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Biomedical subjects

I Extein

Publications and source records attributed to I Extein.

At least 73 records · Page 4Linked to original sources

The thyroid-stimulating hormone response to thyrotropin-releasing hormone in mania and bipolar depression.

The release of thyroid-stimulating hormone (TSH) from the pituitary after infusion of 500 microgram of thyrotropin-releasing hormone (TRH) was decreased (p < 0.01) in manic patients and increased (p < 0.01) in bipolar depressed patients compared to a control group of patients with personality disorders. These results suggest that the TRH test may be useful in the diagnosis of psychiatric disorders and in the prediction of response to pharmacotherapy. We discuss the role of central monoaminergic systems in changes in the TSH response to TRH.

Affective Disorders, Psychotic

Serum prolactin and opiate withdrawal.

To evaluate the dopamine hyperactivity hypothesis for opiate withdrawal, we measured serum prolactin (PRL) in 21 male methadone addicts during significant opiate withdrawal and after clonidine suppression of opiate withdrawal signs and symptoms. We also measured serum PRL in these addicts 4 weeks after they were free of clonidine and opiates. Serum PRL was significantly decreased during opiate withdrawal and after clonidine reversal of withdrawal symptoms when compared to serum PRL measured in the drug-free baseline samples. These data suggest that dopaminergic hyperactivity is present in opiate withdrawal, but may not be related to the signs and symptoms of withdrawal. A noradrenergic hyperactivity hypothesis is proposed to explain the neurobiological system that becomes activated in withdrawal, generates symptoms, and is inhibited after clonidine administration.

Clonidine

Failure of naloxone to reduce manic symptoms.

The authors conducted a double-blind placebo-controlled study in which patients with a wide range of manic symptoms were administered 20 mg of naloxone subcutaneously. Naloxone failed to improve manic severity, activation-arousal, or elation-grandiosity for intervals up to 3 hours. Global nurse ratings of mania did not improve over an 8-hour period. The authors suggest that the question of endorphin involvement in mania has not been resolved and recommend clinical studies with longer acting oral narcotic antagonists such as naltrexone.

Affective Disorders, Psychotic

Comparative pharmacokinetics of zimelidine and desipramine in man following acute and chronic administration.

Single dose and steady-state pharmacokinetics of zimelidine and desipramine were compared in eight depressed patients who were subjects in a double-blind crossover study. Within the same patient, there was no relationship between the pharmacokinetics of desipramine (pharmacokinetically similar to all other tricyclic antidepressants) and those of zimelidin, a bicyclic antidepressant. The weight-corrected dose of zimelidine gives a reasonable index of the concentration of its active metabolite norzimelidine, which predominates over zimelidine by a ratio of approximately 3 to 1. The variation in steady-state concentration of norzimelidine for a given dose of zimelidine in adults is about twofold and can be reduced by correcting for weight.

Adolescent

Dopamine-mediated behavior produced by the enkephalin analogue FK 33-824.

Intraperitoneal injection of FK 33-824 produced apomorphine-like stereotyped behavior in rats. Antagonism of this stereotypy by naloxone and neuroleptics suggests that FK 33-824 can activate opiate and dopamine receptors in the brain. Because increased dopaminergic neuronal activity is thought to be involved in schizophrenia and dopamine-mediated stereotypy has been used as an animal model for this illness, these results are consistent with an involvement of endogenous opiate-like peptides in schizophrenia. This involvement provides a possible mechanism for the reported improvement in schizophrenic psychosis produced by naloxone.

Animals

Changes in lymphocyte beta-adrenergic receptors in depression and mania.

The beta-adrenergic receptors were studied in vitro in lymphocytes obtained from patients with major affective disorders and controls. Specific L-[3H]-dihydroalprenolol binding was decreased in both depressed and manic patients compared to controls and euthymic patients. Isoproterenol-stimulated, but not prostaglandin El-stimulated, cyclic adenosine-3',5'-monophosphate production was decreased in manic and depressed patients. These results suggest decreased lymphocyte beta-receptor functioning in depression and mania. This decrease may be an index of changes in brain beta-receptors in mania and depression, or may simply reflect homeostatic regulation of peripheral beta-receptors in response to stress-induced increases in circulating catecholamines.

Adult

State and trait in psychiatric practice.

The authors present a schema for conceptualizing psychiatric illness in terms of state and trait disorders. These disorders are relatively independent components, one or both of which can be present in one patient. They usually require treatment by different methods. State disorders, such as schizophrenic psychosis, mania, and depression, are time-limited and autonomous and respond better to pharmacological than psychosocial therapy. Trait disorders, such as neurotic and characterological disturbances, are long-lasting and respond better to psychosocial therapies. The authors discuss the implications of this schema for the integration of pharmacological and psychosocial treatments.

Humans

14C-homovanillic acid in the cerebrospinal fluid of parkinsonian patients after intravenous 14C-L-dopa.

Six patients with Parkinson's disease and five controls were premedicated with probenecid and the peripheral decarboxylase inhibitor alpha-methyldopathydrazine (Carbidopa) before intravenous administration of 50 muc of 14C-L-dopa in tracer quantity. Seven-and-one-half hours later lumbar CSF was obtained. 14C-homovanillic acid (HVA), a major metabolite of brain dopamine, was isolated by thin-layer chromatography and measured. The statistically significant positive correlation between endogenous HVA and 14C-HVA in the entire patient group and the slightly lower values of endogenous HVA and 14C-HVA in the CSF of the parkinsonians support the assumption that the concentration of HVA in the CSF after probenecid treatment reflects brain dopamine turnover. Measurement of labeled HVA here seems to have little advantage over measurement of endogenous HVA alone.

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