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Biomedical subjects

M E Tancer

Publications and source records attributed to M E Tancer.

36 records · Page 2Linked to original sources
PubMed1991

Phenomenology and neurobiology of social phobia: comparison with panic disorder.

Like panic disorder, social phobia is a common, frequently severe, anxiety disorder that can cause significant work and social impairment. Unlike panic disorder, social phobia has only recently begun to undergo neurobiologic study and to receive pharmacotherapeutic attention. There is a high comorbidity between social phobia and panic disorder; however, many differences exist--including age at onset, gender distribution, contextual framework of anxiety, help-seeking and help-avoidance behavior, quality of sleep and sleep patterns, caffeine and lactate sensitivity, and, most probably, pharmacologic responses. Social phobia can now be included among the growing number of anxiety disorders that respond to pharmacotherapy.

Adult↗
PubMed1990

Paradoxical growth-hormone responses to thyrotropin-releasing hormone in panic disorder.

Thyrotropin-releasing hormone (TRH) has been reported to stimulate growth hormone (GH) release in a variety of pathological conditions, including some studies of major depression. Because of the considerable phenomenological and neuroendocrine overlap between major depression and panic disorder, we investigated the rate of positive GH responses to TRH in 38 patients with panic disorder and 23 normal controls. There were no between-group differences in mean GH response to TRH or in the proportion of subjects with positive responses. These findings are discussed in the context of neuroendocrine regulation of GH secretion and the relationship between anxiety and affective disorders.

Adult↗
PubMed1990

Behavioral effects of chronic imipramine treatment in genetically nervous pointer dogs.

The genetically nervous pointer dog has been proposed as a model for human anxiety disorders. In a double-blind placebo-controlled study, seventeen nervous pointer dogs were treated for four weeks with imipramine hydrochloride (10 mg/kg), a potent antipanic agent in humans. Although three of the dogs demonstrated marked improvement to imipramine but not placebo treatment after short-term administration, chronic imipramine failed to modify the aberrant behavior in any of the dogs. These findings are discussed in the context of the nervous pointer dog as a model for human anxiety disorders.

Animals↗
PubMed1990

Major depression in patients with panic disorder: factors associated with course and recurrence.

The relationship between anxiety and depressive disorders has been the subject of considerable interest and controversy. In this study, the occurrence and course of affective illness was systematically examined in 63 patients meeting DSM-III-R criteria for panic disorder. Forty (63%) of the patients had experienced at least one major depressive episode. Of these, 13 (32.5%) experienced their first depressive episode prior to the onset of panic disorder, 15 (37.5%) experienced their first depressive episode after the onset of panic disorder, and in 12 (30.0%) the onset of the disorders was concurrent. Patients with agoraphobia had comparable rates of depression (68%) to patients without agoraphobia (53%, P = NS), and they had similar temporal patterns of depressive illness. Comorbidity with social phobia was associated with an increased longitudinal likelihood of major depression compared to patients without this comorbid diagnosis (P less than 0.05). Patients with longer duration of illness, early onset depression, melancholic depression, or family histories of anxiety or depression had an increased likelihood of having experienced recurrent depression. These findings are discussed in the context of current theories regarding the development of affective illness in patients with anxiety disorders.

Adult↗
PubMed1990

Impaired effortful cognition in depression.

Depressed patients have been reported to have deficits in "effortful," but not effortless, cognitive functions compared to healthy volunteers. To test the hypothesis that the effortful cognitive deficits in major depression are not simply a function of psychiatric illness or hospitalization, we administered both effort-demanding and effortless cognitive tasks to 17 inpatients with major affective disorder and 17 hospitalized psychiatric controls. The depressed patients performed significantly more poorly than the controls on the effort-demanding task. The groups did not differ on the effortless task. These findings suggest that depressed patients are impaired in performing effort-demanding cognitive tasks compared to nondepressed psychiatric patients.

Adjustment Disorders↗
PubMed1990

Growth hormone (GH) response to clonidine and growth hormone releasing factor (GRF) in normal controls.

To investigate the relationship between the plasma growth hormone (GH) response to provocative challenge with the hypothalamic peptide growth hormone-releasing factor (GRF) and the alpha 2-adrenergic agonist clonidine, we administered GRF (1 microgram/kg), clonidine (2 micrograms/kg), and placebo to 21 healthy normal controls (13 men and eight women). Both clonidine and GRF caused significant increases in plasma GH levels over baseline. The peak GH-responses to GRF and clonidine were similar (GRF = 8.7 +/- 6.7 ng/ml; clonidine = 6.5 +/- 5.9 ng/ml; Wilcoxon test: s = 361, z = -1.31, p = NS). The GH responses to GRF and clonidine were significantly correlated (rs = 0.62, n = 20, p = 0.004). Unexpectedly, we found that five of the 21 (26%) normal controls had no GH secretory response to either GRF or clonidine. There was a modest gender effect with clonidine (men greater than women; p less than 0.06) and a negative correlation between GH secretion and age with both GRF and clonidine. Neither GRF nor clonidine had an effect on cortisol levels (DRUG x TIME interaction: F(8,152) = 0.60, p = NS). These findings are consistent with animal studies suggesting that the GH response to clonidine is mediated by GRF. The age and gender effects underscore the importance of careful matching for these factors in studies measuring the GH secretory response.

Adult↗
PubMed1990

Major depression in patients with social phobia.

