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Biomedical subjects

R Noyes

Publications and source records attributed to R Noyes.

At least 19 recordsLinked to original sources
PubMed1992

A family study of obsessive-compulsive disorder.

First-degree relatives of probands with obsessive-compulsive disorder (OCD) (n = 32) and psychiatrically normal controls (n = 33) were blindly interviewed with the use of the Diagnostic Interview Schedule. The morbidity risk for anxiety disorders was increased among the relatives of obsessional subjects compared with that for the relatives of controls, but the risk for OCD was not. Risk for a more broadly defined OCD (including relatives with obsessions and compulsions not meeting criteria for OCD) was increased among the parents of obsessional subjects but not among the parents of controls (16% vs 3%). The findings suggest that an anxiety disorder diathesis is transmitted in families with OCD, but that its expression within these families is variable. The findings also support the current practice of classifying OCD as an anxiety disorder.

Adolescent↗
PubMed1992

A comparison of patients with illness phobia and panic disorder.

Fourteen subjects with illness phobia, a subtype of hypochondriasis, were compared with an equal number of subjects with panic disorder who had been matched for age and sex. The illness phobic subjects differed from panic subjects in not having spontaneous panic attacks or agoraphobic symptoms, the characteristic features of panic disorder. The onset of illness phobia was related to experience with illness in half the subjects. Half of the illness phobic subjects also had family histories of anxiety disorders. The results suggest that illness phobia is distinct from panic disorder and that it is a disorder in which environmental and genetic factors are etiologically important.

Adult↗
PubMed1992

Generalized anxiety disorder vs. panic disorder. Distinguishing characteristics and patterns of comorbidity.

In order to examine the validity of the distinction between generalized anxiety disorder (GAD) and panic disorder (PD) we compared 41 subjects with GAD and 71 subjects with PD. The GAD subjects had never had panic attacks. In contrast to the symptom profile in PD subjects suggestive of autonomic hyperactivity, GAD subjects had a symptom pattern indicative of central nervous system hyperarousal. Also, subjects with GAD had an earlier, more gradual onset of illness. In terms of coexisting syndromes, GAD subjects more often had simple phobias, whereas PD subjects more commonly reported depersonalization and agoraphobia. GAD subjects more frequently had first-degree relatives with GAD, whereas PD subjects more frequently had relatives with PD. A variety of measures indicated that our GAD subjects had a milder illness than those with PD. Also, fewer GAD subjects gave histories of major depression than did PD subjects. Among GAD subjects, coexisting major depression was associated with simple phobia and thyroid disorders and among PD subjects, comorbid depression was associated with social phobia and hypertension. Our findings indicate that the separation of GAD from PD is a valid one. They also indicate that, within disorders, unique patterns of comorbidity may exist that are important both clinically and theoretically.

Adult↗
PubMed1992

Adrenergic receptor genes as candidate genes for panic disorder: a linkage study.

OBJECTIVE: Several lines of investigation suggest that the noradrenergic neurotransmitter system may be involved in the pathogenesis of panic disorder. Since a mutation in a gene coding for one of the adrenergic receptors could account for both the familial nature and autonomic dysfunction of panic disorder, the authors performed analyses of the linkage between panic disorder and five adrenergic receptor loci. METHOD: The subjects were 14 multiplex pedigrees with DSM-III panic disorder or agoraphobia with panic attacks. The loci tested were the alpha 1/beta 2 pair on chromosome 5q32-q34, the alpha 2/beta 1 pair on chromosome 10q24-q26, and a second alpha 2 locus on chromosome 4. Flanking loci were included in the analysis on chromosomes 5 and 10 to increase the informativeness of the adrenergic receptor loci. RESULTS: Lod scores less than -2.0 were found at all five receptor loci. CONCLUSIONS: These findings provide strong evidence against the possibility that genetic mutation at any of these loci is responsible for panic disorder in these pedigrees.

Adolescent↗
PubMed1992

Discontinuation of alprazolam after long-term treatment of panic-related disorders.

