Panic Disorder: The Pinnacle of Anxiety
Authors: Randy A. Sansone, MD, Associate Professor, Departments of Psychiatry and Internal Medicine, Wright State University School of Medicine, and Director of Psychiatry Education, Kettering Medical Center, Dayton, Ohio; and Lori A. Sansone, MD, Kettering Medical Center Physicians Incorporated (family practice), Dayton, Ohio.
Peer Reviewers: Donald M. Hilty, MD, Assistant Professor of Clinical Psychiatry, University of California, Davis, Sacramento, CA; and Lucy J. Puryear, MD, Assistant Professor of Psychiatry, Department of Psychiatry; Director, Baylor Psychiatry Clinic; Director, Medical Student Education, Baylor College of Medicine, Houston, Texas.
Editor’s Note—Panic disorder is a common psychiatric diagnosis in the primary care setting. Symptoms are intense and disabling. Misdiagnosis can result in the unwarranted and excessive use of resources. The following review of panic disorder includes a discussion of description, epidemiology, etiology, diagnosis, treatment, and outcome. In many cases, effective treatment of panic disorder can be undertaken in the primary care setting.
Description
According to DSM-IV,1 panic disorder is defined by recurrent panic attacks as well as a one-month history of concern, worry, or behavioral change as a consequence of these attacks. The classic or typical panic attack is highlighted by cardiac symptoms and characterized by at least four of the following: palpitations or accelerated heart rate, sweating, tremulousness, shortness of breath, choking sensation, chest pain or discomfort, nausea or abdominal distress, light-headedness or dizziness, derealization (i.e., the perception that things outside oneself don’t appear normal or real), fears of dying, fears of losing control or going crazy, paresthesias (particularly around the mouth or fingertips), and chills or hot flushes. These symptoms are intense, well circumscribed, last approximately 15 minutes, and can be difficult to discern from a genuine heart attack. As an example, 38% of patients who were referred to cardiology clinics for the evaluation of chest pain met criteria for panic disorder.2
There appear to be other versions or subtypes of panic disorder3 in addition to those highlighted by cardiac symptoms. These include a respiratory version in which respiratory symptoms predominate (e.g., hyperventilation), a gastrointestinal version highlighted by intense, discrete episodes of queasiness and nausea, and a vestibular version characterized by light-headedness.4,5 The comparative prevalence of these subtypes is unknown, although the cardiac version of panic disorder appears to be the most common. All versions are characterized by well-circumscribed symptoms with no long-term medical sequelae. Whether treatment differences exist among the subtypes of panic remains unknown.
Epidemiology
Prevalence. Community surveys indicate that the lifetime prevalence of panic disorder is about 3% internationally6 and 3.6% among the U.S. general population.7,8 The prevalence of panic disorder in the primary care setting is estimated around 7%. According to the National Comorbidity Study,9 the lifetime prevalence of panic disorder among men is 2% and among women 5%. Women may have a greater likelihood of comorbid social phobia or post-traumatic stress disorder.10
Onset. The onset of panic has a bimodal distribution with one peak in the teens to early 20s and a second in the mid-30s to early 40s.11 However, there are case reports of late-onset panic disorder12; the clinical and demographic profiles of these patients have been found to be similar to those of early-onset patients.12
Timing of Attacks. The symptoms of panic disorder may have seasonal overtones, with exacerbation during the winter months.13 Panic attacks may also occur during sleep,14-16 which may indicate greater psychiatric comorbidity, including mood and anxiety disorders as well as a history of trauma.17
With regard to times of hormonal change in women, up to 40% of patients experience premenstrual exacerbation of panic.18 During pregnancy, up to 20% of women with panic disorder experience worsening of symptoms,19 whereas during the postpartum, 35% experience symptom exacerbation.20,21 Finally, triphasic oral contraceptives22 and progesterone23 have been linked with exacerbations of panic symptoms in predisposed individuals.
