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Increasing evidence suggests that impulsivity may play an important role in the mechanism of the central nervous system disorders including drug abuse. Clinical studies suggest that patients with increased aggresivity and persons who commit suicide as well as drug abusers show increased impulsivity. Likewise, animal laboratory studies show correlation between drug-seeking and impulsive behavior. Based on animal and clinical studies suggesting that brain serotonergic system plays a critical role in the regulation of impulse-control mechanism, it seems possible that dysfunction of serotonergic neurotransmission contributes to the drug addiction.

In article was presented characteristic features of mental disorders from spectrum obsessive compulsive disorder and spectrum impulse control disorders. Author underlined frequent occurrence of various forms of aggression (auto aggression, and verbal, as well as aggressive behavior in the presence of other people) in patients with these diagnosis, and coincidence some of these disorders as well as similar effects of treatment with similar psychotropic drugs.

The aim of the presented research was to elaborate a criminal behaviour model of juveniles taking into account, on one side the risk factors, diagnosed by means of SAVRY questionnaire, and on the other side, the psychological processes and mechanisms underlying the asocial activity of youth.

The examined group consisted of 98 juveniles, who underwent psychological examination by means of SAVRY questionnaire and the following testing methods: Eysenck Personality QuestionaireRevised (EPQ-R), A. Antonowsky's Sense of Coherence Scale (SOC-29), J.B. Rotter's I-E Scale, Coping Inventory for Stressful Situations (CISS) Scale of Emphaty, Mehrabin's and Epstein's.

The analysis of the obtained results allowed for the differentiation of juvenile groups having similar profile of risk factors. In the analysis, a K-means clustering method was applied. Three groups of juveniles were differentiated, according to the intensity and the risk profile. In the first group there was the highest historical, social and individual factor with a low (or a very low) security factor. In the second group the lowest were historical and social factors, whereas the individual factor was on the average scale, with the security factor being the highest. In the third group the historical and the socal factors were average, the lowest was the individual factor, while the security factor was low or very low.

The paper will present the analysis of the relationship between the group of the juveniles and the selected personality traits of juveniles.

Impulsivity is potentially leading to autoadestructive acts, including suicide. Abnormalities in the brain's serotonin symptoms may predispose to aggressive behavior. But probable not all serotoninergic and anxiolytic agents are safe in patients with impulsive behavior. An open, double blinded, randomized study found that the long-term therapy with lithium reduced the suicidality in patients with affective disorder. Clozapine and second generation antipsychotics have autoaggressive effects in schizophrenic patients.
In patients with personality disorders both, valproic acid and carbamazepine, reduced impulsive aggression. The benzodiazepines, serotoninergic and noradrenergic reuptake inhibitors can in patients with impulsivity facilitate achievement of autoaggressive action.

