PubMed · 10784487
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S Burton, K Heslop, K Harrison, M Barnes. 2000. Ziprasidone overdose.. https://doi.org/10.1176/appi.ajp.157.5.835
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A review of 65 studies of individuals with schizophrenia who had never been treated with antipsychotic medications indicates significant abnormalities in brain structure and function. Neurological and neuropsychological measures show the most consistent and largest group differences between those affected and normal controls. Measures of structural differences and cerebral metabolic function are significant but less impressive. Electrophysiological differences also are found, but most such studies are older and have methodological problems. The brain abnormalities implicate a variety of interrelated brain regions, primarily the medial temporal, prefrontal, thalamic, and basal ganglia areas. It is concluded that schizophrenia is a brain disease in the same sense that Parkinson's disease and multiple sclerosis are, and that the brain abnormalities in schizophrenia are inherent in the disease process and not medication-related. The challenge for the future is to use the new molecular techniques to study these brain areas and elevate our understanding of schizophrenia's etiology to the next level.
We report the identification of four novel histamine 1 (H1-17-C/T, -974-C/A, -1023-A/G and -1536-G/C) and four novel histamine 2 promoter polymorphisms (H2-294-A/G, -592-A/G, -1018-G/A and -1077-G/A) which we have investigated for involvement in susceptibility to schizophrenia, and in clinical response to clozapine treatment. We identified a weak independent association between variants at the H1-1536-G/C locus and schizophrenia, where an excess of the H1-1536-C allele was observed amongst such patients (P = 0.036). However upon correction for multiple testing this relationship was no longer statistically significant. Similar investigation of the H2 receptor polymorphisms revealed association between genotype at the H2-1018-G/A locus and clinical response to clozapine treatment (P = 0.027), though upon correction for multiple testing this difference was no longer significant. We have concluded that the participation of these variants in the disorder is unlikely, particularly in view of their apparent lack of function and unlikely influence on receptor expression. However their nature alludes to the potential presence of other more important alterations further along these regions, where sequences encoding alternate promoters have recently been identified for each receptor that may yet be found to harbour such polymorphisms.
A precise and feasible high-performance liquid chromatographic (HPLC) method for the analysis of the novel antipsychotic drug quetiapine in plasma has been developed. The analysis was carried out on a C8 (150x4.6 mm i.d., 5 micrometer) reversed-phase column, using a mixture of acetonitrile, methanol and pH 1.9 phosphate buffer as the mobile phase; triprolidine was used as the internal standard. Careful pretreatment of the biological samples was implemented by means of solid-phase extraction (SPE). A good linearity was found in the 4-400 ng ml(-1) quetiapine plasma concentration range. The application to some plasma samples of patients treated with Seroquel(R) tablets gave satisfactory results. The accuracy was good (quetiapine mean recovery=92%), as well as the precision (mean RSD=3.3%). The method seems to be suitable for the clinical monitoring of patients treated with quetiapine.