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Biomedical subjects

S C Risch

Publications and source records attributed to S C Risch.

At least 109 records · Page 6Linked to original sources
PubMed1984

A cholinomimetic model of motion sickness and space adaptation syndrome.

The space adaptation syndrome is one of the more vexing problems confronted by our nation's astronauts during their journeys. This syndrome may be a variant of motion sickness, although this possibility has been questioned. Physostigmine, a centrally active cholinesterase inhibitor which increases brain acetylcholine, was found to cause a motion sickness-like syndrome--in psychiatric patients and normals--including nausea, emesis, malaise, dysphoria, increases in serum ACTH, beta-endorphin, cortisol, and prolactin, Neostigmine, a non-centrally acting cholinesterase inhibitor, and saline placebo caused no such effects. The above effects closely parallel those of motion sickness. Thus, the effects of physostigmine may be a convenient model for screening for treatments for motion sickness or space adaptation syndrome, or for predicting who will develop these syndromes.

Adaptation, Physiological↗
PubMed1983

Plasma measures of beta-endorphin/beta-lipotropin-like immunoreactivity in chronic pain syndrome and psychiatric subjects.

This study compared basal concentrations of plasma beta-endorphin/beta-lipotropin-like immunoreactivity and dexamethasone suppression of cortisol in seven chronic pain patients, seven psychiatric disorder patients, and seven normal volunteers. Pain patients and psychiatric patients showed significantly higher basal concentrations of beta-endorphin/beta-lipotropin-like immunoreactivity compared to normal volunteers. Pain patients also had significantly higher beta-endorphin/beta-lipotropin-like immunoreactivity than psychiatric patients, even though there was no significant difference in severity of depressive symptomatology as assessed by Beck and Hamilton scores. Resistance to dexamethasone occurred in 57% of pain patients. These results may indicate that biological markers for depression occur in populations of chronic pain patients, or may reflect levels of central nervous system arousal in response to stress, pain, or nonaffective phenomena.

Adult↗
PubMed1983

Bright white light alleviates depression.

Studies of biological rhythm disorders among manic-depressive patients have suggested that depressed patients may have an early photosensitive interval. If so, exposure to bright light during the photosensitive interval might relieve depressive symptoms. As a test of this hypothesis, 12 depressed patients were exposed to bright white light from roughly 5 to 6 a.m. On the afternoon following this treatment, depressive symptoms were reduced in comparison to baseline ratings and as compared to afternoons following similar exposures to dim red light.

Arousal↗
PubMed1983

Adrenergic-cholinergic balance and the treatment of affective disorders.

Centrally acting cholinomimetic drugs cause anergia, behavioral inhibition and depression. Centrally acting cholinomimetic drugs have antimanic properties. Combinations of acetylcholine precursors and centrally active cholinomimetic agents may cause augmented muscarinic effects, as may a combination of an antiadrenergic and cholinomimetic drugs. Centrally active anticholinergic agents may exert antidepressant effects. Affective disorder patients may show hyperreactivity to cholinomimetic agents, a phenomena which may have diagnostic significance.

Acetylcholine↗
PubMed1982

The relationship between blood and cerebrospinal fluid prolactin in nonhuman primates.

We studied the relationship between plasma and cerebrospinal fluid (CSF) concentrations of prolactin (PRL) in repeated and simultaneous samples of blood and CSF from chair-restrained rhesus monkeys. Following administration of thyrotropin releasing hormone (TRH), each of 4 monkeys showed increased plasma and lumbar CSF PRL concentrations. Increases in CSF PRL concentrations were muted and delayed until 60 min after peak plasma concentrations were attained. In 3 other monkeys we compared PRL concentrations in simultaneous lateral ventricular and lumbar CSF samples. ALthough we found no difference in PRL concentrations under baseline conditions, a ventricular-lumbar PRL concentration gradient became apparent after TRH stimulation. These studies demonstrate that changes in plasma PRL concentrations are reflected in CSF concentrations. They suggest that a significant blood-CSF barrier exists for PRL and the PRL may enter the CSF selectively via the ventricles.

Animals↗
PubMed1982

Blunted prolactin response. A neuroendocrine abnormality manifested by depressed patients.

Prolactin concentrations of 30 unmedicated psychiatric inpatients and 11 normal controls were measured at baseline and at 30 and 60 minutes after the administration of 10 mg of intramuscular methadone hydrochloride. Methadone raised the prolactin level at 60 minutes to more than twice the mean baseline level for the full subject sample. Patients with depressive disorders had lower mean basal prolactin levels than did the other subjects, and also manifested attenuated prolactin responses to methadone. Eight of 16 depressives had markedly blunted prolactin responses, a finding consistent with other studies reporting deficient responses in depression. These data are consistent with the hypothesis that the pathophysiology of depressive disorders involves dysfunctions in the anterior pituitary itself or in the hypothalamic neurotransmitter and neuromodulator systems (eg, endorphins) that regulate the secretion of prolactin and other neurohormones.

Adult↗
PubMed1982

The effect of methadone on the behavioral and neuroendocrine responses of manic patients.

In a double-blind, crossover design, 10 mg of methadone or an inert placebo were administered intramuscularly to nine acutely manic patients in identical experimental sessions separated by 1 day. Standardized behavioral observations, self-ratings of mood and affect, and blood samples for prolactin and cortisol were obtained at baseline and 30, 60, and 120 minutes after the administration of methadone or placebo. Methadone decreased symptoms of euphoria, elation, and grandiosity in these manics. There was a significant rise in prolactin, peaking at 60 minutes, and a significant decrease in cortisol, maximal at 120 minutes following methadone administration. There appeared to be a correlational consistency between the subduing effects of methadone on behavior and its effect upon prolactin and cortisol secretion. These findings, together with data from previous studies of our own and others, suggest that a potentially important interrelationship may exist between the central endogenous opioid peptide systems, various neuroendocrine regulatory factors, and the pathophysiology of affective disorder.

Adult↗
PubMed1982

The effects of psychotropic drugs on the cardiovascular system.

Clinicians may encounter substantial numbers of patients with cardiovascular disease who may be receiving cardiovascular medications and who also need psychopharmacologic intervention. To provide information regarding the management of such patients, the pharmacology of the major classes of psychoactive agents is reviewed with respect to their cardiotoxicity, cardiovascular side effects, and drug-drug interactions. Management of the cardiovascular complications of psychotropic overdose is discussed, and potential therapeutic uses of psychoactive medications in patients with cardiovascular pathology are noted.

Antidepressive Agents, Tricyclic↗