Healthcare Use. Of those diagnosed with panic disorder, twice as many seek care in medical settings such as a primary care physician’s office or an emergency department compared to mental health settings.24 Not surprisingly, panic disorder patients demonstrate high rates of use of both psychiatric25 and nonpsychiatric services.26-28 Even compared with other anxiety disorders, panic disorder patients have higher levels of healthcare use.29 As expected, quality of life among these patients is meaningfully diminished.30
Etiology
The explicit cause of panic disorder remains unknown, although a variety of factors have been implicated. Because of this, we conceptualize panic disorder as a final common pathway disorder with multiple contributory factors (see Figure).
Psychological Variables. A number of psychological variables have been reported as causative factors. For example, sexual abuse,31,32 a nonspecific contributory factor for many types of psychopathology, as well as physical abuse33 and chaotic families-of-origin34 have been associated with panic disorder. Airway compromise (e.g., near-drowning, choking, airway obstruction) has been found among some patients with panic disorder.35 Finally, there has been an association between separation anxiety in childhood (e.g., fears of leaving home, separating from parents, staying overnight with friends, going to school) and panic disorder in adulthood.36-38
Nonpsychological Variables. A number of neurotransmitters have been implicated, including GABA,39 serotonin,40,41 and neuropeptide Y.42 Alterations in the hypothalamic-pituitary-adrenal axis43 and abnormal lung function44 have also been identified as potential causative factors. Genetic factors appear to be relevant among some patients and families45-47 and hypersensitivity to CO2 challenge may identify those with a greater likelihood of genetic predisposition.48,49 The intersection of these various risk factors is likely to enhance the probable expression of panic disorder in a given individual.
Exacerbating Factors. Psychosocial stressors appear to exacerbate panic episodes, as well as illness, certain types of drugs (e.g., stimulants, marijuana), antidepressants initially prescribed at routine doses, and weight loss.
Diagnosis
Pattern of Symptom Expression. The diagnosis of panic disorder is based on: 1) the epidemiological context (e.g., age, gender); 2) type and pattern of symptoms; and 3) the exclusion of medical causes. With regard to epidemiology, most convincing is the initial emergence of symptoms during one of the bimodal peaks of onset regardless of the current age of the patient as well as female gender.
Symptoms that reflect the classic panic attack (i.e., cardiac subtype) are highly suggestive of the diagnosis. The symptom pattern is distinctive and characterized by intense, recurrent, and dramatic symptoms during a discrete but brief period (e.g., 15 minutes), with no medical deterioration over time (i.e., months to years). The symptoms of panic disorder usually worsen with stress but, paradoxically, many patients focus on their physiological symptoms and initially appear to dismiss stress factors. With continued exploration, the clinician can usually elicit a relationship between emerging panic attacks and psychosocial stressors.
Medical Evaluation/Differential Diagnosis. Medical evaluation focuses on the predominant symptom complex (i.e., cardiac, respiratory, gastrointestinal, vestibular). The extent of the evaluation is dependent upon the context of the presentation; the more atypical the history, the more necessary a detailed medical work-up. With the cardiac subtype, medical evaluation in suspicious cases might include an echocardiogram, electrocardiogram, or event monitor to exclude certain cardiac conditions such as severe mitral valve prolapse or paroxysmal supraventricular tachycardia,50 both of which may mimic panic symptoms.
