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Biomedical subjects

T W Uhde

Publications and source records attributed to T W Uhde.

At least 55 records · Page 3Linked to original sources
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

Plasma 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) and growth hormone responses to yohimbine in panic disorder patients and normal controls.

Eleven patients with a DSM-III diagnosis of panic disorder and seven normal controls received yohimbine (20 mg) or placebo orally in a double-blind paradigm on two separate days. Compared to normal control subjects, the panic disorder patients had similar behavioral responses to placebo but a greater anxiogenic response to yohimbine. Compared to placebo, yohimbine produced a significant increase in plasma 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) levels (p less than 0.02), with a trend toward greater MHPG rises in the panic disorder patients compared to the normal controls. In the patients, but not in the controls, there was a significant positive correlation between yohimbine-induced peak changes in MHPG and increased ratings of panic anxiety. Yohimbine had no effect on plasma growth hormone (GH) levels in either patients or controls. These results are discussed within the context of the noradrenergic theory of panic disorder.

Adult↗
PubMed1990

Thyrotropin and prolactin responses to protirelin (TRH) prior to and during chronic imipramine treatment in patients with panic disorder.

The effects of protirelin [thyrotropin-releasing hormone (TRH)] administration on the release of thyrotropin (TSH) and prolactin (PRL) were examined in 14 patients with panic disorder prior to and during chronic treatment with imipramine. During imipramine treatment, the patients exhibited an increase in their TSH response to TRH (delta delta max TSH = 3.65 +/- 6.02 mu IU/ml, p less than 0.05) and in their PRL response to TRH (delta AUCPRL = 734 +/- 965 ng/ml/45 min, p less than 0.005). Several behavioral measures correlated with the neuroendocrine measures during imipramine therapy. These preliminary findings might suggest a role for changes in dopaminergic function in the clinical effects of imipramine in patients with panic disorder.

Adult↗
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

Anxiety disorders in patients with Parkinson's disease.

To study the prevalence and importance of anxiety disorders in patients with idiopathic Parkinson's disease, the authors systematically evaluated 24 parkinsonian patients for the presence of DSM-III-R axis I syndromes. Nine subjects (38%) had a clinically significant current anxiety disorder. Severity of anxiety was not correlated with severity of parkinsonian symptoms, cumulative duration of L-dopa exposure, or current dose of L-dopa. These findings suggest that anxiety disorders should be considered in the medical evaluation and treatment of parkinsonian patients and that further attention should be paid to the role of the dopaminergic system in anxiety and phobic disorders.

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↗
PubMed1990

Biogenic amines distribution in the brain of nervous and normal pointer dogs. A genetic animal model of anxiety.

Nervous pointer dogs have been suggested as an animal model for pathological anxiety. In order to study possible disturbances in neurotransmitter functions in this animal model, we measured brain biogenic amines (norepinephrine, dopamine, and serotonin) and their metabolites in both nervous and normal dogs. Eight nervous and six normal dogs were behaviorally tested and later anesthetized and killed. Brains were removed and dissected while frozen using a punch technique. Samples were assayed using high-performance liquid chromatography (HPLC) with electrochemical detection. The nervous dogs had higher [NE] in the reticular formation and lower serotonin, and its metabolite 5-hydroxyindoleacetic acid, in the septal nuclei, indicating possible important differences in noradrenergic and serotonergic functions in the nervous dogs. There was a trend for lower [HVA] and [DOPAC] levels and a significantly lower [DOPAC]/[DA] ratio in the nervous dogs, suggesting decreased dopaminergic function.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Inefficacy of single-dose nifedipine in the treatment of phobic anxiety.

Single-dose nifedipine was given to 13 phobic patients with increased generalized anxiety. Nifedipine failed to demonstrate anxiety-reducing effects on baseline anxiety ratings. Furthermore, in a subset of four patients, the drug failed to show an anxiolytic effect in exposure-related anxiety.

Arousal↗
PubMed1990

Dysequilibrium and audiovestibular function in panic disorder: symptom profiles and test findings.

Patients with panic disorder commonly report symptoms of dizziness and imbalance. We studied the relationship between objective measures of audiovestibular function, phenomenologic, and self-report measures of dysequilibrium and related somatic symptoms in a sample of panic disorder patients with and without agoraphobia, unselected for the complaint of dysequilibrium. Of seventeen patients evaluated by electronystagmography, 71 percent exhibited abnormal vestibular test findings. These latter patients had higher total anxiety ratings than patients without vestibular abnormalities. We conclude that patients with panic disorder warrant evaluation of audiovestibular function.

Adult↗
PubMed1990

Patients with frequent sleep panic: clinical findings and response to medication treatment.

The authors present 12 cases of panic disorder patients whose sleep panic attacks represented their primary complaint at the time of admission. The patients averaged 18 sleep panic attacks per month before admission. Seven patients were treated with tricyclic antidepressants and demonstrated marked global clinical improvement and a reduction in the frequency of sleep panic attacks. The clinical and theoretical implications of these preliminary findings are discussed within the context of current theories regarding the spontaneous nature of panic attacks.

Adolescent↗
PubMed1990

Cerebral glucose metabolic differences in patients with panic disorder.

Regional glucose metabolic rates were measured in patients with panic disorder during the performance of auditory discrimination. Those regions examined by Reiman and colleagues in their blood flow study of panic disorder [Nature 310:683 (1984)] were examined with a higher resolution positron emission tomography (PET) scanner and with the tracer [F-18]-2-fluoro-2-deoxyglucose (FDG). In contrast to the blood flow findings of Reiman et al., we did not find global gray metabolic differences between patients with panic disorder and normal controls. Consistent with the findings of Reiman et al. [Nature; Am J Psychiatry 143:469 (1986)], we found hippocampal region asymmetry. We also found metabolic decreases in the left inferior parietal lobule and in the anterior cingulate (trend), as well as an increase in the metabolic rate of the medial orbital frontal cortex (trend) of panic disorder patients. It is unclear whether the continuous performance task (CPT) enhanced or diminished findings that would have been noted in a study performed without task.

Acoustic Stimulation↗
PubMed1989

Behavioral and physiologic effects of short-term and long-term administration of clonidine in panic disorder.

We evaluated the behavioral and physiologic effects of clonidine hydrochloride, a centrally active alpha 2-adrenergic agonist, in two separate studies of patients with panic disorder. In the first study, intravenous clonidine (2 micrograms/kg) and placebo were administered on a blind basis to 12 patients with panic disorder and ten normal controls. Clonidine produced significantly greater decrements in anxiety at one hour in the patients with panic disorder than in the controls. The changes in pulse, blood pressure, and ratings of sleepiness did not differ significantly between patients and controls. In the second study, oral clonidine was administered to 18 patients in a double-blind, flexible-dose treatment trial averaging ten weeks in duration. While anxiolytic effects were noticed in some patients, these effects did not persist in the group as a whole. These two studies indicate that while clonidine has short-term anxiolytic effects in patients with panic disorder, these effects do not persist with long-term administration in most patients.

Administration, Oral↗