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Biomedical subjects

R M Post

Publications and source records attributed to R M Post.

At least 235 records · Page 13Linked to original sources
PubMed1988

Effects of thyroid alterations and carbamazepine on cortical beta-adrenergic receptors in the rat.

The effect of alteration in thyroid status on beta adrenergic receptors in the cortex of the rat was assessed. Normal animals were treated with large doses of thyroxine (T4) and triiodothyronine (T3) and thyroidectomized animals were treated with physiological replacement doses of T4 and T3 in order to assess the possible differential effects of these hormones. In addition, a group of rats was treated with a diet of carbamazepine (an anticonvulsant also used in the treatment of manic-depressive illness), which has been shown to reduce peripheral levels of thyroid hormone in humans. The intended manipulations of the thyroid were achieved by the various treatments with thyroid hormone, and carbamazepine-diet-treated animals had significantly lower plasma T4 levels as compared with controls. No significant alteration in the density or affinity of beta-adrenergic receptors in the cortex was noted with major, short-term alterations in thyroid status or with treatment with carbamazepine. It is concluded that even marked, but relatively short-term, changes in thyroid status do not necessarily affect beta-receptors in the cerebral cortex and that carbamazepine may represent an exception to the general proposition that antidepressant agents decrease the number of beta-receptors.

Animals↗
PubMed1988

Ventricular-brain ratio and life course of illness in patients with affective disorder.

The relationship between ventricular-brain ratio (VBR) on computed tomography of the brain and life course of illness was assessed in 59 hospitalized patients with recurrent affective disorder. In contrast to the implications of some, but not all, prior studies. VBR was not positively related to episode frequency, severity, pattern, or chronicity. In fact, when analyzed by sex, in both males and females, VBR was inversely related to several measures of illness chronicity.

Adult↗
PubMed1988

Somatostatin in neuropsychiatric disorders.

1. Somatostatin is a peptide that is widely and discretely distributed throughout the central nervous system. 2. Its relevance to neuropsychiatric disorders is suggested both by the existence of disease-related alterations in somatostatin content in brain and cerebrospinal fluid as well as by the manifold neuroregulatory capabilities of somatostatin and related peptides. 3. This article will summarize the central nervous system effects of somatostatin, identify those neuropsychiatric disorders that are characterized by changes in somatostatin, and review the evidence for and potential significance of decreases in cerebrospinal fluid somatostatin in depression.

Central Nervous System↗
PubMed1988

Graphic representation of the life course of illness in patients with affective disorder.

The authors illustrate methods for the graphic depiction of the course of unipolar and bipolar affective illness. The utility and advantages of such an approach include 1) accurate assessment of episode patterns, 2) elucidation of relationships to environmental events, endocrine and seasonal factors, and psychosocial stressors, 3) better delineation of treatment response, 4) a greater understanding of the longitudinal and characteristic patterns of illness, and 5) the associated better patient management with psychotherapeutic and pharmacological interventions.

Bipolar Disorder↗
PubMed1988

Lack of efficacy of carbamazepine in the treatment of panic disorder.

The authors conducted a controlled study of carbamazepine in the treatment of 14 patients with panic disorder. Although there was a statistically significant reduction in symptoms of anxiety on several measures, only one of the patients was judged to have a marked and sustained clinical improvement while taking carbamazepine. Forty percent of the patients had a decrease in frequency of panic attacks during carbamazepine treatment, 50% had an increase, and 10% showed no change. The presence of either EEG abnormalities or prominent psychosensory symptoms did not predict response to carbamazepine. These findings are discussed within the context of an epileptiform model for panic disorder.

Adult↗
PubMed1988

Time course of clinical effects of carbamazepine: implications for mechanisms of action.

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.

Affect↗
PubMed1987

Lack of effect of chronic carbamazepine on brain somatostatin in the rat.

We investigated the effects of chronic carbamazepine treatment in rats on brain somatostatin. Following 12 days of carbamazepine treatment, no changes in somatostatin levels were found in any of the brain areas examined which included: amygdala, hippocampus, caudate-putamen, median eminence, arcuate nucleus, nucleus accumbens, nucleus interstitialis of the stria terminalis, nucleus periventricularis, parietal cortex, and occipital cortex. Thus, carbamazepine in low doses does not affect basal levels of brain somatostatin in the rat, in contrast to the previous reports of decreased somatostatin in the cerebrospinal fluid of affectively ill patients.

Animals↗
PubMed1987

Motor activity in depressed patients treated with carbamazepine.

Motor activity in 19 depressed patients treated with carbamazepine was assessed using self-contained monitors worn on the wrist. Those whose depression improved demonstrated significant increases in motor activity. Nonresponders as a group did not show decreased motor activity, suggesting that carbamazepine was not producing sedation or hypoactivity at clinically relevant doses. Activity counts were negatively correlated with ratings of global severity of depression on the Bunney-Hamburg Scale and with degree of motor retardation rated on the BPRS during treatment. The selective increases in motor activity in those who improved are consistent with psychomotor changes related to amelioration of depression.