Discontinuation of alprazolam after long-term treatment of 142 patients with panic-related disorders was examined in five study sites using a telephone interview. The majority (67%) of patients interviewed discontinued alprazolam for a period of at least 3 days after a gradual dosage reduction schedule over a 4-week period at the end of the long-term treatment study. A marked difference among the study sites in percentages of patients discontinuing therapy with alprazolam suggests that physician intervention played an important role in determining the ability of patients successfully to discontinue use of alprazolam: 90% and 95% of patients ceased therapy at two sites whereas only 21%, 38%, and 66% of patients discontinued therapy at the other three sites. The mean daily dosage for patients who continued using alprazolam decreased from 5.1 mg/day at the end of the long-term segment to 2.7 mg/day at the time of the poststudy interview. This decline indicates a lack of tolerance to the therapeutic effectiveness of alprazolam over an extended period of time.

Adult↗
PubMed1991

The prognostic significance of HPA-axis disturbance in panic disorder: a three-year follow-up.

Seventy-seven patients with DSM-III panic disorder underwent a baseline dexamethasone suppression test (DST), participated in an 8-week controlled treatment trial, and provided follow-up interviews 2-4 years later. The 20 patients who had exhibited DST nonsuppression at baseline had more symptoms of anxiety, more work and social disability, and a greater likelihood of ongoing major depression than did patients who had had normal DST results. DST nonsuppression in panic disorder apparently indicates a more persistent and chronically disabling condition.

Adult↗
PubMed1991

Controlled discontinuation of benzodiazepine treatment for patients with panic disorder.

OBJECTIVE: The purpose of this study was to compare the effects of discontinuing treatment with intermediate- and long-acting benzodiazepines. METHOD: Fifty patients with panic disorder who had taken part in a double-blind treatment study and had responded to alprazolam, diazepam, or placebo for 8 months were asked to stop taking these medications gradually. RESULTS: After a relatively rapid dose reduction, the majority of patients relapsed. Rebound anxiety and withdrawal symptoms were identified in a substantial minority of patients. Those who were taking alprazolam showed earlier and more intense rebound anxiety and withdrawal symptoms than did the patients who received diazepam. Both the level of pretreatment anxiety and the drug the patient was taking predicted the level of anxiety when drug treatment was discontinued. CONCLUSIONS: The findings indicate that withdrawal phenomena commonly occur after patients stop taking benzodiazepines and that they are more frequent after discontinuation of treatment with shorter-acting drugs.

Adult↗
PubMed1991

The first double-blind, placebo-controlled trial of a partial benzodiazepine agonist abecarnil (ZK 112-119) in generalized anxiety disorder.

This is the first reported controlled trial of a partial benzodiazepine agonist, abecarnil, utilized in the treatment of generalized anxiety disorder (GAD). It was a sequential dose-finding study comparing 15-30 mg/day, 7.5-15 mg/day, and 3-9 mg/day to placebo for 3 weeks of treatment followed by abrupt discontinuation through placebo substitution. Although the two higher dose groups had high incidence of central nervous system (CNS) sedative adverse effects, the 3-9 mg/day group tolerated the medication well with no dropouts. The 3-9 mg/day group, in comparison to the two higher doses and placebo, demonstrated efficacy in global improvement ratings and Hamilton Anxiety Scale (HAM-A) scores. At Week 3, 61 percent of the abecarnil 3-9 mg/day group was rated as at least 50 percent improved on the HAM-A, compared to 30 percent of the placebo group. With abrupt discontinuation there were mild to moderate withdrawal symptoms and loss of efficacy in the two higher dose groups. However, in the 3-9 mg/day abecarnil group, there were few withdrawal symptoms and almost no loss of efficacy following discontinuation.

Adult↗
PubMed1991

Treatment of ADHD with fluoxetine: a preliminary trial.

