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Biomedical subjects

R M Nesse

Publications and source records attributed to R M Nesse.

51 records · Page 3Linked to original sources
PubMed1985

Anxiety in patients with pheochromocytomas.

Anxiety has been considered an important clinical feature of patients with pheochromocytomas. We studied 17 patients with active pheochromocytoma to determine whether they experienced anxiety that met criteria of the Diagnostic and Statistical Manual of Mental Disorders, third edition, for either panic disorder or generalized anxiety disorder. Fifty-two patients with primary anxiety disorders were used as a comparison group. Six patients with pheochromocytomas had norepinephrine-secreting tumors and 11 had mixed-secretion tumors, with elevated levels of both epinephrine and norepinephrine. None of the 17 patients described the severe apprehension or fear characteristic of panic attacks and none described agoraphobia. One patient received a diagnosis of possible panic disorder, two met criteria for generalized anxiety disorder, and two met criteria for major depressive episode. Thus, the elevated levels of catecholamines secreted by pheochromocytomas are not sufficient to elicit an anxiety disorder.

Adolescent↗
PubMed1984

Adrenergic function in patients with panic anxiety.

Increased beta-adrenergic receptor sensitivity could account for many aspects of panic disorder. We tested this hypothesis by comparing 14 patients with six normal control subjects. The controls and eight patients had 14 blood samples taken, and heart rate and BP measured, during a four-hour protocol that included supine rest, a posture and isometric exercise stimulus, and a series of up to seven logarithmically increasing bolus intravenous doses of isoproterenol hydrochloride. The other six patients were studied only at rest. Patients had markedly elevated resting heart rate, substantially elevated levels of plasma epinephrine, cortisol, and growth hormone, mildly elevated plasma norepinephrine levels, and decreased heart rate responses to isoproterenol. These results suggest that beta-adrenergic receptor response is not increased, and may be decreased, in patients with panic disorder. Receptor down-regulation could result from the increased adrenergic function that these patients demonstrate, even in the absence of panic attacks.

Adult↗
PubMed1984

Platelet alpha 2-adrenergic receptor binding and plasma catecholamines. Before and during imipramine treatment in patients with panic anxiety.

Specific binding of tritiated clonidine, an alpha 2-adrenergic receptor agonist, and tritiated yohimbine, an alpha 2-adrenergic receptor antagonist, to platelet membranes was measured in persons with panic attacks or major depression and in normal subjects. Plasma catecholamine levels were measured in patients with panic attacks and in normal subjects. The number of binding sites in patients with panic attacks, as measured with tritiated clonidine, was lower than in depressed persons and was the same as in normal subjects. The number in patients with panic attacks, as measured with tritiated yohimbine, was lower than in either depressives or normal subjects. Catecholamine levels were somewhat higher in patients with panic attacks than in normal subjects. Treatment with imipramine hydrochloride decreased the number of sites, as measured with either ligand, in both patient groups and increased catecholamine levels in patients with panic attacks.

Adolescent↗
PubMed1982

The dexamethasone suppression test in panic disorder and agoraphobia.

Reports that imipramine and phenelzine prevent panic attacks in agoraphobia suggest the possibility that agoraphobia and/or panic disorder might be a clinical manifestation of underlying depression. To test this hypothesis, dexamethasone suppression tests (DSTs) were performed in 10 patients meeting DSM-III criteria for agoraphobia with panic attacks, 6 for panic disorder, and 4 whose diagnosis could have been either panic disorder or agoraphobia except that another axis I disorder precluded such a diagnosis. Abnormal DSTs were observed in only 3 patients and appeared to be attributable to causes other than panic attacks or agoraphobia. The results suggest that panic attacks and endogenous depression are separate disorders and that the antipanic properties of imipramine and phenelzine are separate from their antidepressant actions.

Adult↗
PubMed1980

Anxiety induced by flooding therapy for phobias does not elicit prolactin secretory response.

Eight subjects with severe phobias to insects and small animals had blood samples taken for measurement of prolactin concentration at regular intervals during five sessions of 3 hr duration each. Severe anxiety was induced by treating the phobia with in vivo flooding during the middle hour of the third and fourth sessions. Despite intense anxiety experienced by the subjects, they showed no change in plasma prolactin levels.

Anxiety↗
PubMed1980

Pretreatment nausea in cancer chemotherapy: a conditioned response?

Many patients receiving cancer chemotherapy become nauseated as they anticipate their treatments. We studied this phenomenon in eighteen cancer chemotherapy patients. The eight patients who reported pretreatment nausea had more extensive disease than the other patients and had received twice as much chemotherapy. In most cases pretreatment nausea developed only a after a number of months of treatment. Nausea was usually precipitated by the odor of the clinic and similar odors elsewhere also caused nausea. Patients continued to experience nausea during follow-up visits after treatment was completed. This syndrome of pretreatment nausea can be understood as a classically conditioned response. Clinical recommendations can be made on this basis.

Adult↗
PubMedDate not supplied

Endocrine and cardiovascular responses during phobic anxiety.

In vivo exposure therapy for phobias is uniquely suited for controlled studies of endocrine and physiologic responses during psychologic stress. In this study, exposure therapy induced significant increases in subjective anxiety, pulse, blood pressure, plasma norepinephrine, epinephrine, insulin, cortisol, and growth hormone, but did not change plasma glucagon or pancreatic polypeptide. Although the subjective and behavioral manifestations of anxiety were consistent and intense, the magnitude, consistency, timing, and concordance of endocrine and cardiovascular responses showed considerable variation.

