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Biomedical subjects

R M Post

Publications and source records attributed to R M Post.

At least 271 records · Page 15Linked to original sources
PubMed1986

The effects of lithium on neuroendocrine function in affectively ill patients.

Lithium is the primary treatment for manic-depressive illness. The mechanism of action of lithium and its endocrine effects remain unclear. Therefore, the hormone responses to sequential stimuli, namely arginine, TRH, and LHRH, were studied in eight patients with major depression before and during treatment with lithium. The drug was found to elevate baseline TSH and prolactin and to augment both their responses to TRH. No clinically significant effect on sex hormones was noted. The advantages of the experimental design and the implications of the findings for lithium's mechanism of action are discussed.

Adult↗
PubMed1986

Antidepressant effects of carbamazepine.

Thirty-five depressed patients diagnosed by DSM-III criteria participated in a double-blind study of the acute antidepressant effects of the anticonvulsant carbamazepine, at average doses of 971 mg/day, achieving mean +/- SD blood levels of 9.3 +/- 1.9 micrograms/ml (range, 3-12.5 micrograms/ml). Twenty patients (57%) showed at least mild improvement, and 12 showed more substantial improvement. Possible clinical predictors of antidepressant response to carbamazepine are discussed. These preliminary data suggest that carbamazepine has some acute antidepressant efficacy in addition to the growing evidence that it has acute antimanic and longer-term prophylactic efficacy in both phases of manic-depressive illness.

Adult↗
PubMed1986

Preliminary evidence for the utility of carbamazepine in alprazolam withdrawal.

Alprazolam treatment is effective for panic disorder, but its major disadvantages include possible dependence and withdrawal symptoms upon discontinuation. The authors report three cases in which carbamazepine, a clinically effective anticonvulsant without abuse potential, successfully attenuated alprazolam withdrawal symptoms.

Adult↗
PubMed1986

Reduced TSH and prolactin responses to TRH in patients with panic disorder.

The authors studied the TSH and prolactin responses to a standard 500-micrograms thyrotropin-releasing hormone (TRH) stimulation test in 12 patients with panic disorder and 10 control subjects. As a group, panic disorder patients had lower mean TSH and prolactin responses, and female patients accounted for the lower prolactin response. The clinical and theoretical implications of these findings are discussed.

Adult↗
PubMed1986

The corticotropin-releasing hormone stimulation test in patients with panic disorder.

Eight patients with panic disorder had significantly lower ACTH and cortisol responses to corticotropin-releasing hormone and a significantly lower ratio of ACTH to cortisol response than 30 normal control subjects. These responses resemble those previously reported for depressed patients except that they occurred in the face of significantly elevated basal cortisol and ACTH levels. These results suggest that patients with panic disorder have an element of chronic hypercortisolemia, like depressed patients, but also a more acute perturbation in ACTH secretion, not previously seen in depressed patients.

Adrenocorticotropic Hormone↗
PubMed1986

Conditioning and sensitisation in the longitudinal course of affective illness.

Few biological theories of manic-depressive illness have focused on the longitudinal course of affective dysfunction and the mechanisms underlying its often recurrent and progressive course. The authors discuss two models for the development of progressive behavioural dysfunction--behavioural sensitisation and electrophysiological kindling--as they provide clues to important clinical and biological variables relevant to sensitisation in affective illness. The role of environmental context and conditioning in mediating behavioural and biochemical aspects of this sensitisation is emphasised. The sensitisation models provide a conceptual approach to previously inexplicable clinical phenomena in the longitudinal course of affective illness and may provide a bridge between psychoanalytic/psychosocial and neurobiological formulations of manic-depressive illness.

Behavior↗
PubMed1986

The clinical phenomenology of multiple personality disorder: review of 100 recent cases.

The clinical syndrome of multiple personality disorder (MPD) is an unusual dissociative condition that has been poorly characterized. In an attempt to better delineate the clinical phenomenology of MPD, 100 recent cases were collected on a 386-item questionnaire completed by clinicians involved in the treatment of MPD patients. This study documents the existence of a clinical syndrome characterized by a core of depressive and dissociative symptoms and a childhood history of significant trauma, primarily child abuse.

Acting Out↗
PubMed1986

Effect of carbamazepine on body weight in affectively ill patients.

The effect of carbamazepine on body weight was studied in 24 patients with affective illness. Carbamazepine caused significant increases in body weight in the depressed but not the manic patients. Furthermore, the weight gain in the depressed patients seemed to be related to the response to treatment. These preliminary findings suggesting that weight gain is related to improvement in depression and not to a direct effect of the drug require further study.

