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Biomedical subjects

R M Post

Publications and source records attributed to R M Post.

At least 289 records · Page 16Linked to original sources

Dissociative states in multiple personality disorder: a quantitative study.

Multiple personality disorder (MPD) patients may experience themselves as several discrete alter personalities who do not share consciousness or memories with one another. In this study, we asked whether MPD patients are different from controls in their ability to learn and remember, and their ability to compartmentalize information. MPD patients were not found to differ from controls in overall memory level. Learning of information by MPD patients in disparate personality states did not result in greater compartmentalization than that of which control subjects were capable. However, there were qualitative differences between the cognitive performance of patients and that of controls attempting to role-play alter personalities. Our results suggest that simple confabulation is not an adequate model for the MPD syndrome, and we consider a possible role for state-dependent learning in the phenomenology of MPD.

Adult↗

Normal pain sensitivity in patients with panic disorder.

The pain sensitivity of 18 patients with panic disorder and age- and sex-matched controls was assessed by signal detection analysis. The authors failed to demonstrate any difference in pain sensitivity between the two groups. The relationship between state anxiety, as assessed by the Spielberger scale, and pain in panic patients tended to be in the opposite direction from that in normals.

Adult↗

Longitudinal course of panic disorder: clinical and biological considerations.

The longitudinal course of panic disorder and its associated symptoms were investigated in thirty-eight patients. The temporal relationships among panic attacks, generalized anxiety, agoraphobia and depression are described. Similar and different biological alterations in the tricyclic-responsive disorders of primary depression and panic disorder are reviewed and discussed.

Adult↗

CSF somatostatin in affective illness and normal volunteers.

Somatostatin is a hypothalamic tetradecapeptide with many central nervous system actions. We investigated a potential role for altered somatostatin activity in affective disorder by measuring somatostatin in the cerebrospinal fluid (CSF) of 47 patients with affective disorder and of 39 normal volunteers. Medication-free depressed patients showed significantly lower levels of CSF somatostatin than normal volunteers (p less than .001) or patients during the improved state (p less than .01). Somatostatin levels were significantly and inversely correlated with duration of sleep on the night of the lumbar puncture (p less than .05). Treatment with carbamazepine reduced CSF somatostatin (p less than .01) in contrast to the absence of effect of imipramine, desmethylimipramine, and lithium carbonate and the significant increase in CSF somatostatin seen in a small group of patients treated with zimelidine. The implications of these findings with respect to attempts to explore the neurobiology of depression are discussed.

Bipolar Disorder↗

The longitudinal course of recurrent affective illness: life chart data from research patients at the NIMH.

Using data gathered in a naturalistic study of 95 research patients at the NIMH, a retrospective method of documenting the life course of recurrent affective illness is presented, along with a partial prospective validation of this method. In these patients, the severity, frequency, and duration of manic and depressive episodes, as well as their pattern and distribution, are characterized. These variables are examined in different patients subgrouped according to gender and age of onset, polarity, and rapidity of cycling of illness. The findings are compared with data on the life course of affective illness found in studies from the pre-pharmacologic era.

Adult↗

Relationship between cerebrospinal fluid somatostatin and peripheral thyroid hormones with carbamazepine treatment.

The relationship between CSF somatostatin and peripheral thyroid hormones was assessed in 11 affectively ill patients before and during carbamazepine treatment. A direct relationship between CSF somatostatin and plasma thyroxine and free thyroxine, but not triiodothyronine, was observed both while patients were medication-free and during carbamazepine treatment. These first data in man are consistent with those in animals, suggesting a close interrelationship between somatostatin and thyroid regulation.

Adult↗

Hematological effects of carbamazepine in patients with affective illness.

The hematological effects of carbamazepine, a drug effective in the acute and prophylactic treatment of manic-depressive disorder, were assessed in 43 subjects with affective disorder. Carbamazepine was found to cause statistically significant, but clinically insubstantial, decreases in white blood cell indexes. The consistent decreases in white cell counts observed with carbamazepine should be differentiated from the extremely rare, idiosyncratic blood dyscrasias reported in the literature.

Adult↗

Premenstrual mood disorder and psychiatric illness.

The results of several studies suggest that a special relationship exists between premenstrual syndromes and major psychiatric disorders, particularly affective illness. These studies in general have not employed prospective criteria to diagnose premenstrual syndrome. In this paper the authors report a significant difference in the lifetime history of psychiatric illness between women with prospectively confirmed menstrually related mood disorder and those without it.

Adult↗

Premenstrual syndromes: past and future research strategies.

Premenstrual Syndrome remains a poorly understood controversial disorder largely because of the errors in design found in research into this subject. The first task is to clearly define the entity to be studied. It is necessary to look at the nature, intensity and time of occurrence of symptoms in relation to menstruation. One must further differentiate the appearance of symptoms premenstrually from the premenstrual exacerbation of symptoms present throughout the menstrual cycle. Research has clearly shown the superiority of prospective versus retrospective data in establishing a linkage between symptoms and menstruation. Premenstrual Syndrome research offers a unique opportunity to study classical psychiatric disorders. A relationship appears to exist between this syndrome and major affective disorders. Studies of the appearance or exacerbation of mood disturbances in relation to the menstrual cycle may inform us about the development, course and vicissitudes of psychiatric illness.