The authors examined the longitudinal course of affective illness retrospectively in 63 patients with social phobia and 54 patients with panic disorder. Significantly fewer (35%) of the patients with social phobia than patients with panic disorder (63%) had experienced at least one major depressive episode. Patients with generalized social phobia and patients with specific social phobia had comparable past rates of major depression (37% and 30%, respectively). The clinical and theoretical implications of these findings are discussed within the context of current concepts regarding the development of depressive symptoms in patients with anxiety disorders.

Adolescent↗
PubMed1990

The hypothalamic-pituitary-thyroid axis in social phobia.

The authors investigated indices of hypothalamic-pituitary-thyroid (HPT) axis function in patients with social phobia. They found no differences between patients with social phobia and age- and sex-matched control subjects in plasma T3, T4, free T4, or TSH levels or in the proportion of subjects with positive antithyroid antibodies. Patients with social phobia and control subjects also did not differ in three of the four measures used to assess TSH response to TRH. These data suggest that abnormalities in thyroid function are not requisite neuroendocrine correlates of social phobia.

Humans↗
PubMed1989

Use of electroconvulsive therapy at a university hospital: 1970 and 1980-81.

The use of electroconvulsive therapy (ECT) at a university teaching hospital in 1970 and in 1980-81 was reviewed. The percentage of psychiatric patients who received ECT declined modestly over the period, from 4.4 percent to 2.9 percent, despite compelling evidence of its safety and efficacy. Its use as a first-line treatment appeared to drop markedly in 1980-81, however, as indicated by a significantly longer mean period of hospitalization before administration of ECT. Overall length of hospitalization was significantly longer for patients who received ECT in 1980-81. These patients were also more likely to have had previous psychiatric admissions, suggesting they may have been more seriously ill. The findings are compared with use of ECT in other settings.

Adolescent↗
PubMed1987

Iron homeostasis in beta-thalassemic mice.

To explore the pathogenesis of nontransfusional iron overload in iron-loading anemia, we examined features of external iron exchange, internal iron kinetics, and tissue iron burden in adult mice with inherited gene-deletion beta-thalassemia. Mice homozygous for beta-thalassemia display moderate anemia, reticulocytosis, and shortened red cell survival, whereas heterozygous carriers appear hematologically normal. Quantitative iron determination revealed that iron content and concentration in liver, spleen, and kidney, but not heart, were far higher (P less than .01) in 15-to 35-week old homozygous thalassemic mice than in age-matched normal and heterozygous controls; of these tissues, iron content increased with age only in kidneys (P = .01) of homozygous affected mice. Although plasma iron levels were only minimally elevated in homozygotes, plasma iron turnover was threefold greater (P less than .001) than that seen in heterozygote controls. Nevertheless hyperabsorption of enteric radioiron, discernible among homozygous thalassemic mice as late as 6 to 8 weeks after birth, was not observed in older mice, additionally, thalassemic and control mice at 18 to 34 weeks showed comparable iron excretion after intravenous radioiron. We conclude that adult mice with beta-thalassemia regain balanced external iron exchange, despite substantial tissue iron excess and accelerated internal iron transit.

Animals↗
PubMedDate not supplied

Short stature, growth hormone deficiency, and social anxiety.

OBJECTIVE: We have reported high rates of social phobia in growth hormone-deficient (GHD) adults who had been treated with growth hormone during childhood. This follow-up study was conducted to determine whether the increased social phobia observed in GHD subjects was secondary to the effects of short stature. METHODS: Twenty-one age- and sex-matched non-GHD short adults were evaluated for social anxiety and compared with the previously studied 21 GHD subjects. RESULTS: Thirty-eight percent (8 of 21) of GHD and 10% (2 of 21) of short subjects met DSM-III-R criteria for social phobia. GHD subjected scored significantly higher than short subjects on the following self-report questionnaires: Fear of Negative Evaluation (p = .03), Fear Questionnaire (p = .01), Social Avoidance and Distress Scale (p = .01), Beck Depression Inventory (p = .007), and the Tridimensional Personality Questionnaire-harm avoidance subscale (p = .0004). CONCLUSIONS: These data suggest that the high prevalence of social phobia in GHD adults is not explained by short stature alone.

Adolescent↗
PubMedDate not supplied

Neuroendocrine responsivity to monoaminergic system probes in generalized social phobia.

We examined neuroendocrine correlates of central monoamine function in patients with the generalized type of social phobia compared to healthy volunteers in order to test hypotheses of dopaminergic, noradrenergic, and/or serotonergic dysregulation in patients with this disorder. A double-blind, placebo-controlled, neuropharmacological challenge study was performed using probes for the serotonergic (fenfluramine), dopaminergic (levodopa), and noradrenergic (clonidine) systems. Twenty-one patients with DSM-III-R social phobia (generalized type) and 22 "never mentally ill" volunteers participated in the study after providing informed consent. Patients with social phobia had an augmented cortisol response to fenfluramine administration compared to the volunteers. In contrast, we found that neither the prolactin response to fenfluramine, the growth hormone or norepinephrine response to clonidine, nor the prolactin or eye-blink responses to levodopa, differed between patients with social phobia and healthy volunteers. The findings suggest that patients with social phobia may exhibit selective supersensitivity of serotonergic systems, but that dopaminergic and noradrenergic function appear normal. Further challenge studies with more specific serotonin probes before and after treatment may assist in the clarification of the pathophysiology of social phobia.

Adrenergic alpha-Agonists↗