Biomedical subjects
Publications and source records attributed to R E Becker.
Inhibitory activity against the enzyme monoamine oxidase is present in low molecular weight fractions (less than 100,000) of human cerebrospinal fluid. These endogenous substances of different molecular weights (3000 to more than 35,000) act like monoamine oxidase inhibitor drugs to inhibit both type A and type B monoamine oxidase.
A rater-bind, ABA's design study of 21 cases indicates that diazepam significantly improves tardive dyskinesia and that some of the improvement persists for an extended period after diazepam is withdrawn. Since benzodiazepine receptors and sites of action seem to be mainly in the neocortex (especially frontal), limbic cortex, and deep limbs nuclei, and these structures provide most of the input into the nigrostriatopallidal system that probably regulates its role in voluntary movement, it may be suggested that impaired corticolimbic control of basal ganglia may be a factor in the pathogenesis of tardive dyskinesia.
Hemiballism is an involuntary uncontrollable movement disorder with grave prognosis. Post stroke anatomical lesions of the subthalamic nucleus are the most frequent but not sole site. Increased cerebrospinal fluid homovanillic acid levels and successful management of hemiballistic symptoms with neuroleptics have suggested a dopaminergic overactivity as the neurochemical pathology. Diazepam, a gamma amino butyric acid (GABA) mimetic drug, has recently been reported to possess therapeutic efficacy. Hemiballism is a treatable condition which responds to neuroleptics and possibly GABA mimetic drugs.
Vibrio cholerae serotype Ogawa was recently isolated from the estuarine waters of Apalachicola Bay, Fla., in areas that are subject to consistent fecal contamination and in areas that are remote from any apparent source of contamination. The significance of these organisms in the environment has not been determined.
The ineffectiveness of antidepressants, and the effectiveness of neuroleptics alone, in the treatment of depressed schizophrenic patients is evidence that a pharmacologically definable depression cannot be demonstrated in schizophrenia. The author reports findings from a double-blind 1-month study of 52 anergic and depressed schizophrenic patients given thiothixene-placebo or chlorpromazine-imipramine. These findings support DSM-III, which does not diagnose intercurrent, secondary depression in the presence of schizophrenia. Consistent with most of the clinical literature, this study also supports the use of a single neuroleptic rather than neuroleptic-antidepressant combinations to treat depressive symptoms secondary to schizophrenia.
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Plasma from normal subjects and chronic schizophrenic patients produced nearly equal inhibitory effects on platelet and bovine brain monoamine oxidase (MAO) activity. Plasma from controls and patients with high platelet MAO activity caused less decrease in platelet MAO kinetic variables (Km, Vmax) than plasma from subjects with midrange or low MAO activity. When bovine striatal MAO was used, with serotonin as substrate, plasma from schizophrenic patients caused less decrease in Vmax than plasma from controls. These inhibitory effects are associated with the presence in plasma of one or more nonalbumin proteins with low molecular weight.
The authors assessed perceptual changes in 12 depressed patients treated wih bupropion, 12 patients given other antidepressants, and 12 drug-free controls. Bupropion was associated with vivid dreaming and changes in attention, memory, and perception. which may have contributed to its therapeutic effectiveness.
Using an ABA' research design, the effects of a benzodiazepine gamma-aminobutyric acid (GABA)-ergic agent, diazepam, on various aspects of tardive dyskinesia (TD) were investigated in 21 patients. Videotaped recordings of the examinations were rated blind on the Abnormal Involuntary Movements Scale. In nonsedating amounts, diazepam had a significant anti-TD effect, especially in terms of limb dyskinesia. A significant portion of the therapeutic effect persisted after the medication was withdrawn. The results suggest that diazepam has a specific anti-TD action and that in some cases it may be able to produce a somewhat lasting correction of the deranged neurobiological mechanisms in TD. Since the main sites of action of benzodiazepines and the highest concentrations of benzodiazepine-linked GABA receptors are in the limbic and cortical structures that provide principal sources of inputs to the basal ganglia, it is suggested that the supra-striato-pallidal mechanisms of voluntary movement control should be considered in understanding the pathogenesis and treatment of TD.
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A telomian-beagle hybrid has been studied as a possible model for the hyperkinetic syndrome in children. Behavior tests showed that hybrids, like children, exhibit hyperactivity, impulsiveness, and impaired learning. Two groups of hybrid could be differentiated; the behaviour of one improved after amphetamine (responders) while that of the other did not (nonresponders). Moreover hybrids were less responsive than beagles to other effects of amphetamine such as stereotyped behaviour and hyperthermia. Measurement of blood levels of amphetamine and its active metabolite p-hydroxyamphetamine (pOA) showed that hybrids form less pOA. We propose that the lesser response of hybrids to toxic effects of amphetamine is due to this difference in amphetamine metabolism. Responders showed higher peak blood levels of amphetamine than nonresponders and their improvement on amphetamine correlated with blood levels of amphetamine. Therefore high levels of amphetamine appear to be necessary for its 'paradoxical' effect in this model. This suggests that amphetamine acts by activating both noradrenergic and dopaminergic neuronal systems in the CNS.
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A gas-chromatographic method for simultaneously measuring p-hydroxyamphetamine (pOA) against amphetamine (A) in plasma and CSF is presented. The time course of body temperature (Tb), stereotyped behavior (St), and A and pOA levels in plasma and CSF were studied after administration of 0.6 and 1.5 mg/kg p.o. of A to dogs. Stereotyped behavior reached maximal value 2.5 h after A, as did levels of A in CSF. The A levels in CSF decreased steadily in the following hours and simultaneously with the levels of A in plasma. St remained elevated and began to decrease after 6.5 h. The relationship between St and amounts of A was not linear but exponential. This suggest that both A and its metabolite contributed to this effect. In fact, a linear relationship was found between St and the amounts of pOA in CSF. Body temperature had a time course similar to A plasma levels, reaching peak value after 1.5 h and declining thereafter simultaneously with A. A linear relationship was found between Tb and the amounts of A in plasma. Thus Tb seems to be a peripheral A effect related to the presence of the drug in plasma.
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