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Effectiveness of a clozapine-aripiprazole combination in Tourette syndrome and bipolar spectrum disorder.
No full textAntipsychotic combination is a common strategy used in both bipolar disorder and schizophrenia, although just a few trials are available exploring its effectiveness. We report herein the case of a patient suffering from severe Tourette syndrome (TS) and bipolar spectrum disorder who benefited from a combination of clozapine and aripiprazole
The glutamate and the immune systems: new targets for the pharmacological treatment of OCD
No full textIn the last decades the pharmacological treatment of obsessive-compulsive disorder (OCD) has been significantly promoted by the effectiveness of selective serotonin (5-HT) reuptake inhibitors (SSRIs) and the subsequent development of the 5-HT hypothesis of OCD. However, since a large majority of patients (between 40% and 60 %) do not respond to SSRIs or strategies based on the modulation of the 5-HT system, it is now essential to search for other possible therapeutic targets
SSRIs do not worsen Parkinson's disease: Evidence from an open-label, prospective study
No full textSelective serotonin reuptake inhibitors (SSRIs) have been reported to be useful in the treatment of depression in patients with Parkinson's disease (PD). However, a few reports have suggested that SSRIs may worsen parkinsonian motor symptomatology and extrapyramidal side effects have been reported in depressed patients treated with SSRIs. So far, no prospective trial comparing the effects of different SSRIs in depressed patients with PD has been performed. The aim of the present study was to assess the effects of four SSRIs (citalopram, fluoxetine, fluvoxamine, and sertraline) on motor performance and their efficacy on depression in a group of patients with PD. Sixty-two consecutive nondemented, nonfluctuating, depressed patients with PD were included in four treatment groups (15 patiens received citalopram, 16 fluoxetine, 16 fluvoxamine, and 15 sertraline). The evaluation of extrapyramidal and depressive symptomatology was performed with use of the Unified Parkinson's Disease Rating Scale (UPDRS), Beck Depression Inventory, and Hamilton Depression Rating Scale at baseline and after 1, 3, and 6 months. Fifty-two patients completed the study. UPDRS scores were not significantly modified by the add-on therapy with each of the SSRIs studied. A significant improvement in depressive symptoms from baseline to the end of the trial was obtained with all SSRIs (Beck and Hamilton scores improving; p < 0.05 according to an analysis of variance). Our findings suggest that SSRIs do not significantly worsen extrapyramidal symptomatology and may ameliorate depression in patients with PD
Current Trends on Antipsychotics: Focus on Asenapine
No full textOver the years, both first- (FGAs) and second-generation antipsychotics (SGAs), continue to gain increasing evidence of being effective in the treatment of psychotic symptoms. Currently, they represent the first-line treatment of schizophrenia and bipolar disorder, although they are widely used in psychotic depression and other clinical conditions, such as agitation and/or behavioural disturbances. Despite representing an indispensable tool for the treatment of severe psychotic disorders, they are widely known to have a number of unwanted side effects that the clinician must be aware of, and handle carefully to provide the patient the best available treatment in the short and long-term. However, even with respect to the long-term use of some of the most effective SGAs, it is imperative for clinicians not to overlook the risk linked to the onset of potentially severe metabolic side effects such as weight gain, dyslipidaemia, insulinresistance and type II diabetes. Asenapine is one of the newest SGAs licenced in Europe for the treatment of manic episodes and in the US for schizophrenia. It belongs to the same class of clozapine, olanzapine and quetiapine, sharing with them a rather complex pharmacological binding profile. In fact, asenapine shows a high affinity for the serotonin (5HT) receptor of the type 2A (5HT2A) and to a lesser extent for the dopamine receptor of the type 2 (D2), similar to other SGAs. Asenapine behaves also as an antagonist at the level of 5HT2C, H1 and α2-receptors. Asenapine has been reported to be effective either in monotherapy or in combination with mood stabilers (lithium and valproate) in the treatment of manic or mixed episodes, with a lower propensity to induce, or being followed by, depressive symptoms, when compared to other SGAs. These unique properties may explain the increasing interest towards the use of this drug in mixed states, besides schizophrenia and acute mania. The aim of this paper was at reviewing current data on pharmacological properties and clinical use of asenapine, as well as on possible future indication of this SGA
Nuovi sviluppi dell’ipotesi serotoninergica della depressione: shunt del triptofano
No full textRIASSUNTO. A partire dalla fine degli anni Sessanta, il deficit di serotonina, ampiamente dimostrato nella depressione maggiore, fu messo in relazione con un aumento dell’attività dell’enzima triptofano-pirrolasi epatica stimolato dall’eccesso di corticosteroidi circolanti, che avrebbe deviato il metabolismo del triptofano dalla produzione di serotonina verso quella della chinurenina. La scoperta che la chinurenina provocava diversi effetti a livello del sistema nervoso centrale suggerì che una up-regulation della via che dal triptofano porta alla chinurenina determinava non solo un deficit di serotonina, ma poteva essere implicata nello sviluppo di ansia, sintomi psicotici e deterioramento cognitivo associati alla depressione.
Questa review si propone di passare in rassegna i vari fattori ormonali e genetici che regolano il metabolismo del triptofano lungo la via della chinurenina, e di evidenziare come tale via metabolica possa essere coinvolta nell’eziopatogenesi della depressione. Gli enzimi limitanti la formazione di chinurenina sono due: la triptofano 2,3-diossigenasi (TDO), attivata dagli ormoni dello stress, e l’indolammina 2,3-diossigenasi (IDO), attivata da citochine pro-infiammatorie. L’aumentata espressione dei geni che producono citochine pro-infiammatorie (interferone-gamma e fattore di necrosi tumorale alfa) potrebbe determinare una predisposizione genetica a sviluppare la depressione mediante una up-regulation della via della IDO, mentre gli stressor ambientali attivano la via ormonale della TDO. Si potrebbe quindi ipotizzare che la via della triptofano-chinurenina rappresenti uno dei principali punti di incontro dell’interazione tra fattori genetici e ambientali coinvolti nella fisiopatologia della depressione e anche un nuovo target per strategie terapeutiche innovative
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