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Physical activity has always been attributed with a favorable effect on human health. In recent years, the evidence for a positive impact of physical activity also on mental health, as well as for its neurobiological mechanisms, has been accumulated. Physical exercises cause an intensification of neurogenesis, mainly associated with increased production of the brain-derived neurotrophic factor (BDNF), and exert an anti-inflammatory effect on the immune system. These phenomena as well as a motivation for taking exercise show an association with polymorphism of the BDNF gene. Studies on the effect of physical activity on psychological status included various groups of patients. Physical exercises caused a decrease of depressive symptoms and also a decrease of negative and positive symptoms in schizophrenia. In schizophrenia patients such exercises resulted in an improvement of cognitive functions. In patients with symptoms of dementia, physical activity brought about an amelioration of cognitive functions, reduced behavioral disorders, improved level of independent functioning and regulates sleep. Physical activity can be also a protective factor for the development of dementia in the high-risk population. Physical exercises improved a number of sleep parameters in primary insomnia. In addictions to psychoactive substances, the exercise is important both for primary prevention as well as for reducing symptoms of withdrawal and for prolonging the abstinence. The data obtained so far allow to consider physical activity as a valuable and safe method, complementary to pharmacotherapy in many psychiatric disorders.

Calcitonin gene-related peptide (CGRP) is a 37-amino acid neuropeptide. It has two forms: α and β. CGRP is widely expressed in the central and peripheral nervous systems. Great attention is paid to examining the role of CGRP in pain transmission, including modulation of the function of other neurotransmitters. CGRP is regarded as a key mediator in pain response; it is released from the trigeminovascular system after stimulation of sensory nerve endings. It is well documented that CGRP has a very important role in the pathogenesis of migraine. The concentration of CGRP increases in response to stimulation of the trigeminal ganglion. CGRP may affect the activity of sensory neurons by direct control of the pain response in the course of a migraine attack. Therefore, trials are being conducted to develop effective medicines, which could block CGRP’s activity or decrease its concentration. The efficacy of a few CGRP receptor antagonists in the treatment of migraine has been demonstrated in clinical trials. The potential use of monoclonal antibodies directed against CGRP or its receptors is also highlighted. They should decrease severity and frequency of migraine attacks by reducing the levels of CGRP or block its action. These drugs can become an effective alternative to triptans in migraine treatment and to other medicines used in the treatment of disorders associated with dysfunction of the trigeminal nerve.

Valproic acid is a well-known drug long used in neurology as an antiepileptic drug and in psychiatry because of its mood-stabilising effect. Various mechanisms of valproic acid activity have been described (through gamma-aminobutyric acid system – GABA, glutamatergic activity, monoamines, ion channels, gene expression modulation and others), resulting in a decrease of neuronal activity but also affecting other processes, such as apoptosis, inflammation and differentiation of neurons. A wide range of possible activity mechanisms enables the potential use of this “old drug” in new indications. One of the considered aspects of valproic acid activity is its neuroprotective effect, which has been noted so far both in the cellular and in the animal models. The aim of this article is to recapitulate current knowledge on the well-known and novel mechanisms of valproic acid activity in the context of its possible neuroprotective effect.

Aims. A demonstration of therapeutic effect of ketamine infusion in depression initiated the attempts of using it as an anaesthetic agent for electroconvulsive therapy (ECT). As ketamine exerts significant influence on the heart and circulatory system, the aim of this study was to assess it by measuring serum concentration of brain natriuretic peptide (BNP) in patients for whom thiopental was used in all ECT sessions, compared to those for whom ketamine was used in 5 out of 10 sessions.

Material and methods. The study was performed on 27 patients (11 males, 16 females) aged 21–81 years (mean 54±15), treated for drug-resistant depression or drug-resistant schizophrenia (1 patient) in the Department of Adult Psychiatry, Poznań University of Medical Sciences, between 2013-2014. Each patient had at least ten ECT sessions. In the first group (16 patients), 2–5 mg/kg of thiopental was used as an anaesthetic for all sessions and in the second group (11 patients) – 1.0–1.5 mg/kg of ketamine was used for the 2nd, 4th, 6th, 8th, and 10th session. Measurements of BNP were performed prior to and after the 2nd, 6th and 10th sessions.

Results. No significant difference was found taking into consideration the BNP levels between the group with thiopental anaesthesia alone and the group with alternating anaesthesia of thiopental and ketamine. Either, no significant difference was observed while comparing successive BNP levels during the course of ECT within each group.

Conclusions. The results show that BNP levels reflecting the load of circulatory system are similar for patients with alternating anaesthesia with thiopental and ketamine as in patients having anaesthesia with thiopental alone.

The aim of the publication is to present topics covered during the ECNP School of Children and Adolescent Neuropsychopharmacology which took place in Venice (1–6.03.2015). Prominent experts from abroad presented latest research results in the field of child and adolescent psychiatry.