Regardless of panic-disorder subtype, we advise obtaining a thyroid-stimulating hormone (TSH) on all patients presenting with possible panic disorder to exclude the rare possibility of thyroid storm. Also, a drug and caffeine history (including cocaine, marijuana, amphetamines, and caffeine) should be obtained, as exposure may mimic or exacerbate panic attacks.51
A rare diagnosis that may be confused with panic disorder is severe paroxysmal hypertension, or pseudopheochromocytoma. This condition is characterized by abrupt elevations in blood pressure and acute physical symptoms that may be confused with panic attacks (e.g., headache, chest pain, dizziness, nausea, palpitations, flushing, diaphoresis).52 These episodes last from 30 minutes to several hours and are apparently not provoked by psychosocial stressors or accompanied by feelings of panic. Afflicted patients tend to fail treatment with anti-hypertensives and may respond to psychotherapy, alpha or beta blockers, tricyclic antidepressants, or selective serotonin reuptake inhibitors.52
Psychometric Scales. To date, there is not a formally recognized panic disorder scale that is generally accepted for use. The MINI Patient Health Survey53 is a brief self-report survey that explores major depression, alcohol dependence, social phobia, and panic disorder. The panic disorder subscale consists of four primary questions and may be of value in the primary care setting as a screening measure. Shear et al54 have developed the Panic Disorder Severity Scale, a seven-item interview that assesses the severity of panic.
Comorbid Psychiatric Conditions. Up to 70% of patients with panic disorder have a comorbid psychiatric disorder.27 The relationship between and among these comorbid disorders is unknown. Comorbid psychiatric conditions include agoraphobia (50%), alcoholism,55 major depression,56,57 other anxiety disorders,58 and personality disorders.58 Weissman et al59 found that, compared with other psychiatric disorders, there was a substantial risk of suicidal ideation and attempts among panic disorder patients. However, several investigators attribute this finding to psychiatric comorbidity, not to panic disorder itself.60,61
Treatment
Overview. For most patients, the treatment of panic disorder entails several components including psychotropic medication, cognitive-behavioral intervention, and exercise. The preceding interventions can be initiated in the primary care setting. Patients with trauma histories, significant psychosocial stressors, and/or separation difficulties may benefit from psychotherapy. Finally, among those with agoraphobia, systematic desensitization is recommended.
Psychotropic Medication. Several classes of psychotropic medication appear to be efficacious in the treatment of panic disorder. These include the selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), benzodiazepines, and monoamine oxidase inhibitors (MAOIs).1 In the primary care setting, SSRIs and TCAs have the best risk/benefit ratio, with SSRIs emerging as first-line therapy.62 Whether prescribing an SSRI or a TCA, these drugs need to be started in very low doses and gradually titrated to a therapeutic dose to prevent an overly activating response in the patient (i.e., jitteriness, worsening of panic symptoms). For panic disorder, the duration of the drug-evaluation trial for an antidepressant is approximately six weeks with beneficial effects accruing up to 12 weeks.1
The SSRIs, currently the starting point of pharmacologic treatment, include five members: fluoxetine, sertraline, citalopram, paroxetine, and fluvoxamine. SSRIs have the advantages of mild side effect profiles, no addiction, and safety in overdose.63 Limitations include sexual dysfunction among some patients (e.g., decreased libido, delayed orgasm), discontinuation syndromes (i.e., the emergence in some patients of acute symptoms in response to the abrupt cessation of the SSRI), and the possibility of drug interactions via the P-450 isoenzyme system.
Both sertraline and paroxetine have been approved by the FDA for use in panic disorder,64 although the remainder of the SSRIs have been found effective as well.65-67 In comparing sertraline and paroxetine in terms of possible side effects, sertraline is more likely to cause loose stools. Paroxetine is more likely to cause mild sedation, dry mouth, constipation, and sexual dysfunction.
Sertraline can be initiated at 12.5 mg per day and gradually titrated (i.e., increased by 12.5 mg every 4-7 days or as tolerated) to the usual effective dose, which is 50 mg per day. Paroxetine can be initiated at 10 mg per day and gradually titrated (increased by 10 mg every 4-7 days or as tolerated) to the usual effective dose, which is 20 mg per day. On occasion, some patients may be sensitive to these recommended initial starting doses. In these cases, starting doses of both drugs can be reduced to 6.25 mg of sertraline or 5 mg of paroxetine (i.e., ¼ of sertraline 25 mg or ½ of paroxetine 10 mg). When cutting apart pills, patients report no significant pill fragmentation or unpleasant taste.
