With panic attacks, alarming physiologic symptoms mount swiftly—tachycardia, chest pain, sweating, trembling, smothering or choking, dizziness, fear of losing control or going crazy—even fear of dying.1 Patients constantly fear the next attack, worry about its consequences, and change their behaviors to avoid or withdraw from anxiety-provoking situations.
To relieve their suffering, cognitive-behavioral therapy (CBT) may offer benefits you would not realize with medication alone. CBT can:
- improve long-term patient outcomes
- enhance medication management
- boost treatment response when medication alone is inadequate
- ease drug discontinuation.2
Whether you or a CBT-trained psychotherapist guides the sessions, you can achieve optimal results for your patients with panic disorder.
How Effective is CBT?
Panic disorder is chronic, often disabling, and characterized by spontaneous, unpredictable panic attacks (Boxes 1 and 23-11). When treated with CBT, about three-quarters of patients become panic-free and maintain treatment gains at follow-up, and one-half become both panic-free and free of excess anxiety.9
Typical therapy is 12 individual, once-weekly visits for psycho-education, relaxation, and breathing training; cognitive restructuring; and exposure therapies.
Briefer protocols, “reduced therapist contact,”12 and group therapy13 also can help patients and in some studies have been as beneficial as 12 weeks of individual therapy. Although trained psychotherapists have higher success rates than nonbehaviorists when treating panic patients, nonbehaviorists also can provide effective therapy after relatively brief training.14
American Psychiatric Association15 treatment guidelines recommend medications—such as selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), and benzodiazepines—as well as CBT as first-line therapies for panic disorder. Other treatment guidelines concur16 and note that CBT is more cost-effective than medications.
In comparison studies, CBT has been at least as effective for panic symptoms as SSRIs,17,18 TCAs,19 and alprazolam.20 Antidepressants are the preferred drug for panic disorder16 because they lack benzodiazepines’ dependence and abuse potential.
Providing medication during CBT may maintain patients’ therapeutic gains better than CBT alone if the medication is continued after CBT is completed. Interestingly, patients who use benzodiazepines during CBT may have higher relapse rates than those who do not use benzodiazepines, particularly when the benzodiazepines are withdrawn.9
CBT produces improvement rates similar to those of pharmacologic treatment at one-quarter to one-half the cost in the first year. Patients also appear to have better clinical outcomes if they receive CBT while SSRIs or benzodiazepines are being discontinued, compared with simply stopping the medications.8
Panic attacks typically begin between ages 10 and 40. The cause is unknown, but evidence points to multiple factors, including heredity, neurobiology, provocations, and psychological conditioning (Box 2).3-9 prevalence is approximately 5%,10 and about three-fourths of panic disorder patients are female.11
Comorbidity. Up to 50% of persons with panic disorder also experience agoraphobia.1 Depression, other anxiety disorders, and substance abuse may complicate the clinical picture.
Genetics. About 10% of persons who experience panic attacks have first-degree relatives with panic disorder. Twin studies suggest heritability of up to 43%
Neurobiology. Anxiety responses appear to be organized at different neuroanatomic levels:
- automatic responses by periaqueductal grey matter or locus coeruleus
- practiced responses by the amygdala and septohippocampal regions
- cognitively complex responses by higher cortical regions.
The hypothalamus mediates neurohormonal responses. Panic disorder patients’ response to SSRIs, tricyclic antidepressants, and benzodiazepines suggest a link with neurotransmitters serotonin, norepinephrine, and GABA. Adenosine, cannabinoids, neuropeptides, hormones, neurotrophins, cytokines, and cellular mediators may also be involved.
Provocation. Panic disorder may have a physiologic mechanism. When exposed in the laboratory to panicogenic substances (such as carbon dioxide, sodium lactate, yohimbine, and caffeine), persons with panic disorders experience greater numbers of panic attacks than do those without panic disorders. These laboratory-induced panic attacks resemble real attacks, and anti-panic medications block the induced panic attacks.
The cognitive-behavioral model postulates that panic disorder patients:
- have a predisposed vulnerability to respond with physiologic arousal to negative stressors
- tend to see anxiety symptoms as harmful
- have negative and catastrophizing cognitions about those symptoms.
With conditioning, patients associate early physiologic arousal with other panic symptoms as the arousal progresses. Ultimately, they become hypervigilant for symptoms and develop a learned escalation of anxiety and apprehension (with accompanying negative cognitions) when the early symptoms re-occur.
Source: References 3-9
To diagnose panic disorder, conduct a thorough psychiatric evaluation that includes assessing for comorbid mental and substance use disorders. The history and physical exam are essential to rule out medical causes of the patient’s symptoms, such as heart disease causing dizziness or palpitations. Asking patients to keep panic attack records can help you identify panic symptoms’ frequency and triggers.9
An assessment tool such as the Albany Panic and Phobia Questionnaire (Figure) can be a useful starting point. It has 27 items and three subscales to quantify a patient’s fear of agoraphobic situations, social phobia situations, and situations that produce bodily sensations (interoceptive symptoms). Items on the interoceptive subscale include activities such as exercising vigorously, ingesting caffeine, and experiencing intense emotion.21 Using the Anxiety Sensitivity Index is another assessment option.22