1,721,070 research outputs found
The sequential treatment approach to resistant schizophrenia with risperidone and clozapine: results of an open study with follow-up
No full textd-cycloserine adjuvant therapy to conventional neuroleptic treatment in schizophrenia: an open-label study
No full textD-cycloserine, a partial agonist at the strychnine-insensitive glycine site of the NMDA receptor complex, was tested as adjuvant treatment to conventional neuroleptics in chronic schizophrenic volunteers. The drug was administered, o.a.d., at the daily dose of 250 mg for six weeks. Mental status outcome measures were completed at the end of each week of treatment. The major finding was a deterioration of the patients' clinical condition, specifically of their psychotic symptoms. These preliminary results are discussed among others in view of d-cycloserine pharmacologic properties and recent findings on the interaction between NMDA agonists and dopamine system. This study, finally, suggests the need for a controlled dose-finding trial to establish the activity and a therapeutic "window" of this drug in schizophrenia
Clozapine-induced hypersensitivity myocarditis
No full textA rare, but frequently fatal, side effect of the antipsychotic drug clozapine is myocarditis. We report a case of hypersensitivity myocarditis secondary to clozapine administration that was diagnosed in vivo for the first time through endomyocardial biopsy and was successfully treated with corticosteroids. Histologic diagnosis was based on the evidence of eosinophilic infiltration of the endomyocardium and eosinophil degranulation. Endomyocardial biopsy was performed in order to establish or exclude a clear-cut relationship between cardiac dysfunction and clozapine, and was crucial to establish a correct diagnosis and appropriate treatment. Clozapine withdrawal and targeted 8-day, low-dose corticosteroid therapy resolved the symptoms and restored cardiac function
Increased concentrations of various amino acids in schizophrenic patients. Evidence for heterozygosity effects?
No full textThe hypothesis is examined that heterozygosity for amino acid disorders (AAD) is a genetic component of susceptibility for schizophrenic psychoses. To detect possible heterozygotes, urinary and blood amino acid levels were analyzed in a sample of subjects with a diagnosis of schizophrenia and in their biological parents and compared with those of a sample of healthy volunteers. The results showed increased blood and urinary levels of certain amino acid in those patients who have at least one parent with the same amino acid abnormality. This finding points to the possibility of heterozygosity for AAD in schizophrenic patients
Genetic approach to the study of heterogeneity of affective disorders
No full textIn the present paper we compared the results of the application of segregation analysis, under two different single major locus (SML) transmission hypotheses, a dominant one with sex effect and a recessive one, to the families of 202 probands with major depression, recurrent and bipolar disorder. In the first analysis we considered only secondary cases with major affective disorders (bipolar disorders and major depression, recurrent), in the second one we included as affected phenotypes also relatives with atypical depression, dysthymic and cyclothymic disorders. Results indicated that considering spectrum disorders greatly modified familial segregation patterns
The search for genetic homogeneity in affective disorders
No full textIn the present study we tested the fit of the Single Major Locus (SML) hypothesis, using segregation analysis for single families of affective probands treated with lithium salts, with second degree relatives included. We tested the segregation pattern for every family with two different sets of parameters: one dominant for a group that did not relapse on lithium treatment and one recessive for a group that did. We calculated the likelihood ratios for each family. The results of this study partially confirm the importance of outcome on lithium treatment in susceptibility to affective disorders. However, application of segregation analysis suggested that there is genetic heterogeneity that cannot be completely detected when using only the simple pharmacological criterion of outcome on lithium
NEUROFUNCTIONAL ASSESSMENT OF SCHIZOPHRENIA - A PRELIMINARY INVESTIGATION OF THE PRESENCE OF EYE-TRACKING (SPEMS) AND QUALITY EXTINCTION TEST (QET) ABNORMALITIES IN A SAMPLE OF SCHIZOPHRENIC-PATIENTS
No full textThis preliminary study evaluated the simultaneous presence of abnormalities in the regulation of eye-tracking and neuropsychological tests performance (tactile extinction) in a sample of schizophrenic patients. Both those measures of central malfunctioning appears to be quite specific to schizophrenic disorders and more related to the trait, rather than state characteristics. Even though preliminary, the results indicate a significant relationship between abnormalities in SPEM regulation and the distribution of tactile abnormalities, with more left-side extinguishing patients showing abnormal SPEMs. Some interpretations of the findings are given in the context of current hypotheses on the neurofunctional abnormalities of schizophrenics
Interference between anti-HLA antibodies and CPZ metabolites
No full textThe interference of chlorpromazine (CPZ) and several preincubated CPZ metabolites on the lymphocyte absorption of antibodies directed against HLA-A1 and other nonrelated HLA specificities were investigated. Both CPZ and metabolites 7-OH-, Nor1-, and Nor2-CPZ were found to interfere with the specific absorption of anti-HLA-A1 antibodies. The meaning of such a result is discussed
PRESYNAPTIC CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE-II - AUTOPHOSPHORYLATION AND ACTIVITY INCREASE IN THE HIPPOCAMPUS AFTER LONG-TERM BLOCKADE OF SEROTONIN REUPTAKE
No full textIt is known that long-term treatment with antidepressants induces an enhancement of neurotransmission in the pathway projecting from raphe nuclei to the hippocampus. In the case of selective serotonin (5-HT) reuptake inhibitors, this enhancement is due to a desensitization of presynaptic 5-HT autoreceptors and a concomitant increase in 5-HT release in terminal areas. To investigate whether this effect is accompanied by adaptive changes in the molecular machinery regulating transmitter release at serotonergic terminals, autophosphorylation and activity of Ca2+/calmodulin-dependent protein kinase II were measured in subsynaptosomal fractions from hippocampus and total cortex. Long-term treatment with two selective serotonin reuptake inhibitors (paroxetine and fluvoxamine) and with a nonselective reuptake inhibitor (venlafaxine) induces a large increase of kinase autophosphorylation in synaptic vesicles and synaptic cytosol in the hippocampus but not in synaptosomal membranes. No significant change was detected in total cortex. The change is not reproduced by the direct addition of the drugs to the phosphorylation system and is not elicited by acute treatment of the animals. The increase in autophosphorylation is not accounted for by neosynthesis or translocation of the kinase to synaptic terminals. The change is restricted to the kinase located inside the terminals and is not detected in synaptosomal membranes, containing predominantly postsynaptic kinase, suggesting that only presynaptic kinase is affected. In the same fractions, the kinase activity is increased. These results are in agreement with reports suggesting a presynaptic effect for the SSRIs and disclose a new putative site of action for psychotropic drugs
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