TCAs are also effective in the treatment of panic disorder. They are a reasonable consideration when either cost is a barrier to SSRI treatment or there are failed drug trials with SSRIs. As with SSRIs, the initial dose should be very small, for example 10 mg of imipramine. Unlike SSRIs, TCAs have both anticholinergic and cardiovascular effects and are lethal in overdose. However, some patients may respond to TCAs and not to SSRIs.
Among the benzodiazepines, alprazolam and clonazepam are well-recognized interventions for panic disorder. Both are high-potency benzodiazepines and both carry the risk of physiological addiction and withdrawal.68,69 Benzodiazepines can also precipitate disinhibited behavior70 and depression70,71 as well as impair recent memory72,73 and psychomotor performance.74 They may be helpful among some patients for rapid symptom control while awaiting the effects of an antidepressant medication. However, their combined use with an antidepressant may sabotage the antidepressant trial due to the patient’s recognition of the immediate efficacy of the benzodiazepine. In addition, we believe that benzodiazepines should not be prescribed in patients with prior drug or alcohol abuse histories.
The fourth and final group of antipanic medications are the MAOIs. While effective, these medications require strict adherence to low-tyramine diets as well as the avoidance of many medications; admixtures may precipitate hypertensive crises. Therefore, while an academic possibility, few patients in clinical practice are willing to undergo these restrictions or risk a hypertensive crisis.
At times, monotherapy may be insufficient for symptom control, and the addition of a second drug (i.e., augmentation strategy) may be helpful. In the primary care setting, one uncomplicated option includes gabapentin (an anticonvulsant). While not approved by the FDA for use in psychiatric disorders, gabapentin appears to have an augmenting effect among some patients. Unlike other anticonvulsants, gabapentin does not require initial laboratory studies or ongoing serum levels. It is renally excreted, has few drug interactions, and is safe in overdose. We usually begin with 100 mg at bedtime and titrate to 300 or 400 mg per day. Augmenting effects with these drugs are usually apparent in 2-3 weeks or longer.
The duration of pharmacological treatment for panic disorder remains unknown. The minimum duration is probably one year. However, patients with long histories of the disorder and significant functional impairment may continue on lifelong treatment.
Cognitive-Behavioral Intervention. Cognitive-behavioral intervention has been found efficacious in the treatment of panic disorder,75 whether in group76 or abbreviated77 format. The combination of cognitive-behavioral therapy with psychotropic medication is reported as more effective than either treatment alone.78 Most clinicians, particularly primary care physicians, do not have the time to undertake this type of treatment in the office setting. In response to this dilemma, we have provided a list of several books and manuals for patients who teach cognitive-behavioral techniques.
Exercise. Few studies in the psychiatric literature have examined the effects of exercise on any disorder, but one in panic patients found significant clinical improvement compared with the placebo group.79
Psychotherapy. Psychotherapy can be helpful in resolving acute stressors80 as well as sorting out trauma-related issues. There is currently an available treatment manual for mental health professionals on this type of therapy.81
Systematic Desensitization. Nearly half of the patients with panic disorder also have agoraphobia. The academic intervention is to recommend systematic desensitization, which is reasonable in those locales that have a therapist trained in this procedure. For communities that do not have this resource, clinicians may rely on the sections in the cognitive-behavioral manuals that deal with this procedure.
Management in the Primary Care Setting. In the Table, we have outlined the general management strategy for treating panic disorder patients in the primary care setting. We believe that partial responses or treatment failures are most often due to comorbidity. In these cases, referral to a psychiatrist for further evaluation and treatment is suggested. For cases involving psychosocial stressors and/or trauma, referral to a mental health professional for psychotherapy is advised.
Clinical Pitfalls. In our experience, the most common clinical errors in the treatment of panic disorder include the following: 1) initial doses of antidepressant that exceed those recommended, resulting in an overly activating effect; 2) use of a benzodiazepine among those patients with alcohol and substance abuse histories, resulting in addiction; 3) benzodiazepine coprescription with an antidepressant that unintentionally sabotages a successful antidepressant trial; 4) inadequate drug-evaluation trial (i.e., < 6 weeks); 5) patient resistance to taking medication82; and 6) partial responses due to psychiatric or medical comorbidity.
