PubMed · 8753593
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N Sakamoto, Y Sakamoto, J Kawano, M Uehara. 1995. [Haloperidol].. https://pubmed.ncbi.nlm.nih.gov/8753593/
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Plasma homovanillic acid (pHVA) levels were compared in a large number of neuroleptic-resistant and -responsive schizophrenic patients (male/female = 161/46) and normal controls (67/27), and correlated with various measures of psychopathology. Psychopathology was evaluated with the brief psychiatric rating scale, the Schedule for Affective Disorders and Schizophrenia-Change version (SADS-C) and SADS-C Global Assessment Scale, the Scale for Assessment of Negative Symptoms, the Scale for Assessment of Positive Symptoms (SAPS), and the Quality of Life Scale. No significant differences in pHVA levels between neuroleptic-resistant (n = 104) or -responsive (n = 103) schizophrenic patients, and normal controls, were found; however, there was a main effect for sex, due to higher pHVA levels in women than men. There were no diagnosis x gender or age effects on pHVA levels. No significant correlations were observed between psychopathology ratings and baseline pHVA levels, except with the Hallucinations subscale of SAPS in neuroleptic-responsive patients. Neither duration of neuroleptic washout nor plasma prolactin levels correlated with pHVA levels. Further studies on the origin and significance of the gender difference in pHVA are indicated.
Though conceptualised originally as a deteriorating disorder, some contemporary studies have been interpreted as challenging these foundations; more radically, it has been proposed that schizophrenia may be a 'static encephalopathy' of neurodevelopmental origin. The argument offered here is that schizophrenia is indeed a neurodevelopmental disorder, but that this is not in itself antithetical to later disease progression. Rather, the onset of psychosis may reflect the maturationally-mediated triggering of an active disease process that is associated with progressive deterioration unless attenuated by antipsychotic drugs. A developmental trajectory is proposed to link first or early second trimester dysplasia to the chronic course of the illness; from this, it is argued that schizophrenia is inherently a progressive disorder but that antipsychotic drugs may act to ameliorate this progressive component and thus confer on the disease course some of the characteristics of a 'static encephalopathy'. The 'true' natural history of an illness cannot be determined from studies in treated populations.
This is a study of the morphology and transbilayer lipid distribution of human erythrocytes treated with chlorpromazine (CPZ) over extended time courses. At 0 degree C, treatment of dilauroylphosphatidyl[1-14C]choline-labeled erythrocytes with 120 microM CPZ produced an immediate stomatocytic transformation (t1/2 < 5 min) with no concurrent change in transbilayer distribution of radiolabeled lipid, as determined by bovine serum albumin extractability. At 37 degrees C, CPZ treatment of cells produced two sequential morphological effects: immediate stomatocytosis (t1/2 < 1 min) with no concurrent change in radiolabel transbilayer distribution, followed by gradual increase in stomatocytic extent over several hours, with concurrent redistribution of radiolabeled lipid to the inner monolayer. Cells pretreated with vanadate at 37 degrees C exhibited a triphasic morphological response: CPZ produced immediate stomatocytosis, followed by a transient reversion to echinocytes lasting about 2 h, before returning to stomatocytic morphologies over the next several hours. The echinocytic reversion was accompanied by exposure of phosphatidylserine on the cell surface, as indicated by increased activation of exogenous prothrombinase. These findings suggest that while CPZ induces transbilayer lipid redistribution over extended time periods (which may mediate the complex morphological transformations observed), the early stomatocytic response elicited by addition of CPZ is not due to lipid reorganization.