Adult↗
PubMed1987

Intravenous procaine as a probe of limbic system activity in psychiatric patients and normal controls.

Evidence from animal and human studies suggests that procaine hydrochloride may selectively activate limbic system structures and suppress neocortical structures. We administered a series of intravenous bolus doses of procaine hydrochloride to 31 subjects (7 with affective disorders, 17 with borderline personality disorder, and 7 healthy normal volunteers). Dose-related cognitive and sensory distortions and illusions were observed; affective experiences ranged widely from euphoric to dysphoric. Topographic electroencephalogram (EEG) analysis indicated selective increases in fast activity (26-45 Hz) over the temporal lobes; the degree of increase in this activity correlated with degree of dysphoria experienced. Procaine was associated with increases in secretion of cortisol, adrenocorticotrophic hormone (ACTH), and prolactin, but not with growth hormone. These preliminary data are consistent with the possibility that procaine might serve as a clinically useful probe of psychosensory, affective, electrophysiological, and endocrine effects referable to the limbic system.

Adrenocorticotropic Hormone↗
PubMed1987

Platelet [3H]imipramine binding in patients with panic disorder.

[3H]imipramine binding to platelets was measured in 17 drug-free panic disorder patients and 14 healthy controls. No difference in Bmax or Kd values was found between the two groups. Patients with a past history of major melancholic depression or severe agoraphobia had similar binding parameters as panic disorder patients without a history of depression or severe agoraphobia.

Adult↗
PubMed1987

Glucose utilization in the temporal cortex of affectively ill patients: positron emission tomography.

As temporal lobe dysfunction has been postulated in the affective disorders, the authors investigated glucose utilization in the temporal lobes of 13 affectively ill patients in comparison with 18 normal volunteer controls and 17 previously reported schizophrenic patients, following injections of fluorine 18-2-deoxy-D-glucose (FDG) during somatosensory stimulation to the right forearm. Using a boundary-finding algorithm to outline each temporal lobe, maximum glucose use relative to maximums elsewhere in the same positron emission tomography (PET) slice were calculated. In a small group of moderately to severely depressed patients, this relative measure was significantly reduced in the right (with a similar trend in the left) temporal lobe compared to normal volunteers and the other comparison groups. The lack of a significant increase in glucose utilization, measured either as a maximum or in relation to other areas in the PET scan slice, suggests that a temporal lobe activation or a seizure-like process is not generally occurring during active depressive phases of the illness.

Affective Disorders, Psychotic↗
PubMed1987

Differential time course of antidepressant effects after sleep deprivation, ECT, and carbamazepine: clinical and theoretical implications.

The pattern and time course of antidepressant response to different treatment modalities provide important clinical information and hints about underlying neurobiological mechanisms. Depressed patients who responded to 1 night's sleep deprivation (11 of 33 patients) showed maximal improvement on day 1 and deterioration in mood thereafter. In contrast, slower onset and more sustained effects were observed following carbamazepine (12 of 37) or electroconvulsive therapy (ECT) (8 of 8). Nearly maximal improvement required about 2 weeks for ECT and 3 weeks for carbamazepine. Possible differential or common biological mechanisms with differential times of action are implied by these data, which are of importance to the neuroscientist attempting to uncover neural substrates of antidepressant response and the clinician attempting to find rapid onset, yet sustained antidepressant treatments.

Carbamazepine↗
PubMed1987

Correlates of antimanic response to carbamazepine.

Nineteen acutely manic patients were studied in a double-blind trial of carbamazepine in doses averaging 1240 mg/day, achieving blood levels of 10.4 +/- 2.2 micrograms/ml. Clinical improvement in mood and psychomotor components of the manic syndrome was rapid in onset, generally parallel to that observed in previous patients treated with neuroleptics, and was associated with increases in the total hours of nighttime sleep. Compared to the seven nonresponders, the 12 patients who improved were significantly more manic during the baseline placebo period, tended to be more dysphoric, and were significantly more rapid cyclers over their entire course of illness as assessed by episodes in the year before NIMH admission (7.0 +/- 5.6 vs. 2.7 +/- 2.4 in the nonresponders). While improvement was robust in responders, it was not always complete, and some of these patients remained mildly to moderately symptomatic. All seven patients with a negative family history of affective illness in first degree relatives were responders, while those with a positive family history were equally divided. These preliminary data suggest that several predictors of poor response to lithium carbonate (manic severity, anxiety and dysphoria, rapid cycling, and negative family history) may be associated with good antimanic response to carbamazepine.

Antipsychotic Agents↗