2005, Number 1
Psychophisiological and behavioral treatment of anxiety disorder.
Campos CP, Jurado CS, Mendieta CD, Zabicky ZG, Silva CM
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Language: Spanish
References: 33
Page: 28-37
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ABSTRACT
Panic disorder is a complex phenomenon according to its biochemical and psychosocial etiology. Therapeutic interventions of panic disorder are aimed to promote effectiveness through the combined use of medication and behavioral cognitive therapy.Anxiety is a normal human response. Moderate levels of anxiety are well accepted because they act as an aid to improve performance, and high levels of anxiety are experienced as normal if they are consistent with the demands of the situation.
Persons with anxiety disorders complain of experiencing anxiety too often but they seek help also to overcome fears they recognize as irrational and intrusive. From a psychological point of view, behavioral cognitive techniques -such as hyperventilation control, exposure, and cognitive therapy- and structured problem solving have been successful in the treatment of the symptoms associated to anxiety. It is worth to emphasize that graded exposure is perhaps the most powerful technique assisting patients to overcome fearful situations.
Cognitions are also important because it has been found that panic attacks occur when people process information in the external environment, as well as internal somatic stimuli, as though they were threatening experiences. In other words, they feel they have no control over their sensations. Panic attacks prevalence in Mexico City is 1.1% in men and 2.5% in women. It is more frequent among 25-to 34- year old single men and married women, with an average scholarity between 7 and 9 years.
From a biological point of view, it is suggested that the etiology of panic attacks involves the participation of the serotonergic and adrenergic neurotransmitter systems, as well as the GABA/benzodiacepine. Studies based on the noradrenergic theory had lead to conclude that panicking patients have more sensitive brainstem carbon dioxide receptors than normal control subjects. At the same time, other lines of work indicate that serotonergic transmission may also play an important role in the genesis of panic attacks. It has been found that patients with panic disorder may have a lower tolerance threshold to methocloro-phenylpiperazine response than control subjects because of hypertensive serotonergic receptors.
The accumulated laboratory evidence seems to support the idea that panic attacks begin with the stimulation of irritable foci in one of three brainstem areas: the medullary chemoreceptors, the noradrenergic pontine locus coeruleus, or the serotonergic midbrain dorsal raphe.
On the other hand, biofeedback is a psychophysiological intervention that allows in the first place for the external control of some of the physical symptoms involved in this disorder, which is later transferred to internal control of psychophysiological cognitions and behaviors that enable the patient to prevent symptom´s occurrence. Based on the principles of the General Systems Theory, biofeedback utilizes the concepts of self regulation and disregulation to describe the conditions under wich normally integrated self-regulatory systems may become imbalanced with regard to their positive and negative feedback loops.
Technically, all that a person needs to do is to attend to the signals feedback and not to “try” to control them; the effects of a positive feedback loop should occur automatically, without conscious awareness, as long as the person processes the stimuli. Biofeedback has been effectively used in the treatment of essential hypertension, migraine headaches, Raynaud´s disease, tension headaches, temporomandibular joint syndrome, asthma, primary dysmenorrhea, peptic ulcers, fecal incontinence, and conditioning of electroencephalographic rhythms, among other problems.
The present study reports data from 32 panic disorder outpatients from the National Psychiatry Institute, Mexico City. They were randomly assigned to:
Control Group (N=14): daily doses of 75 milligrams of imipramine. The participants of this group were required to assist to the psychology department in order to obtain a baseline (pre-test and post-test) with the biofeedback equipment. In addition, every two weeks they visited a psychiatrist who verified that there were no collateral effects from the medicament.
Experimental Group (N=18): besides daily doses of imipramine, and visits to the psychiatrist, these patients went through eight multimodal biofeedback and behavioral cognitive techniques which were assisted with relaxation training sessions.
All biofeedback sessions lasted 30 minutes divided in six five-minute trails. The first and final trials served to stabilize the biological responses, and the four middle trials were used to give biofeedback and reinforcement to the response being trained in addition to the verbal explanation of the changes occurring on the screen of the computer.
All patients were assessed with the Anxiety Sensitivity Index, and with Beck’s Anxiety and depression Inventories. Results showed that patients in the experimental group reported significant lower scores in the anxiety sensitivity index than the control group. Post-test differences showed that the electromiographic and electrodermic activity from the experimental group was lower than the one from the control group. Diaphragmatic respiration training and progressive muscular relaxation and imagery proved to be effective in reducing the symptoms associated to panic attacks.
The overall final result is that all patients improved clinically. They verbally reported that the intensity, frequency and evitative behaviors derived from panic attacks had almost disappeared. However, the cognitive factor of anxiety sensitivity changed significanty only in the experimental group. These findings support the hypothesis that clinical improvement results from a symptom “reattribution” which gives them cognitive skills to cope with stressing stimuli.
Further studies should reassess the effectiveness of the combined treatment (imipramine and behavioral cognitive techniques). It is also recommended to expand the study to generalized anxiety disorder and to adjust the experimental design in order to incorporate a second phase with neurofeedback as independent variable. Equally important is to investigate the mechanisms of the hypnotic ability and its impact on the clinical improvement of anxiety disorders.
REFERENCES