Outcome
The long-term outcome of panic appears to be variable. Approximately one-third of patients attain a stable remission, a third experience exacerbations and relapses, and a third appear to have a chronic course.83-86 These data indicate that a subgroup of panic disorder patients have a chronic course with rare remissions.87
Coexisting psychiatric disorders such as major depression88,89 and personality disorders90,91 have empirically been associated with poorer outcomes. The role of comorbid anxiety disorders such as social phobia or generalized anxiety requires further study, although agoraphobia may predict an unfavorable course.86 A higher risk of suicide has been reported among panic patients,59 but this risk appears attributable to comorbid psychiatric conditions.92 Finally, women may have less favorable outcomes compared with men.93
On a final note, Battaglia and colleagues found that from generation to generation, the onset of panic disorder was earlier in each succeeding generation.94 This finding, called "anticipation," requires additional study to determine if illness-affected parents are more sensitive to earlier signs of the disorder in their children.
Conclusion
Panic disorder patients are relatively common in clinical practice. There appear to be multiple contributory factors for this disorder and diagnosis is based upon the epidemiology, pattern and type of symptoms, and the exclusion of medical causes among those with atypical presentations. Treatment in the primary care setting consists of antidepressants (SSRIs being first-line), use of cognitive-behavioral techniques (patient handouts), and recommendation of exercise. Psychiatric comorbidity often accounts for partial or nonresponsiveness, and psychiatric referral is advised. Psychotherapy can be useful for patients with stressors and trauma histories, and agoraphobia may be addressed through systematic desensitization. Future studies of this perplexing disorder need to explore the efficacy of other newer antidepressants and drug combinations, panic disorder subtypes and differences in treatment, outcome factors among special populations (especially women), and prevention strategies. All of these empirical endeavors need to consider effective use of assessment and treatment resources.
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Suggested Reading
1. Wilson RR. Don’t Panic: Taking Control of Anxiety Attacks. New York, NY: HarperCollins; 1996.
2. Rachman S. Panic Disorder: The Facts. New York, NY: Oxford University Press; 1996.
3. Getting Treatment for Panic Disorder: Information for Patients, Families, and Friends. Bethesda, MD: National Institutes of Health, National Institute of Mental Health; 1995.
4. Swede S, Jaffe S. The Panic Attack Recovery Book. New York, NY: New American Library; 1987.
5. Kleinknecht RA. Mastering Anxiety: The Nature and Treatment of Anxious Conditions. New York, NY: Plenum Press; 1991.
6. Puerifoy RZ. Anxiety, Phobias, and Panic: Taking Charge and Conquering Fear. Lifeskills; 1988.
Other Resources
1. National Institute of Mental Health, Panic Campaign, 5600 Fishers Lane, Room 7C-02, Rockville, MD 20857; 1-800-64-PANIC (brochures on panic disorder).
2. Anxiety Disorders Association of America, 6000 Executive Boulevard, Suite 513, Rockville, MD 20852; 301-231-8368.
Physician CME Questions
74. All of the following are true except:
a. the lifetime prevalence of panic disorder is 3.6%.
b. men are more prone to panic disorder than women.
c. panic symptoms may show seasonal exacerbations.
d. panic attacks can occur during the night.
e. panic attacks can occur in late life.
75. Panic disorder may be caused by all of the following contributory factors except:
a. disturbances in GABA or 5HT.
b. genetic factors.
c. trauma.
d. early childhood separation difficulties.
e. neurological events.
76. In the treatment of panic, all of the following are true except:
a. SSRIs are first-line treatment.
b. TCAs are effective.
c. an augmentation strategy includes gabapentin.
d. exercise should be avoided.
e. benzodiazepines may sabotage the antidepressant trial.
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