Volume 8, Issue 1, March 2006

Editoral in Hungarian

Mátyás Trixler

Abstract

Anxiety itself, and anxiety disorders in particular, seem to represent an independent risk factor for cardiovascular diseases as important as obesity, hypertension, sendentary lifestyle or hyperlipidemia. Anxiety-related noradrenaline and HPA overactivity, excessive sympathetic nervous system activation, and the permanently elevated level of several neuropeptides and cytokines result in hypertension and arrhythmias, endothel lesions, detrimental hemodynamic changes and platelet overactivation facilitating thrombosis. Patients with severe and sustained anxiety usually have additional adverse health behaviors which further aggravate the hazards. Epidemiological studies agree in finding markedly increased incidence of myocardial infarct, coronary heart disease or other cardiovascular conditions, often with earlier age of onset, faster progression and higher letality, in anxiety disorder patients. Better recognition and adequate treatment of anxiety disorders may therefore contribute to curbing the excessive–and typically early-onset–cardiovascular morbidity and mortality in Hungary.

Keywords: anxiety, cardiovascular risk factor, biochemical link, mortality

 

Abstract

Although antidepressants undoubtedly treat depression and decrease suicidality in case of severely ill depressives in the case of good clinical response, there is evidence that antidepressants can worsen depression and can increase suicidality in a very small subpopulation. Some individual case histories were published that of SSRIs can induce suicidal behaviour, mainly at the beginning of the treatment, during akathisia, restlessness and agitation. Some clinical trials suggested that provocation of suicidality could be a serious side-effect of antidepressants. The almost double frequency of suicidal behaviour of patients on antidepressants compared to patients on placebo; it is in sharp contrast with the 2-6 fold lower suicide risk of antidepressant treatment versus untreated patients.

Keywords: depression, suicide risk, antidepressants, side-effect

Polymorphisms in glycine transporter with schizophrenia

Shih-Jen Tsai, Chih-Ya Cheng, Chen-Jee Hong, Ding-Lieh Liao, Ying-Yay Liou

Abstract

Glycine acts as an obligatory co-agonist with glutamate on N-methyl-D-aspartate (NMDA) receptors. Brain glycine availability is determined by glycine transporters (GlyT1 or SLC6A9), which mediate glycine reuptake into nerve terminals. Since hypofunction of NMDA receptors has been implicated in the pathophysiology of schizophrenia, this study tests the hypothesis that GlyT1 genetic variants confer susceptibility to schizophrenia. Four GlyT1 polymorphisms were studied in a sample population of 249 people with schizophrenia and 210 normal controls. One polymorphism (rs16831541) was not informative in our Chinese population while the other three polymorphisms (rs1766967, rs2248632 and rs2248253) were analysed with chi-square tests and haplotype analysis. Significant linkage disequilibrium was obtained among the three polymorphisms. Neither single marker nor haplotype analysis revealed an association between variants at the GlyT1 locus and schizophrenia, suggesting that it is unlikely that the GlyT1 polymorphisms investigated play a substantial role in conferring susceptibility to schizophrenia in the Chinese population. Further studies with other GIyT1 variants, relating either to schizophrenia, psychotic symptoms or to therapeutic response in schizophrenia, are suggested.

Keywords: association study, polymorphism, glycine transporter, schizophrenia, haplotype

Abstract

Excessive self-grooming in animal models of obsessive-compulsive disorder (OCD) is regarded as an equivalent of compulsive behaviour in OCD patients. Previous studies have suggested a key modulatory role of certain serotonin2 receptor subtypes both in grooming behaviour and OCD. Certain 5-HT2 receptor agonists were reported to exacerbate symptoms in OCD patients. Here we report that activation of the serotonin2c (5-HT2c) receptor induces self-grooming in rats, which result supports the hypothesis that selective stimulation of central 5-HT2c receptors exacerbates symptoms also in OCD. The present findings may help to understand serotonergic mechanisms underlying psychiatric disorders of the obsessive-compulsive spectrum and may progress the development of novel anxiolytic and anti-OCD medications.

Keywords: self-grooming, obsessive-compulsive disorder, serotonin, 5-HT2C receptor, 5-HT2B receptor

Abstract

The atypical antipsychotic aripiprazole was administered once a day by peroral dose–10-15 mg–in 103 schizophrenics; they were hospitalized or in day-hospital or outpatient department. During the simple blind clinical trial it was compared by 70 schizophrenics administered by haloperidol treatment (9-15 mg/day dose). The aripiprazole had good therapeutic effect at the positive and negative symptoms of acute schizophrenia, and at the other antipsychotic non-responder patients, and had no serious side-effects. The hypothesis, that of aripiprazol had good effect on the mesolimbic dopamine system as dopamine antagonist, causes improvement on positive symptoms; also good effect on the mesocortical dopamine system as partial agonist, causes improvement on negative symptoms of schizophrenia. The patients had good compliance with aripiprazol.

Keywords: schizophrenia, aripiprazol, mesolimbic and mezocortical dopamine systems, sideeffects

Abstract

The 59 year-old, high-qualified male patient had been treated for psychiatric illness due to depressive symptoms, “pathological crying”, amplified somatic style and severe insomnia. Earlier he had one depressive episode. There was no psychotrauma detected to cause these symptoms and no neurological symptoms, either. The clinical appearance was psychotic depression, so combined antidepressant, anxiolytic, hypnotic, and antipsychotic therapy was started. The MAWI examination showed mild intellectual deficit, so cerebral MRI was done, also. This examination helped to verify the correct diagnosis: post-stroke depression.

Keywords: post-stroke depression, pathological crying, amplificated somatic style, MRI