Pathogenic and therapeutic concepts of psychiatric disturbances gradually evolved in recent decades from an abnormality of neurotransmission in central nervous system (CNS) to an abnormality of neuronal plasticity. In 1977, a molecular and cellular theory of depression was proposed, according to which, in the pathogenesis of depression disturbances of neuronal plasticity in CNS occur, such as atrophy of hippocampal cells, decrease of expression of neurotrophic hormones and impairment of neurogenesis, resulting from interaction of stress factors and genetic predisposition. Antidepressant drugs counteract these processes by preventing „toxic action of hypercotisolemia on hippocampal cells, increasing expression of neurotrophic factors, mainly brain-derived neurotrophic factor (BDNF) and stimulating neurogenesis.
The evidence of neuroprotective properties of mood-normalizing drugs (mainly lithium salts and valproates) which may contribute to the therapeutic activity of these drugs has been accumulated for many years. Such properties may be connected with the effect of these drugs on the processes of intracellular signalling such as phosphatydilinositol system, protein kinase C activity, neuroprotective factor bcl-2 and glycogen synthase kinase 3-beta, as well as stimulation of BDNF expression and neurogenesis. A supposition has been made (mainly for lithium salts) that these drugs may favourably influence neurodegenerative brain diseases.
In recent years, assumptions have also been made that an action on neuronal plasticity may be of importance in the mechanism of therapeutic action of neuroleptic drugs, especially those of second generation. Many studies point on the effect of typical and atypical neuroleptic drugs on different parts of the brain. In the course of long-term administration, new generation neuroleptic drugs exert „sparing” effect on brain structures and may even have a neuroprotective effect. This may be connected with an action of these drugs on a broad spectrum of psychopathological symptoms and with their favourable effect on cognitive functions. Pathogenic and therapeutic concepts of psychiatric disturbances gradually evolved in recent decades from an abnormality of neurotransmission in central nervous system (CNS) to an abnormality of neuronal plasticity. In 1977, a molecular and cellular theory of depression was proposed, according to which, in the pathogenesis of depression disturbances of neuronal plasticity in CNS occur, such as atrophy of hippocampal cells, decrease of expression of neurotrophic hormones and impairment of neurogenesis, resulting from interaction of stress factors and genetic predisposition. Antidepressant drugs counteract these processes by preventing „toxic action of hypercotisolemia on hippocampal cells, increasing expression of neurotrophic factors, mainly brain-derived neurotrophic factor (BDNF) and stimulating neurogenesis.
The evidence of neuroprotective properties of mood-normalizing drugs (mainly lithium salts and valproates) which may contribute to the therapeutic activity of these drugs has been accumulated for many years. Such properties may be connected with the effect of these drugs on the processes of intracellular signalling such as phosphatydilinositol system, protein kinase C activity, neuroprotective factor bcl-2 and glycogen synthase kinase 3-beta, as well as stimulation of BDNF expression and neurogenesis. A supposition has been made (mainly for lithium salts) that these drugs may favourably influence neurodegenerative brain diseases.
In recent years, assumptions have also been made that an action on neuronal plasticity may be of importance in the mechanism of therapeutic action of neuroleptic drugs, especially those of second generation. Many studies point on the effect of typical and atypical neuroleptic drugs on different parts of the brain. In the course of long-term administration, new generation neuroleptic drugs exert „sparing” effect on brain structures and may even have a neuroprotective effect. This may be connected with an action of these drugs on a broad spectrum of psychopathological symptoms and with their favourable effect on cognitive functions.

The psychiatrist has commonly dealt with hiponatremia (sodium blood level lower than 135 mEq/l) in psychiatry department, and by consulting other hospital departments. The prevalence of hiponatremia is estimated as about 0,36% to 4% in general hospitals, and 0,36% to 6,4% in psychiatric departments. By the sodium level lower than120 mEq/l, the psychiatric and neurological symptoms are appearing, with the threat of irreversible brain damage and death. The possible causes of hiponatremia in chronic mentally ill patients are psychogenic polidypsia, somatic illnesses, and undesirable drug effects. The common mechanism is the induction of inappropriate high secretion of anti diuretic hormone (ADH).
Sodium level correction is urgently needed, but it is necessary to consider carefully the risk of quick intravenous infusion of NaCl solution. According to the causes of hiponatremia, the correction of previous pharmacotherapy, and needed somatic or psychiatric treatment must be undertaken.

Clinical assessment and neuropsychological tests measuring working memory were performed in 23 patients with depression secondary to cerebrovascular changes, before and after three-month treatment with moclobemide. Before treatment, significant global cognitive deficit and working memory disturbances were found in all investigated patients. Treatment with moclobemide resulted in an improvement of depressed symptoms and cognitive functions. The improvement of performance on neuropsychological tests, except for Stroop test B, did not show correlation with the level of improvement of depressed symptoms.

The topic of the article is a case report of hebephrenic schizophrenia diagnosed in 23-year old male patient who had apparently attention deficit and hyperactivity disorder in his childhood. The patient since 21 year of his age had been repeatedly admitted to psychiatric hospital and treated with poor therapeutic effects. It was not until administration of clozapine in high doses that his mental status significantly improved.

Case report of 43-year old patient who have suffered from bulimia for over 20 years is presented. The patient has posed marked therapeutic difficulties and the illness resulted in negative somatic consequences. During last hospitalization a comorbid bipolar mood disorder was diagnosed and mood-normalizing drug, lamotrigine, has been introduced. This resulted in a significant improvement of both mood disorder and bulimic behaviour.