and motor retardation subscores with Pearson coefficients of (.78, .82, and .76). Participant feature data plotted longitudinally exposes subtle changes in objective measures humans would find difficult to identify from memory. We demonstrate the range of objective digital features that can be generated in the normal course of a relatively brief, unstructured clinical interactions and correlate these objective features with subjective clinical ratings and patient trajectories. (DB) NIH T32 MH019961, (DB) R25 MH071584.

Novel bi-allelic variants expand the SPTBN4-related genetic and phenotypic spectrum

Neurodevelopmental disorder with hypotonia, neuropathy, and deafness (NEDHND, OMIM #617519) is an autosomal recessive disease caused by homozygous or compound heterozygous variants in SPTBN4 coding for type 4 βIV-spectrin, a non-erythrocytic member of the β-spectrin family. Variants in SPTBN4 disrupt the cytoskeletal machinery that controls proper localization of ion channels and the function of axonal domains, thereby generating severe neurological dysfunction. We set out to analyze the genetic causes and describe the clinical spectrum of suspected cases of NEDHND. Variant screening was done by whole exome sequencing; clinical phenotypes were described according to the human phenotype ontology, and histochemical analysis was performed with disease-specific antibodies. We report four families with five patients harboring novel homozygous and compound heterozygous SPTBN4 variants, amongst them a multi-exon deletion of SPTBN4. All patients presented with the key features of NEDHND; severe muscular hypotonia, dysphagia, absent speech, gross motor, and mental retardation. Additional symptoms comprised horizontal nystagmus, epileptiform discharges in EEG without manifest seizures, and choreoathetosis. Muscle histology revealed both characteristics of myopathy and of neuropathy. This report expands the SPTBN4 variant spectrum, highlights the spectrum of morphological phenotypes of NEDHND-patients, and reveals clinical similarities between the NEDHND, non-5q SMA, and congenital myopathies.

Early-onset familial Alzheimer's disease in a family with mutation of presenilin 2 gene.

Alzheimer's disease (AD) is the most common senile neurodegenerative disease characterized by progressive cognitive dysfunction, psychological and behavioral abnormalities, and impaired ability of activities of daily living. A family with a total of 3 patients were admitted to the Department of Neurology of Xiangya Hospital, Central South University in 2018. The proband showed memory decline as the presenting symptoms, and subsequently showed psychological and behavioral abnormalities, personality changes, seizures, and motor retardation. Definite diagnosis of early-onset familial AD (EOFAD) with missense mutation of presenilin 2 (PSEN2) (c.715A>G p.M239V) was established by whole exome sequencing (WES) technology. We reported the mutation in Chinese Han population for the first time, which expanded the mutation spectrum ofPSEN2 gene and aid to enrich the characterization of clinical phenotype in EOFAD associated to PSEN2 mutations. Patients with early onset age and complex clinical manifestations of AD can be diagnosed with the help of genetic testing to avoid misdiagnosis.

Clinical Features in Patients with Xq23 Microdeletion: A Case Report and Literature Review

Xq22.3-q23 microdeletion is a rare genomic disorder. The purpose of this study was to emphasize the correlation between clinical phenotype and genotype of proximal deletion on chromosome Xq22.3-q23. A 5 years old boy had a 671 KB microdeletion on Xq23 by chromosomal microarray analysis, including AMMECR1 and CHRDL1 genes. He presented with microsomia, midface hypoplasia, right kidney dysplasia and mildly motor retardation, which have not previously been reported in relation to Xq23 deletion. To the best of our knowledge, this is the first case with Xq23 microdeletion. A total of nine cases with microdeletion at Xq22.3-q23 affecting AMMECR1 and two cases with CHRDL1 mutation were reviewed. This review showed that Xq23 microdeletion with microsomia, midface hypoplasia, kidney dysplasia, and mild motor retardation was rare. The previous literature showed two novel point mutations in AMMECR1 and CHRDL1 with some phenotype difference from the presented case. Xq23 microdeletion should be considered for patients with microsomia, midface hypoplasia, kidney dysplasia and growth retardation.

Coexistence of Severe Acute Respiratory Syndrome-Coronavirus-2 and Human Metapneumovirus in a Child with Severe Pneumonia

Coronavirus disease-2019 (COVID-19) is a respiratory system disease caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). In cases with COVID-19 pneumonia, other respiratory viral agents may be simultaneously present. An 11-monthold male patient diagnosed with hydrocephalus, epilepsy and mental-motor retardation was referred to our hospital with fever, cough, and vomiting. The nasopharyngeal swab sample was positive for SARS-CoV-2 and human metapneumovirus. The patient's respiratory distress increased on the third day of the follow-up, and hydroxychloroquine sulfate was added to his treatment. On day 11 of follow-up, based on the deteriorating general condition of the patient and increased acute phase reactants, sepsis secondary to nosocomial infection was considered. Acinetobacter baumannii growth was seen in the blood culture. After antibiotic treatment, the patient's clinical condition improved. Our findings support the idea that COVID-19 can be severe in young children when it coexists with viruses that cause other respiratory tract infections.

