Academic journal article American Journal of Psychotherapy

Crisis Intervention Techniques for Panic Disorder

Academic journal article American Journal of Psychotherapy

Crisis Intervention Techniques for Panic Disorder

Article excerpt

Panic disorder is estimated to affect more than 4% of the U.S. population. It is assumed that this incident rate increases during crisis situations. While the professional literature is replete with references on the treatment of panic disorders, few authors address the use of nondrug treatment in conjunction with crisis intervention. This article provides an overview of the latest nonpharmacologic interventions for panic along with a description of their effectiveness in reducing the onset of symptomatology as well as preventing relapse during crisis.


Panic disorder is one of the most common and disabling psychological disorders encountered not only in mental health and general medical settings, but crisis centers as well. For some time, it has continued to rank among the top 10 disorders found in settings involving psychiatric emergencies (1, 2). In past studies, investigators have estimated that the one-month prevalence of panic disorder among primary care patients was 1.4% (3). This appears to hold true to date with a slight increase (4). In addition, statistics derived from a study assessing community-based epidemiological catchment areas estimate that in any given month, 0.5% of the population will be diagnosed with panic disorder (5), a number likely to escalate, especially during crisis situations (e.g., natural disasters, auto accidents, etc.).

According to the Diagnostic and Statistical Manual for Mental Disorders, fourth edition, revised (DSM-IV) (6) panic attacks are diagnosed by the presence of at least four of the following symptoms: 1. shortness of breath or smothering sensation; 2. dizziness, unsteady feelings, or faintness; 3. palpitations or accelerated heart rate; 4. trembling or shaking; 5. sweating; 6. choking; 7. nausea or abdominal distress; 8. depersonalization or derealization-a feeling that the sufferer's body or environment, respectively, is not real; 9. numbness or tingling sensations in one or more parts of the body; 10. hot flashes or chills; 11. chest pain or discomfort; 12. fear of dying; and 13. fear of going crazy or losing self-control. To arrive at a diagnosis of panic disorder, the attacks have to occur "unexpectedly" and the symptoms reach a peak within 10 minutes (6).

Although the literature on crises and crisis intervention in general is abundant (7-10), very little has been devoted to specifically addressing crisis intervention for panic disorder (11-13). This situation is surprising, because it is well documented that physicians have, for the past 120 years, experienced difficulty in differentially diagnosing panic disorder from a variety of physiological disorders (14). Moreover, since the primary goal of crisis intervention is to reduce the patient's self-reported emotional distress, it would be expected that panic would appear near the top of the list of disorders targeted in crisis-intervention settings.

The scarcity of crisis-intervention literature regarding panic may be due to the fact that panic attacks are often viewed as emergencies or crisis manifestations of some other underlying problem. In the medical setting, for example, a physician will usually focus immediately on any chronic underlying physiological condition suspected of precipitating the panic symptoms, such as temporal lobe epilepsy, coronary artery disease, alcohol or tranquilizer withdrawal, hyperthyroidism, pheochromocytoma, electrolyte abnormalities, or stimulant medications/decongestants. (See 14 for a more extensive list). In addition, symptoms of panic can be secondary to other mental disorders, such as major affective disorders, personality disorder, and alcohol withdrawal.


There have been several attempts to explain the etiology of panic. Due to the space limitation, only the more popular theories will be discussed in this article. The psychobiologists have contributed a number of hypotheses, which include the septohippocampal theory (15), the locus coeruleus theory (16, 17) and the gamma-aminobutyric acid-benzodiazepine hypothesis (18). …

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