Adult↗
PubMed1985

Differential mediation of the anticonvulsant effects of carbamazepine and diazepam.

Possible mechanisms of action of carbamazepine and diazepam on amygdala-kindled seizures were studied using compounds acting at the central and "peripheral-type" benzodiazepine binding sites. Ro-15-1788, a selective antagonist at the central benzodiazepine site, blocked the anticonvulsant effect of diazepam, but not of carbamazepine. In contrast, Ro5-4864, which acts at the "peripheral-type" benzodiazepine site, blocked the anticonvulsant effect of carbamazepine, but not of diazepam. The effect of Ro5-4864 was itself reversed by PK-11195, a compound that displaces Ro5-4864 binding in vitro and in vivo. These data indicate that the anticonvulsant effects of carbamazepine and diazepam on amygdala-kindled seizures are differentially mediated and suggest that the "peripheral-type" benzodiazepine binding site is functionally involved in the anticonvulsant effect of carbamazepine.

Amygdala↗
PubMed1985

Motor activity and affective illness. The relationship of amplitude and temporal distribution to changes in affective state.

We measured motor activity with a self-contained monitoring device worn on the wrists of affectively ill patients and volunteer normal control subjects. Decreases in the daytime motor activity level were observed in depressed patients, compared with their improved (euthymic) or manic mood states. Moreover, affectively ill patients, even during euthymic periods, showed lower daytime motor activity levels than the control group housed in the same ward. These data provide objective evidence for decreases in motor activity that occur concomitantly with the depressive phase of illness in patients with affective disorder, and fluctuate in patients in euthymic or manic phases.

Adult↗
PubMed1985

Effects of carbamazepine on cerebrospinal fluid somatostatin.

This paper reports the reduction of the concentration of the neuropeptide somatostatin in the CSF of patients with affective illness during treatment with the anticonvulsant carbamazepine. None of the other psychotropic agents used in this study similarly affected CSF somatostatin, although zimelidine appeared to increase CSF somatostatin in a small number of patients. The potential mechanism and significance of the effects of carbamazepine on CSF somatostatin are discussed in relation to the psychotropic, anticonvulsant, and analgesic properties of carbamazepine.

Adrenocorticotropic Hormone↗
PubMed1985

Effects of carbamazepine on noradrenergic mechanisms in affectively ill patients.

Noradrenergic mechanisms have been postulated to account for the anticonvulsant and psychotropic effects of carbamazepine. In order to assess this possibility in man, cerebrospinal fluid (CSF) was obtained from affectively ill patients before and during treatment with carbamazepine (average duration 29 days) at doses averaging 860 mg/day, achieving blood levels of 8.86 micrograms/ml. Neither plasma nor CSF norepinephrine (NE) nor CSF 3-methoxy-4-hydroxy-phenylglycol (MHPG) was significantly altered by carbamazepine. Baseline medication-free values in 21 depressed patients were not predictive of the degree of subsequent clinical antidepressant response. CSF NE decreased in four manic patients treated with carbamazepine. The many effects of carbamazepine on noradrenergic mechanisms in animals are discussed in relationship to these first studies of carbamazepine in man.

Affective Disorders, Psychotic↗
PubMed1985

CSF substance P immunoreactivity in affective disorders.

CSF substance P immunoreactivity was determined in a group of inpatient controls and acutely manic, euthymic, or depressed unmedicated unipolar and bipolar subjects; a second outpatient group of euthymic bipolar patients (on and off lithium) and normal volunteers was also studied. No group differences and no lithium effects were detected. CSF that was allowed to stand at room temperature for brief periods and then was refrozen contained elevated levels of the immunoreactive substance P, an observation that may account for a previous report of elevated CSF substance P immunoreactivity in psychiatric disorders.

Bipolar Disorder↗
PubMed1985

Adenosine antagonists. Lack of effect on the inhibition of kindled seizures in rats by carbamazepine.

This study investigates the ability of adenosine antagonists to reverse the anticonvulsant effects of carbamazepine on amygdala-kindled seizures in order to elucidate the possible physiological relevance of the potent effects of carbamazepine on adenosine receptors. At large but subconvulsant doses, neither caffeine nor theophylline altered the anticonvulsant potency of carbamazepine, even though caffeine by itself significantly increased the duration of the kindled afterdischarge. The adenosine agonist cyclohexyladenosine (CHA), administered intraperitoneally at a dose that produced sedation, had no effect on the kindled seizures. Although carbamazepine potently displaces the binding of several adenosine ligands in vitro, the present data do not suggest that the anticonvulsant effects of carbamazepine on amygdalakindled seizures are mediated by an adenosine agonist-like action.

Adenosine↗