ВЗАИМОСВЯЗЬ ИНТЕРНЕТ-ЗАВИСИМОГО ПОВЕДЕНИЯ, ИНТЕЛЛЕКТУАЛЬНОГО РАЗВИТИЯ И КУЛЬТУРНОЙ КОНГРУЭНТНОСТИ У ДЕТЕЙ МЛАДШЕГО ШКОЛЬНОГО ВОЗРАСТА

The main purpose of our study was to examine the connection between the Internet addiction in junior school children and their intellectual development and cultural congruence. The study involved 92 schoolchildren from Moscow aged from 9 to 10 years. Our hypothesis was that intellectual abilities of schoolchildren would be related to their cultural congruence, as well as to their Internet dependent behavior. The following methods were used to test the hypothesis: Raven Progressive Matrices, the children's version of Personality Factor Questionnaire by R. Cattell, Chen Internet Addiction Scale, Methodology of determining the cultural congruence of a junior school child by Bayanova and co-authors. The results demonstrated that schoolchildren with good intellectual abilities are highly likely to demonstrate high rates of cultural congruence. At the same time, the study found no statistically significant differences in intellectual development between children with propensity to Internet addiction and children with any Internet addiction. At the same time, it identified significant features in behavior of children prone to online addiction. The behavior of such children is often manifested in demonstrating violations of the regulatory situation at school, as well as in displaying non-congruent behavior; in particular, such children are more likely to tell lies, do not listen to teachers, are late for classes, skip classes, and fight. Besides, such students are characterized by more pronounced impulsiveness and motor retardation, aggressive assertion of their position, self-confidence, and leadership qualities. The school environment is characterized by normative rules and procedures, so children are not always able to realize their motives and desires openly. Thus, we can conclude that more impulsive and motorized children, who are also characterized by displaying aggressive behaviors, will be more likely to be characterized by a tendency to Internet dependent behaviors, because it allows them to express their desires and intentions, which often cannot be realized in a strictly regulated school environment. In this way, our research has demonstrated that high intellectual abilities of junior school children are significantly related to their cultural congruence. In addition, their propensity for Internet addiction can be a factor contributing to non-congruent behavior among children aged 9–10 years.

Культура самокорекції сценічного стресу (на основі науково-методичного проєкту «Практичний експериментаріум “Psy & Art”»)

The relevance of the study. With the need to master the overly stressed psychophysiological state of the artist both on the eve and during a public performance, it became necessary to consider a number of important qualities of the performer, such as concentration of attention and self-observation, the state of will and memory, flexibility and stability of the higher nervous system. The problem of self-correction of stage excitement was discussed within the framework of the scientific and methodological project «Practical Experimentarium “PSY & ART ”» – an open discussion of students and teachers of Borys Grinchenko Kyiv University. Despite the fact that the phenomenon of stage stress has been analyzed in many studies, this problem remains relevant. Methodology of research. The fate of the future musician and the content of his training depend on the percentage of loss of quality and skills on the stage and how much the performer owns the pianist’s acting itself. To continue on stage what has been accumulated in the preparatory work for a creative take-off at a concert, to show your maximum result, significantly exceeding those «approximations» that were achieved at rehearsals – this is the nature of the creative process, that is, the desire to come to something new for yourself, to the top. Motor activity (sensitiveness and controllability of each joint), massage (muscle relaxation), auto-training, breathing exercises, psychological defenses, self-esteem correction (female – often underestimated, and male – overestimated) – all these are coping strategies, that is, possible sources of overcoming stressfulness. Main results and conclusions. Motor retardation, stupor, memory lapses, “special mistakes” as an opportunity to leave the stage as quickly as possible or the painful anticipation of going on stage, perfectionism – from this you need to be able to switch attention to humor, sarcasm, reduce the importance of the performance, to strengthen internal stability. The significance of the research. Stage tension – always access to heightened human resources, to the «ocean» of opportunities, it all depends on the interpretation of the state of the performer and, accordingly, on the mobilization or disorganization of his mental energy.

