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Results for “PSYCHOSES, TOXIC”
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Thioridazine-induced toxic psychosis.
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Psychiatric manifestations of Benzhexol toxicity.
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Isoniazid toxicity and pyridoxine.
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Transdermal scopolamine and toxic psychosis.
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[Isoniazid toxicity in childhood].
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[Demonstration of a case of hallucinosis after atropine toxication].
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Delirium and toxic psychosis: a current appraisal.
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Organic psychoses. Delusional disorders and secondary mania.
Organic delusional disorders and secondary mania are clinical syndromes produced by neurologic diseases and toxic-metabolic disorders. Delusional disorders are associated primarily with limbic system lesions and basal ganglia dysfunction. These two groups of structures are united into a single system involved in the assessment of ongoing perception and experience, and dysfunction in these structures may explain the presence of psychosis. Lesions producing delusional disorders involve dopaminergic projections considered important in idiopathic schizophrenia, and involvement of similar anatomic and biochemical systems may explain the identity of symptoms noted in both disorders. Secondary mania is associated with deep midline lesions and with pharmacologic agents affecting monoaminergic function. Midline lesions may involve reward-system nuclei and euphoriant enkephalins to produce an elevated mood and hypothalamic nuclei to produce alterations in sleep, appetite, and libido. Mania appears to be more common with right-sided than with left-sided lesions. Lesions, metabolic disturbances, and drugs causing mania may disturb serotonergic and noradrenergic transmitters implicated in idiopathic bipolar disease. Study of the organic psychoses is providing insight into the neurophysiologic basis of idiopathic psychotic disorders. Clinically, greater awareness of the organic psychoses may lead to the discovery of additional cases of secondary mania and organic delusional disorders with potentially treatable neuromedical causes.
The nonmedical use of amphetamines among the college age group: recent research concerning epidemiology and toxicity.
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Toxic psychosis caused by preludin.
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[A Halloo-Wach psychosis; maintenance of toxic psychosis by constant excitation].
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Toxic psychosis induced by benzhexol hydrochloride.
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Phenothiazine-induced toxic psychosis after LSD.
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[Toxic mental disorders].
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[On improved prophylaxis of endogenous-phasic psychoses: aspects of parallel determination of lithium in serum and erythrocytes (author's transl)].
In 30% of the psychiatric patients investigated the lithium concentration in erythrocytes (RBC-lithium) is a more reliable indicator for the evaluation of the clinical response and the risk of toxicity. After lithium administration the lithium RBC levels increased within the first three weeks. Lithium RBC/plasma ratios are not different between unipolar, bipolar and schizo-affective psychoses. It was found that low lithium RBC/plasma ratios correspond with low monoamine oxidase (MAO) activity in platelets.
An informative case of Graves' disease with implications for schizophrenia.
The aetiology of schizophrenia and the other psychoses is not yet established. The Knight model, based on genetic and other evidence, proposes that schizophrenia is an autoimmune disease, caused by the development of forbidden clones of B lymphocytes that secrete autoantibodies that accidentally stimulate cell surface receptors on certain neurons, affecting the limbic system of the brain. An unusual defect in a Maori man with Graves' disease rendered him unresponsive to the usually effective antithyroid drugs, prompting his being treated with prednisone, a non-specific immunosuppressant agent. This was highly successful, reducing the blood level of the causative thyroid-stimulating autoantibodies with reduction of thyroid hormone levels and thyroid gland size. Unfortunately, high dosage prednisone can be used for only a month, because of steroid toxicity. A research pathway to effective therapy of receptor-mediated autoimmune diseases, which probably include the psychoses, is now apparent. It involves finding the autoantibodies, then cloning of their antigenic targets, as has been done for Graves' disease. This will provide knowledge of the peptide sequences necessary for constructing therapeutic agents for selectively destroying the pathogenic forbidden clones. Meanwhile, usage of short-term therapy with prednisone could be helpful in the management of schizophrenia and should be explored.