Behavior therapy of phobias: predictors of outcome.
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Biomedical subjects
Publications and source records attributed to G C Curtis.
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The authors used symptom profiles, demographic data, and other variables to compare 316 patients representing all specific DSM-III anxiety disorders except posttraumatic stress disorder to each other and to published norms for both an unselected psychiatric outpatient population and normal subjects. The results support the grouping of these disorders, with the possible exception of obsessive-compulsive disorder, into one general diagnostic category of "anxiety disorders." The distinction between the specific diagnoses of simple phobia and social phobia was also supported; however, the differentiation between panic disorder, agoraphobia, and generalized anxiety was only weakly supported.
The empirical literature that pertains to phobias of blood, injury, or illness (BII) is surveyed. BII phobia is selectively associated with a vasovagal fainting response upon exposure to phobic stimuli, and the clinical entity may represent an exaggeration of a response that is relatively prevalent in the general population. Clinical, demographic and etiological information obtained from a series of 15 BII phobics is presented, and the suggestion is made that this disorder warrants a diagnostic category separate from simple phobia.
Fear Survey Schedule data are presented for a sample of 141 psychiatric patients who met the DSM-III criteria for an anxiety disorder. Diagnostic and gender differences in expressed fears are presented and the results are discussed in light of previous research.
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Free norepinephrine and epinephrine were measured in two consecutive 12-hour urine collections gathered during normal activity and sleep from 23 panic-anxiety patients and 9 normal subjects. Mitral value prolapse (MVP) was found in 7 of 20 patients who had echocardiograms. Mean nighttime norepinephrine and epinephrine excretion in panic-anxiety patients without MVP was significantly higher than that of control subjects, and was significantly higher than that of anxiety patients with MVP. In the daytime, all groups had higher catecholamine (CA) levels, but the differences between the groups were less pronounced. Medication significantly relieved symptoms and was associated with decreased CA levels. Elevated basal CA levels may characterize the subgroup of panic-anxiety patients who do not have MVP.
Antidepressant therapy for panic attacks, exposure therapy for stimulus-dependent anxieties, and, to a lesser extent, clomipramine therapy for obsessive-compulsive symptoms have transformed the treatment of anxiety disorders and ushered in an era of rapid progress in research on anxiety and anxiety disorders. In most cases, these symptomatic treatments should be recommended first. After these approaches have produced maximal benefit, other treatments can be considered if indicated.
Traditionally, it has been assumed that there is only one type of anxiety; recent pharmacologic evidence suggests that there may be several. The psychoanalytic concept of "neurotic" symptoms as depressurizing mechanisms is out of keeping with most evidence now available. Spontaneous or "free-floating" anxiety may be partly biologic and genetic in origin. Anxiety symptoms evoked by specific stimuli behave in part like conditioned responses. Where conditioning theory has failed to propose a plausible unconditioned stimulus for pathologic anxiety, biology, ethology, and psychoanalysis may have been more successful.
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.
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.
The Wolpe-Lange Fear Survey Schedule was administered to 141 psychiatric outpatients who met the criteria for a primary Axis I diagnosis of one of the DSM-III anxiety disorders. Standardization data were obtained for this instrument and their clinical and research implications are discussed.
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The logic of a new design for empirical clinical practice, the repeated pretest-posttest experiment, is described. This design is readily applicable by individual practitioners in the human services, possesses high internal validity, and presents minimal intrusiveness into the delivery of service. A single-case study is used to illustrate the application of the repeated pretest-posttest experiment in clinical research.
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Two patients with phobias for medical procedures and trauma developed "vasovagal syncope" with hypotension and bradycardia while viewing a videotape of a venous cutdown. Eleven hours of exposure therapy per patient eliminated both the phobic and fainting responses. These facts support existing hypotheses that phobias of this type and vasovagal fainting are associated and that vasovagal syncope is a diphasic response. They do not support hypotheses that vasovagal syncope follows sudden cessation of anxiety, that that counter-conditioning is necessary for successful treatment, or that novel symptoms emerge following behavioral treatment of these phobias.