THE EFFECT OF THERAPEUTIC RIDING ON SOME MOTOR SKILLS IN CHILDREN WITH ASPERGER'S SYNDROME

Asperger syndrome (AS) is a developmental disorder associated with autism, characterized by repetitive behaviour, significant movement disturbance, including some poor motor skills and clumsiness. Therapeutic riding (TR) focuses on the cognitive, physical, emotional and social well-being of the rider. TR is a form of the physical, occupational and speech therapy that uses the specific movements of equestrian therapeutic techniques to facilitate normal muscle tone and to enhance balance, coordination, and motor development. PURPOSE: The aim is to evaluate the impact of therapeutic riding on motor skills of children with AS. METHODS: Changes in posture were assessed using the Posture Assessment Scale and child’s coordination in everyday functional activities using the Developmental Coordination Disorder Questionnaire (DCDQ’2007).Five children with AS, aged 4.9-year-old to 7.2-year-old participated in the study. RESULTS: We registered some improvements during the horseback riding course: better head and posture position and fine motor/handwriting general coordination. CONCLUSION: Although the study is only a pilot one with a small group of participants, the results clearly show that Therapeutic riding causes positive changes of some motor skills for children with AS.

Course Of Post-Infarction Depression Taking Into Account The Time Of Its Once

A study of 341 patients with an established diagnosis of acute myocardial infarction was carried out. The patients are divided into 2 groups. The first, main, included 233 patients with acute myocardial infarction, who subsequently developed depressive disorders, confirmed clinically and using diagnostic scales; the second group consisted of 108 patients who also had acute myocardial infarction, but did not subsequently suffer from symptoms of depression. Clinical and dynamic observation of patients in the postinfarction period was carried out with control of the condition in a month, three months, six months, 12 months after myocardial infarction. Clinical observation was used to detect the presence of symptoms of depression. Among patients with MI with DS in the first days after MI, more than half (51.1%) reported a permanent decrease in mood more often than other symptoms, i.e. these patients showed an affective component of depression, while the ideator component of depression, which manifested itself in thinking retardation to one degree or another, was in 27.5% of patients, motor retardation (motor component) was detected in 21.5% of those observed. In patients with almost the same frequency, the anxious and melancholic type of affect was noted (47.0% and 41.2%, respectively), the dysphoric type of affect was found in 11.8% of cases, which is 4 times less than anxious and 3.5 times less than the melancholic type. In cases of prolonged depression, the severity of affective disorders more often directly correlated with the severity of the physical condition. If not so long-term depressive episodes were largely due to "their own vision of the disease", the severity of their symptoms depended on the conversation with the doctor and the information received from him, the degree of awareness of his diagnosis, possible complications, and not very much depended on the general somatic status itself. then the course of prolonged depression in patients worsened with the aggravation of the cardiological and general somatic condition of patients. Psychosomatic parallelism in the majority of protracted depressions was manifested by the generalization of asthenic symptom complexes (increased general weakness, intolerance to exertion, lethargy, adynamia, severe daytime sleepiness in combination with early insomnia) with deterioration of the somatic state. At the same time, it was noted that with prolonged depression, there were always more or less pronounced cognitive disorders (reduced memory for past events, limited ability to comprehend what was happening around, remember new information, impaired concentration). Postinfarction depressive episodes lasting up to six months can be attributed to nosogenies; depressive episodes of postinfarction genesis with a protracted course, probably with a high degree of confidence can be attributed to somatogenias.

State-Independent and -Dependent Structural Connectivity Alterations in Depression.

Some brain abnormalities persist at the remission phase, that is, the state-independent abnormalities, which may be one of the reasons for the high recurrence of major depressive disorder (MDD). Hence, it is of great significance to identify state-independent abnormalities of MDD through longitudinal investigation. Ninety-nine MDD patients and 118 healthy controls (HCs) received diffusion tensor imaging scanning at baseline. After 6-month antidepressant treatment, 68 patients received a second scan, among which 59 patients achieved full clinical remission. Differences in whole-brain structural connectivity (SC) between patients with MDD at baseline and HCs were estimated by two-sample t-tests. Masked with significantly changed SCs in MDD, two-sample t-tests were conducted between the remitted MDD subgroup at follow-up and HCs, and paired t-tests were implemented to compare the differences of SC in the remitted MDD subgroup before and after treatment. Significantly decreased SC between the right insula and the anterior temporal cortex (ATC), between the right ATC and the posterior temporal cortex (PTC), between the left ATC and the auditory cortex as well as increased connectivity between the right posterior cingulate cortex (PCC) and the left medial parietal cortex (MPC) were observed in the MDD group compared with the HC group at baseline (p < 0.05, FDR corrected). The decreased connectivity between the right insula and the ATC and increased connectivity between the right PCC and the left MPC persisted in the remitted MDD subgroup at follow-up (p < 0.05, FDR corrected). The decreased SC between the right insula and the ATC and increased SC between the right PCC and left MPC showed state-independent characters, which may be implicated in the sustained negative attention bias and motor retardation in MDD. In contrast, the decreased SC between the right ATC and the PTC and between the left ATC and the auditory cortex seemed to be state-dependent.