Nineteen children and adolescents with attention-deficit hyperactivity disorder were treated with fluoxetine hydrochloride. The drug was administered in an open-label fashion for 6 weeks. At completion of the study, nearly 60% were judged to be at least moderately improved. No effects on appetite or weight were observed, and side effects were minimal. These findings suggest that fluoxetine may prove to be an alternative treatment for some attention-deficit hyperactivity disorder patients.

Adolescent↗
PubMed1990

A test of the tridimensional personality theory: association with diagnosis and platelet imipramine binding in obsessive-compulsive disorder.

We administered the Tridimensional Personality Questionnaire (TPQ) to a sample of 25 individuals with obsessive-compulsive disorder (OCD) and 35 normal controls. As predicted, OCD cases scored much higher on the harm avoidance dimension than normal controls. Findings for the novelty seeking and reward dependence dimensions were less dramatic, although compatible with the underlying theory. Despite a theoretical link between the harm avoidance dimension and serotonin-mediated neuropathways, we failed to find an association between this dimension and platelet imipramine binding in either OCD cases or controls.

Arousal↗
PubMed1990

Tritiated imipramine binding in obsessive-compulsive volunteers and psychiatrically normal controls.

The authors evaluated platelet tritiated imipramine binding in 22 outpatients with obsessive-compulsive disorder (OCD) and 22 psychiatrically normal controls matched for age and gender. Mean maximal binding site density (Bmax) and equilibrium dissociation affinity (Kd) values were not significantly different. In OCD patients, Bmax was positively associated with age but was not associated with age of onset, gender, personality disorder, or five measures of illness severity. Eight patients with OCD were subsequently treated with clomipramine up to 300 mg/day for 10 weeks. Among these 8 patients, Bmax values had a 65% mean decrease from baseline, but Bmax values did not change among 7 OCD patients receiving placebo. The results suggest that a reduced density of tritiated imipramine binding sites may not be associated with OCD.

Adult↗
PubMed1990

Close linkage between panic disorder and alpha-haptoglobin excluded in 10 families.

We previously reported a lod score of 2.3 suggesting linkage between panic disorder and the alpha-haptoglobin locus on chromosome 16q22 in 26 pedigrees. In the present study we tested for linkage between alpha-haptoglobin and panic disorder in 10 new pedigrees and excluded a gene for panic disorder from 6 centimorgans (recombination fraction, 0.06) surrounding the alpha-haptoglobin locus. The data were analyzed under a variety of assumptions about the transmission of panic disorder, and linkage was excluded by all genetic models but one. When lod scores from the present set of 10 pedigrees were pooled with those from the first 26, no evidence of genetic heterogeneity was found, and the maximum lod score was 0.67 at a recombination fraction of 0.17. Taken as a whole, the present findings do not support the presence of a disease gene for panic disorder closely linked to the alpha-haptoglobin locus on chromosome 16q22.

Adult↗
PubMed1990

Outcome of panic disorder. Relationship to diagnostic subtypes and comorbidity.

Eighty-nine subjects with panic disorder, who had been naturalistically treated, and 46 nonanxious controls were followed up after 3 years. Although they remained symptomatic, most subjects with panic disorder reported relatively little distress or social maladjustment. The course of panic disorder was characterized by fluctuating anxiety and depressive symptoms. Panic subtypes (uncomplicated, limited phobic avoidance, and extensive phobic avoidance) and Axis I and II comorbidity (major depression and personality disorders) were highly predictive of symptoms and social adjustment after 3 years. Abnormal personality was, in fact, the strongest predictor of social maladjustment in both subjects with panic disorder and controls. The results showed that while panic disorder has a favorable outcome, the illness is a chronic one that may require continuing treatment. They also show that subtypes and comorbid disturbances are important predictors of outcome.

Adult↗
PubMed1990

Sequence of improvement in agoraphobia with panic attacks.

In a multi-center comparison of alprazolam to placebo in the treatment of agoraphobia with panic attacks, the sequence of sustained remission in both treatment groups, was panic attacks before phobias. This may suggest that phobias are secondary to panic attacks in the pathogenesis of the disorder, although other explanations may account for these data and are discussed.

Adult↗