Affect↗

Transient sensory, cognitive and affective phenomena in affective illness. A comparison with complex partial epilepsy.

Behavioural changes have often been noted in patients with epilepsy. This study investigated the converse phenomenon--the occurrence of transient sensory, cognitive and affective changes resembling those described by epileptics, in affectively ill patients. Forty-four patients with affective illness, 37 with complex partial seizures, and 30 hypertensive controls were interviewed to determine the lifetime occurrence of these phenomena. Such symptoms occurred frequently in association with episodes of affective illness and epilepsy, but were rare in controls. Visual, auditory, olfactory and epigastric symptoms, illusions, jumbled thoughts and amnesia were common to both epilepsy and affective illness. Greater numbers of symptoms were associated with better response to lithium and tricyclic antidepressants. Transient sensory, cognitive, and affective phenomena may be more common in affective illness and other psychiatric conditions than is generally recognised, and may be clues to the underlying pathophysiology of these conditions.

Adult↗

Metabolic and behavioral consequences of lidocaine-kindled seizures.

Daily administration of lidocaine results in progressive increases in frequency and duration of convulsions in response to a dose of drug which was previously subconvulsive--a pharmacological kindling phenomenon. The effects of such lidocaine-kindling on local cerebral glucose utilization were determined by the 2-[14C]deoxyglucose method. Lidocaine-treated animals, in the absence of convulsions, exhibited decreased glucose utilization in most brain structures compared to saline-treated animals and showed no increase in aggressive behavior. In animals displaying lidocaine-kindled convulsions there were marked increases in glucose utilization in either the hippocampus and amygdala or in perirhinal cortical areas during the seizure administration; these animals also displayed long-lasting increases in irritable behavior. Seizure duration was positively correlated with the rate of glucose utilization in the hippocampus, amygdala and septum, but inversely correlated in several non-limbic areas. These data suggest that lidocaine-kindled seizures are highly localized to limbic and perirhinal structures and are associated with important behavioral consequences.

Aggression↗

Peripheral benzodiazepine binding sites in kidney: modifications by diabetes insipidus.

Using [3H] diazepam as ligand, it is possible to distinguish neuronal binding sites from those present on glial elements and in peripheral tissues (non-neuronal). The function of the "non-neuronal" binding sites is still obscure. Preliminary data showed a distribution of [3H] diazepam binding sites in kidney that could suggest a localization along the renal tubules. This is the site at which a renal peptide, arginine-vasopressin (AVP) is supposed to act. In an attempt to examine the function of these "non-neuronal" sites, we studied the [3H] diazepam binding in kidney of Brattleboro rats which lack AVP and present the symptoms of diabetes insipidus. The homozygous Brattleboro rats showed an increase in the apparent number of benzodiazepine binding sites (Bmax) compared to Long-Evans control rats. Replacement of AVP in these animals results in a reversal of the electrolyte alterations of diabetes insipidus and in an increase of the affinity of the [3H] diazepam binding. These findings may indicate a possible relationship between benzodiazepine binding sites and vasopressin action in kidney and may support receptor function of these "non-neuronal" binding sites.

Animals↗

Increased sensitivity to caffeine in patients with panic disorders. Preliminary evidence.

The results of a caffeine consumption inventory indicated that patients with panic anxiety disorder, but not affectively ill patients or normal controls, had levels of self-rated anxiety and depression that correlated with their degree of caffeine consumption. In addition, this self-report survey suggested that patients with panic disorder had an increased sensitivity to the effects of one cup of coffee. This apparent sensitivity to caffeine was also documented by the observation that more patients with panic disorder reported the discontinuation of coffee intake due to untoward side effects than controls. These results, based on self-reports, suggest that the hypothesis that patients with panic disorder are more reactive to caffeine should be directly tested using caffeine challenges and that the mechanisms underlying caffeine's effects on anxiety should be further explored.

Adult↗

Plasma cortisol responses to clonidine in depressed patients and controls. Evidence for a possible alteration in noradrenergic-neuroendocrine relationships.

Plasma cortisol responses to the intravenous administration of clonidine hydrochloride and placebo were evaluated in depressed patients and controls. Depressed patients had higher mean baseline cortisol levels than controls. Cortisol levels decreased during the morning study period following both placebo and 2 micrograms/kg of clonidine hydrochloride in the depressed patients, but the cortisol decrease was sixfold greater on the day of clonidine administration; these placebo-clonidine differences were statistically significant, whether calculated on an absolute decrement basis or as a percent change. In contrast, controls responded to clonidine with only a 1.5-fold greater cortisol reduction than that found after placebo, a nonsignificant difference from the day of placebo administration. Reductions in the concentration of plasma 3-methoxy-4-hydroxyphenylglycol following clonidine administration were significantly negatively correlated with baseline plasma cortisol levels, raising the possibility that abnormalities in the responsiveness of the alpha 2-noradrenergic system may be associated with the hypothalamo-pituitary-adrenal (HPA) axis dysfunction found in depressed patients.

Aged↗