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The history of antipsychotics began with the discovery of chlorpromazine in the 1950s. Since then this group of medications has become one of the most important element of the armamentarium of psychopharmacology. While initially these pharmacons were used in the treatment of psychotic states (including psychotic mania) in the last approximately 10-15 years new indications - such as treatment of depressive, manic and mixed states and also mood-stabilization in bipolar disorder and also the treatment of major depressive disorder - for several second-generation antipsychotic (SGA) agents have been introduced. Taking this fact into consideration it is not surprising that the market of SGAs has been broadened in several countries. At the same time, safety issues have been raised related to some SGAs, mainly because of their adverse cardiometabolic effects (e.g. weight gain; dyslipidemia; disturbances of glucose metabolism). Related to this, it is worthy of note that the lifespan of patients with serious mental illness (SMIs, such as schizophrenia; bipolar disorder; major depression) is shorter than their healthy counterparts and that somatic comorbidities (mainly cardiovascular disorders) of these patients are primarily responsible for this fact. In this paper, firstly we briefly discuss the history and features of APs then we present data on the shorter than expected lifespan of patients with SMIs and also the possible background mechanisms of it (including the supposed role of AP treatment). Then we provide a short discussion on endothelial progenitor cells (EPC), their role in cardiovascular system and related clinical relevance. Eventually, we also discuss our pilot study with the aim to reveal whether there is any effect of AP therapy on the number of CD34/KDR double-positive EPCs.

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33 year old British male's first presentation to mental health services was prompted by florid paranoid psychosis and volatile aggression. The patient developed agitated catatonia which eventually improved after 12 courses of ECT. The ongoing psychopharmacological management includes a second generation antipsychotic, a mood stabilizer antiepileptic and an anxiolytic. All investigations including blood tests, CSF analysis, urine and hair drug screen, CT and MRI scans with multidisciplinary medical consultations excluded any underlying pathology. The working diagnosis is an enduring paranoid psychosis with prominent signs of cognitive decline, all of which conclude to Kraepelin's Dementia Praecox.

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Irritable bowel syndrome (IBS), a disorder of the brain-gut axis, is characterised by the absence of reliable biological markers. Tryptophan is an essential amino acid that serves as a precursor to serotonin but which can alternatively be metabolised along the kynurenine pathway leading to the production of other neuroactive agents. We previously reported an increased degradation of tryptophan along this immunoresponsive pathway in IBS. Recently, altered cytokine production following activation of specific members of the toll-like receptor (TLR) family (TLR1-9) has also been demonstrated in IBS. However, the relationship between TLR activation and kynurenine pathway activity in IBS is unknown. In this study, we investigated whether activation of specific TLRs elicits exaggerated kynurenine production in IBS patients compared to controls. Whole blood from IBS patients and healthy controls was cultured with a panel of nine different TLR agonists for 24 h. Cell culture supernatants were then analyzed for both tryptophan and kynurenine concentrations, as were plasma samples from both cohorts. IBS subjects had an elevated plasma kynurenine:tryptophan ratio compared to healthy controls. Furthermore, we demonstrated a differential downstream profile of kynurenine production subsequent to TLR activation in IBS patients compared to healthy controls. This profile included alterations at TLR1/2, TLR2, TLR3, TLR5, TLR7, and TLR8. Our data expands on our previous understanding of altered tryptophan metabolism in IBS and suggests that measurement of tryptophan metabolites downstream of TLR activation may ultimately find utility as components of a biomarker panel to aid gastroenterologists in the diagnosis of IBS. Furthermore, these studies implicate the modulation of TLRs as means through which aberrant tryptophan metabolism along the kynurenine pathway can be controlled, a novel potential therapeutic strategy in this and other disorders.

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Glycogen synthase kinase (GSK-3beta) has been implicated in the pathophysiology of mood disorders and schizophrenia. To examine its role in suicide, we determined GSK-3beta messenger RNA (mRNA) in human postmortem brain from suicide and normal control subjects using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) technique. We found that GSK-3beta mRNA was highly abundant in almost all of the 12 brain areas we studied. We also found a significant age effect on GSK-3beta and that GSK-3beta mRNA level were significantly higher in prefrontal cortex (PFC) and hippocampus of teenage normal controls compared with adult normal controls and was significantly decreased in PFC of teenage suicide but not adult suicide victims compared with respective normal control subjects. The decrease observed in the mRNA levels in teenage suicide but not in adult suicide victims may represent a neurodevelopmentally associated decrease and may be important in the pathophysiology of teenage suicide.

