Speaker: Assoc. Prof. Daria Smirnova, MD, PhD (Psychiatry), Russia

Director, Moscow Institute of Mental Health, Moscow Medical University “Reaviz”, Moscow, Russia

This lecture introduces the psycholinguistic approach in schizophrenia research and the central role of language disturbances in the etiopathogenesis of schizophrenia. The variety of manifestations of thought, language and communication disorder in schizophrenia, represents the core features of this heterogenous group of disorders. The topic of language decline in schizophrenia, from the historical perspective of its origins in the early 20th century and through the prism of current research in applied neurosciences, is reviewed in details. In current linguistic models, language neural circuits are described as underlying the basic symptoms of schizophrenia, such as auditory verbal hallucinations, delusions, and formal thought disorder. Moreover, language deterioration is associated with impaired cognition, negative symptoms domain, poor social functioning and poor outcome for people with schizophrenia. Language impairments of schizophrenia, in particular, decreased verbal fluency and a selective deficit in the production of action verbs, are considered to have hereditary nature and to be the part of cognitive endophenotype of schizophrenia. On the other hand, second language acquisition is not impaired in schizophrenia, and bilingualism may serve as a compensatory resource to maintain verbal fluency. Therapeutic strategies such as cognitive remediation or action language treatment, which target to restore language dysfunction, hold some promise for supporting high quality remission from devastating symptoms in schizophrenia.

Prof. Vladimir Mendelevich, MD, PhD, DMSc, Russia

Mental Health Research Centre, Department of Psychiatry and Medical Psychology, Kazan State Medical University, Kazan, Republic of Tatarstan, Russia

The problem of self-harm behaviour is described in a comparative aspects from the standpoint of hierarchical and traditional approaches in psychiatry towards the innovative network analysis. The rationale for highlighting non-suicidal behaviour as an independent diagnosis is discussed in detail. The analysis of the problem of self-harm behaviour demonstrates the presence of many unresolved issues, such as defining the boundaries of “normative” behaviour (based on the youth style preferences), psychopathological self-harm patterns, as well as the search of significant interrelationships between suicidal and parasuicidal behaviour. The innovative approach to the psychopathology network analysis needs further research to evaluate this complicated self-harm behaviour phenomenon.

Professor Paul Cumming, BSc, MSc, PhD, Switzerland

Department of Nuclear Medicine, University of Bern, Bern, Switzerland

School of Psychology and Counselling, Faculty of Health, Queensland University of Technology, Brisbane Australia The technology of molecular imaging of biomarkers in brain has attained considerable maturity as a tool for investigating the pathophysiological basis of schizophrenia. Since the early days of positron emission tomography, much emphasis was placed on positron emission tomography (PET) studies of dopamine synthesis capacity in brain using positron-emitting DOPA decarboxylase substrate such as fluorine-18 FDOPA. Meta-analysis of many such studies confirmed that a group of 300+ untreated patients with schizophrenia had significantly increased dopamine synthesis capacity in striatum. However, there two kinds of schizophrenia with respect to FDOPA-PET results; nearly one half of patients have entirely normal PET results. Other research suggests that high dopamine synthesis in prodromal individuals, and predicts for conversion to psychosis, especially regarding positive symptoms. Other molecular studies link reduced binding sites for muscarinic acetylcholine receptors in patients with schizophrenia, or specific patterns of reduced brain energy metabolism (i.e., glucose consumption) in relation to specific positive or negative symptomatologies. Schizophrenia is a heterogeneous disorder; molecular imaging across a range of markers may eventually support a biochemical typology of its variants, and guide individualized medical therapy.

Professor Paul Cumming, BSc, MSc, PhD, Switzerland

Department of Nuclear Medicine, University of Bern, Bern, Switzerland,
Adjunct Professor, School of Psychology and Counselling, Faculty of Health, Queensland University of Technology, Brisbane, Australia

Huntington’s disease (HD) is a devastating genetic disorder caused by elongation, misfolding and neurotoxic aggregation of the elongated N-terminal polyglutamine (polyQ) in the mutant huntingtin (mHTT) protein. Early efforts in molecular brain imaging of HD depicted the spatial pattern of reduced cerebral metabolism in positron emission tomography (PET) studies with [18F]-fluorodeoxyglucose (FDG). Other PET studies emphasized the characteristic degeneration of medium spiny striatal projection neurons expressing high levels of dopamine D1 and D2 receptors and adenosine A2 receptors. PET studies with markers for microglia activation reveal the pattern of neuroinflammation in parts of the basal ganglia of HD patients. Recent preclinical work has targeted more specific markers such as mHTT aggregates with [11C]CHDI-180R and synaptic density with [11C]UCB. Identification of the most sensitive marker of early degenerative changes would serve as an objective endpoint for studies of disease modifying treatments.

Assoc. Prof. Aleksey Pavlichenko, MD, PhD, Russia

Director, Moscow Institute of Mental Health, Moscow Medical University “Reaviz”, Moscow, Russia

According to the modern international classifications, to diagnose depression it is necessary that five symptoms out of nine (or ten) must be present for most of the time, almost every day, for at least two weeks, with the obligatory presence of depressed mood or decreased interests. The ICD-11 divides depressive symptoms into three clusters (affective, cognitive-behavioral, and somatic) that may be clinically useful. There have been attempts to link specific depressive symptoms to response to different antidepressants and specific psychotherapy. Antidepressants have been shown to be more effective for major affective symptoms and for sleep-related symptoms and not as effective for “atypical” symptoms. Some evidence supports the fact that a symptom profile, in addition to the diagnosis of depression itself, may be of value in predicting response to specific antidepressants or a particular type of psychotherapy.