Prevalence and clinical correlates of explosive outbursts in Tourette syndrome. (9/15)

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Relation of outbursts of anger and risk of acute myocardial infarction. (10/15)

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Acute stress show great influences on liver function and the expression of hepatic genes associated with lipid metabolism in rats. (11/15)

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Physostigmine: an antidote for excessive central nervous system depression or paradoxical rage reactions resulting from intravenous diazepam. (12/15)

A review of the pharmacology and use of the drug physostigmine is presented. Of particular interest is the drug's capability to reverse excessive somnolence or paradoxical responses caused by intravenous diazepam (Valium(R)) and other clinically available benzodiazepines. Its use for the treatment of anticholinergic syndrome is discussed and incidence and characterization of side effects documented. Recommendations are made for appropriate emergency use.  (+info)

Shame in the treatment of schizophrenia: theoretical considerations with clinical illustrations. (13/15)

The phenomenology and dynamics of shame have been largely overlooked in the psychoanalytic and psychological literature. The emerging literature now suggests that shame may play a vital role in autonomy and personality development, symptom formation, character pathology, and interpersonal relationships. This paper attempts to describe shame phenomena and identify shame dynamics. The role of shame in the understanding and treatment of schizophrenic individuals is then demonstrated through reference to the writings of Frieda Fromm-Reichmann and examples from the author's clinical work.  (+info)

Preclinical pharmacology of midazolam. (14/15)

Midazolam, a new imidazobenzodiazepine, forms salts that are stable in water solution, and has an overall pharmacological potency similar to that of diazepam but a much shorter duration of action. It produces all the characteristic effects of the benzodiazepine class. Its metabolites account for only a negligible part, if any, of its pharmacological effects observed in the mouse. The time course of its anticonvulsant activity, studied with different experimental protocols and by different routes of administration, revealed an almost immediate onset of action. Midazolam was slightly more potent, and its duration of action was shorter than diazepam, in enhancing presynaptic inhibition in the spinal cord of cats and in depressing spontaneous activity of cerebellar Purkinje cells in the rat. Midazolam decreased spontaneous multiunit activity (MUA) in different nuclei of the brain in 'encephale isole' rats. This depression was reversed by Ro 15-1788, a recently discovered selective benzodiazepine antagonist. Midazolam and diazepam decreased the cyclic GMP level in the cerebellum of rats with about the same potency; the effect of midazolam was of much shorter duration than that of diazepam. Midazolam had one-third the potency of diazepam in displacing 3H-flunitrazepam in mouse brain in vivo, and also in this case the effect of midazolam was of brief duration, as compared with diazepam. Midazolam in therapeutic doses was virtually ineffective in the cardiovascular system of conscious dogs after p.o. or i.v. administration. No direct effects of the drug on autonomic functions were found. The animal data suggest the usefulness of midazolam as an oral sleep-inducer, as an agent for i.v. induction of anaesthesia and as an i.v. or i.m. anticonvulsant in status epilepticus or tetanus, because of its rapid onset of action and its excellent local tolerance as water-soluble injection form.  (+info)

Effects of psychotropic drugs on the rage responses induced by electrical stimulation of the medial hypothalamus in cats. (15/15)

Effects of psychotropic drugs on the rage responses induced by electrical stimulation were investigated in cats with electrodes chronically implanted in the medial hypothalamus. Diazepam produced marked elevation in the threshold for directed attack and slight elevation in that for hissing. The inhibitory effect of etizolam on hissing was about 6 times as potent as that of diazepam. Anti-anxiety drugs such as diazepam, nitrazepam, lorazepam, clotiazepam and etizolam produced marked elevation in the directed attack threshold dose-dependently. The effect of chlorpromazine on directed attack was far less potent than that of anti-anxiety drugs. The anti-anxiety drugs used in this experiment had anti-pentetrazol activity in mice as well as muscle relaxant activity in cats. There were close correlations between the directed attack inhibition produced by the anti-anxiety drugs and both anti-pentetrazol activity and muscle relaxant activity. These results indicate that the above anti-anxiety drugs have a more potent inhibitory effect on the function of the medial hypothalamus than neuroleptic drugs. The inhibitory effect of anti-anxiety drugs on directed attack may be considered to correlate with clinical anti-anxiety effects.  (+info)