Measurements of beta-endorphin-like immunoreactivity have been performed in CSF and plasma of patients with schizophrenia and other neuropsychiatric disorders. The detection limit of the RIA was between 20--50 pg/ml (6--15 fmole/ml). In CSF the quantity of beta-endorphin-like immunoreactivity ranges up to 65 pg/ml. The data from schizophrenics and other neuropsychiatric patients show no obvious deviation from the results in a control group of medical patients with normal CSF findings. In plasma the immunoreactive beta-endorphin-like material ranges up to 250 pg/ml. There is only a small tendency to higher values in schizophrenic patients, if compared with different types of neuroses and affective and organic psychoses. In a second series of experiments also this tendency could not be reproduced. In 9 electroconvulsive treatments an increase of blood beta-endorphin-like immunoreactivity was observed 7 times. A possible endorphinergic mechanism in the mode of action of electroconvulsion is hypothesized.
A possible antimanic property of the GABA-ergic anticonvulsant valproate was examined by use of a double-blind placebo-controlled ABA design in 5 acutely ill manic patients. In 4 cases a marked improvement was observed after valproate medication whereas one patient showed no response. Seven further patients with frequently recurrent episodes of a manic or maniform schizoaffective psychosis, irresponsive to lithium prophylaxis, were chronically treated with valproate in combination with low doses of lithium (one case only with valproate). Over an observation period of 1 1/2-3 years none of the patients exhibited a relapse. It is proposed that, in general, GABA-ergic anticonvulsants possess antimanic properties and that the specific antimanic effect of lithium is due to a GABA-ergic mode of action. The possible role of GABA-systems in affective disorders and in organic types of psychoses (e.g.,porphyria-psychosis, delirium tremens) is discussed on the basis of pharmacopsychiatric considerations.
Borna Disease Virus (BDV) infections are widespread in animal species. This neurotropic, negative and single-stranded enveloped RNA virus spreads via axonal and transsynaptic pathways quite specifically into olfactoric and limbic structures. The symptoms in BDV-infected animals range from unapparent or subtle clinical manifestations to fatal neurological disorders. The severe and fulminant course of the infection, which is often accompanied by neurobehavioral and "emotional" disturbances, occurs sporadically and, at least in experimentally infected animals (rats), is thought to be mediated by immunopathology. Increases in serum-BDV antibodies have also been detected in neuropsychiatric patients. In addition, viral antigen and viral RNA have been observed in acutely ill major depressive patients, leading to the conclusion that BDV was causally related to psychiatric disorders, in particular to affective disorders. A number of studies have meanwhile furnished evidence of abnormal immune functions in mentally ill patients. In addition, stress has been shown to decrease immune responses to viral infections. On the basis of these findings it is hypothesized that human BDV infection represents a co-factor in the development or course of psychiatric diseases. Stress may cause immunosuppression and thus induce activation of persisting BDV in the limbic system, resulting in an inflammatory reaction of these structures. These neuropathological changes might influence the serotonergic or dopaminergic neurotransmitter systems. In addition, a specific affinity of BDV structural elements for aspartate and glutamate receptors in the hippocampal formation might directly induce an imbalance of these transmitter system interactions, causing affective and behavioral disturbances. The possible interactions between stress-induced immunosuppression, BDV infection and affective disorders in humans, and the theoretical and clinical aspects of this concept are discussed.
The antimanic action of high doses of the beta-receptor blocking agent propranolol was investigated by the use of a double-blind placebo controlled ABA design. For comparison, the d-stereoisomer (which is practically devoid of beta-blocking activity) was used. 6 trials were performed with d-propranolol, 6 trials with the racemic mixture. From dose-effect relations one can conclude that the d-stereoisomer is about half as effective against manic syndromes as the racemic mixture. From this finding it can be concluded that the antimanic action of propranolol is at least partially due to a mechanism independent of its beta-blocking action.
Cognitive impairments during psychotic episodes are assumed to be caused not only by one single putative classical neurotransmitter dysfunction but also to be due to an impaired equilibrium of the interaction between different neurobiological generators of cognitive processes. Here, the perceptual abnormalities induced by psychotogenic agents play a major role as tools for understanding model psychoses. The recently discovered cannabinoid receptor system with its endogenous ligand anandamide can be regarded as an extremely relevant regulation system, a dysfunctionality of which may explain at least one subtype of endogenous psychoses. The present paper discusses the possible associations between the endogenous anandamide/cannabinoid system and schizophrenic psychoses. Neuropsychological experiments with the 3-D inversion paradigm were performed in healthy volunteers intoxicated with delta9-Tetrahydrocannabinol (delta9-THC). The 3-D inversion paradigm represents a visual illusion of binocular depth perception. Such an inversion occurs in many cases, especially when objects with a higher degree of familiarity (e.g. photographs of faces) are displayed. It is assumed that cognitive factors override the binocular disparity cues of stereopsis. We tested the hypothesis that, during psychotic and related prepsychotic states, the human CNS is unable to correct implausible perceptual hypotheses. Our study provides evidence of strong similarities between data acquired from patients, suffering from productive schizophrenic psychoses and delta9-THC-intoxicated healthy volunteers, as concerns disturbances in the internal regulation of perceptual processes.
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