Adult↗
PubMedDate not supplied

Peripheral catecholamine levels and the symptoms of anxiety: studies in patients with and without pheochromocytoma.

We studied the correlation of plasma and urinary epinephrine (E) and norepinephrine (NE) levels with anxiety symptoms in three patient groups: 1) pheochromocytoma (PH+) (n = 17); 2) hypertensives with elevated catecholamine levels shown not to have a PH (PH-) (n = 25); and 3) patients with panic disorder (PD) (n = 23). Structured interviews and four self-rated anxiety scales were used: the SCL-90R Anxiety and Phobic Anxiety scales, and the Spielberger State/Trait Anxiety Inventories. The SCL-90R Somatization scale (which measures 12 somatic symptoms) was also utilized. None of the PH+ patients met DSM-III criteria for PD. Two met criteria for generalized anxiety disorder (GAD). Of the PH- patients, two had PD, two had GAD, and three had both. Urinary and plasma E did not show significant positive correlations with any of the four anxiety scales in any of the three patient groups. In both the PH+ and PH- groups, E was significantly correlated with the SCL-90R Somatization scale. NE was not significantly correlated with any of the four anxiety scales in the PH+ group. In contrast, in the PH- group, plasma NE was significantly correlated with anxiety on all anxiety scales (r = +0.55 to +0.77, p less than 0.05). Furthermore, in the PH- group, plasma NE was significantly correlated with those items of the SCL-90R Anxiety scale measuring the cognitive rather than the noncognitive symptoms of anxiety. In the PD group as well, plasma NE showed a significant correlation with the SCL-90R Anxiety Scale (r = +0.67, p less than 0.05). Taken together, our observations suggest that: 1) the effects of catecholamines in the periphery derived from a source independent of nervous system control (such as a PH) are not sufficient to elicit an anxiety disorder meeting DSM-III criteria; and 2) in patients without an autonomous source of peripheral catecholamines, NE in the periphery results from sympathetic nervous system activation and probably reflects, rather than causes, anxiety.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Platelet alpha 2-adrenoreceptors, catecholamines, hemodynamic variables, and anxiety in panic patients and their asymptomatic relatives.

The objectives of this study were to a) replicate our prior finding of a decreased number (Bmax) of platelet alpha 2-adrenoreceptors in panic disorder, b) determine if binding is also decreased in asymptomatic first-degree relatives of panic patients (known to be at increased risk for developing panic), and c) evaluate the effect of treatment on the presumptive decrease in binding (i.e., is the decrease a state or a trait marker for panic?). Panic patients had clonidine and yohimbine platelet-binding assays, symptom ratings, and measurement of lying and standing plasma epinephrine, norepinephrine, systolic and diastolic blood pressure, and heart rate before treatment, after approximately 2 months of medication (fluoxetine, tricyclics, or alprazolam) and/or cognitive behavioral treatment, and after symptom remission while drug free; normal subjects had determinations of the same measures at approximately the same time intervals. Relatives of both groups had one determination only of all measures. Tritiated clonidine binding was decreased and lying heart rate was increased in patients before treatment. Magnitude of binding decrease was correlated with symptom severity and standing norepinephrine. No binding abnormality was seen in first-degree relatives of patients. Treatment increased clonidine binding in patients. Both patients and relatives of patients showed significantly increased standing plasma norepinephrine in comparison to controls. There is a state-related decrease in binding, associated with symptom severity and norepinephrine, in panic disorder. Abnormal reactivity of norepinephrine to standing might be a marker for increased likelihood of panic development in individuals at risk.

Adult↗
PubMedDate not supplied

Respiratory psychophysiology and anxiety: cognitive intervention in the doxapram model of panic.

UNLABELLED: The goals of this study were to: a) confirm prior evidence that the respiratory stimulant doxapram induces panic attacks and produces excessive hyperventilation in patients with panic disorder and b) explore the impact of cognitive mediators on symptom and respiratory responses. METHOD: Thirty-two subjects (16 patients and 16 controls) received doxapram (0.5 mg/kg) and placebo infusions while symptom, respiratory, and heart rate responses were monitored. Subjects were randomly assigned to receive either a standard introduction or a cognitive intervention designed to reduce the panic responses of panic patients to laboratory challenges. RESULTS: Doxapram was a potent and specific panicogenic agent, inducing panic in 75% of patients and 12.5% of controls. Compared with controls, patients also showed a greater decrease in end tidal carbon dioxide (CO2) and greater increases in minute ventilation, respiratory frequency, and heart rate. The cognitive intervention substantially attenuated the excessive hyperventilatory response of patients but did not fully normalize their breathing patterns. Tidal volume was the only respiratory measure not significantly altered by the cognitive intervention. CONCLUSIONS: In patients with panic disorder, doxapram (0.5 mg/kg) triggers panic attacks about as potently as 7% CO2 and more potently than 5% CO2 or lactate. Psychological factors can modulate the appearance of ventilatory abnormalities in panic patients, but persistent respiratory disturbances were still seen. Psychological factors and respiratory physiology both appear to be important phenomena in laboratory panic.

Adult↗