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To better understand the pathophysiological events associate with suicide in subjects with schizophrenia, we performed a DNA microarray expression profiling of the frontal cortex of subjects with schizophrenia who committed suicide, subjects with schizophrenia who died of non-suicidal causes and matched control subjects. Simultaneous expression profiling for >40,000 genes was performed using HU133A and HU133B Affymetrix oligonucleotide arrays. We conclude that suicide in schizophrenia is associated with a number of gene expression changes in the prefrontal cortex that are distinct from both of that observed in controls and subjects with schizophrenia who did not commit suicide. Furthermore, the observed gene expression signature contains a prefrontal cortical downregulation of the HTR2A serotonin receptor transcript, strengthening previously reported genetic susceptibility reports. As the observed transcript changes are likely developing over days or weeks, these data argue that the molecular predisposition to suicide develops significantly earlier than the act of suicide occurs. Finally, the presented data also strengthens previous reports of neuroimmune transcriptome disturbances in subjects with schizophrenia.

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The rate of smoking is especially high among patients with schizophrenia (SCH) and schizoaffective disorder (SCHAFF). Patients with obsessive-compulsive disorder (OCD) smoke less than the general population. OCD symptoms are more frequent among patients with SCH or SCHAFF than in the general population, but it is still unclear whether schizophrenia patients with OC symptoms suffer from SCH and comorbid OCD, or whether they represent a unique subgroup of SCH with presenting OC symptoms. In our study we hypothetised that the current smoking rate of schizophrenia patients with OC symptoms is lower than in schizophrenia patients without OC symptoms. We assessed OC symptoms with the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), general state with the Brief Psychiatric Rating Scale (BPRS) and smoking habits with a questionnaire among 66 patients with SCH or SCHAFF. We formed two groups by dividing patients according to their Y-BOCS score. Group I consisted of patients with Y-BOCS scores under 16, while group II consisted of patients with Y-BOCS scores above 16, and we compared the current smoking rates of the two groups. We found that the rates did not differ significantly, so we came to the conclusion that OC symptoms are not in a tight relationship with smoking habits among patients with SCH/SCHAFF.

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Pharmacovigilance: permanent collection and assessment of the safety data of the drug, in the interest of precise knowledge of the safety profile of the pharmacon; permanent collection of unexpected adverse drug reactions, effects on special patient populations, drug interactions, adverse drug reactions of long-term treatment, adverse drug reactions of long latency. Our study was performed under the tutelage of the Drug Safety Programme in Psychiatry (AMSP), 2004. We review the side effects occuring in the different organ systems; side effects during the use of antidepressive and antipsychotic therapy. We review how the danger of polypharmacy can be avoided by reducing the dose of the current drug; by using therapeutic drug; or just by monitoring therapeutic and adverse effects.

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In the case of elderly patients, the serious side effects of haloperidol should be taken into account. The 83-year-old schizophrenic patient had had successful haloperidol treatment, but developed a sudden paralytic ileus. The unique side effect of haloperidol calls attention to the danger of neuroleptic treatment of elderly patients. The good solution is to change over from haloperidol to a second-generation antipsychotic agent.

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Treatment of survivors of political terror is an emerging and difficult field. Reports on posttraumatic stress disorder (PTSD) in political prisoners within the former Eastern Block countries is low and mostly restricted to German sources. During the totalitarian period administrative and clinical decisions often had to take into account political realities not found in other treatment environments. That practice might have lead to biased professional training, lack of experience extending into the post-communist era and leading to current underpresentation of PTSD. The authors present a case report of a Hungarian political prisoner with long history of PTSD who had a "carry over" diagnosis of paranoid schizophrenia even 15 years after the collapse of the communist regime. After decades of continuous administration of antipsychotic and antidepressive medications, either alone or in combination, Zeldox monotherapy has proven to be the most effective treatment for this patient.

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UNLABELLED: Three young people developed psychosis during/ after cannabis intake. The 17-year-old male after only a few marihuana cigarettes, the 22-year-old patient after two years of addiction developed schizoid psychosis; the 20-year-old patient after six years of cannabis addiction had schizoaffective psychosis. The first two patients become symptom-free on the antipsychotics and during the drug-free period. The third patient, who had cannabis during the psychotic symptoms, still has the schizoid psychosis. CONCLUSIONS: The connection between cannabis and psychosis is clear in our three patients. Marihuana is working on the dopamine system and may cause schizoid psychosis, sometimes permanent psychosis. Cannabis, this light drug might not be a "safe" agent.

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