Power Over Panic Disorder
Darrell Hulisz, RPh, PharmD, and
Barbara Edocs Strayer, RPh, PharmD
Dr. Hulisz is Assistant Professor of Family Medicine at Case Western Reserve University School of Medicine in Cleveland, OH, and Associate Clinical Professor of Pharmacy Practice at Ohio Northern University College of Pharmacy in Ada, OH. Dr. Edocs Strayer is a Staff Pharmacist at Barberton Citizen’s Hospital in Barberton, OH
Behavioral Objectives
TB is a 22-year-old healthy female who works full time as a nursing assistant and attends evening classes at a local university. She has no medical problems and is not taking any medications, except occasional acetaminophen for dysmenorrhea. TB rarely drinks alcoholic beverages and does not use any recreational drugs. Approximately 3 months ago while sitting in class, TB was struck by a sudden feeling of terror and anxiety; TB felt that she was going to “lose control.” The attack was accompanied by heart palpitations, dizziness, and sweating. The episode lasted about 15 minutes, during which time TB wanted to escape the confines of her front row seat. She later dismissed the episode as being attributed to heavy coffee use in the preceding days and lack of sleep. Over the next 6 weeks, TB experienced three more attacks, two at work and another while studying at home. These episodes were equally frightening and were not associated with any immediate danger, yet TB felt terrified and thought she was going crazy. TB developed considerable anxiety about having recurrent attacks and decided to contact her family doctor. TB’s physician found no remarkable findings on physical examination, except for a very fine macular rash on her back. Her vital signs and laboratory findings, including blood chemistry, thyroid-stimulating hormone (TSH) levels, and parathyroid hormone (PTH) levels, as well as an electrocardiogram, were normal. The physician believes that these episodes are panic attacks and gives TB a diagnosis of panic disorder (PD).
PD is a common anxiety disorder that causes a great deal of psychosocial distress and work-related disability. About 3.5% of Americans are affected by PD, which is characterized by recurrent panic attacks, persistent worry and concern about having another attack, or worry about the implications and consequences of an
attack.1-3 Panic attacks are discrete episodes of intense anxiety, fear, or discomfort. The attacks may vary in frequency and intensity, have an abrupt onset, and often involve intense and irrational anxiety, a feeling of imminent danger, or an urge to escape. Most patients with PD can be treated on an outpatient basis using a combination of psychological or cognitive-behavioral therapy (CBT) and pharmacotherapy.
Traditional pharmacologic treatment of PD has been tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and benzodiazepines. However, these therapies have several limitations, including variable efficacy, potentially serious adverse effects, drug-drug and drug-food interactions, and abuse or dependency. The selective serotonin reuptake inhibitors (SSRIs) lack many of these limitations and are effective for PD. Thus, the SSRIs are now generally considered the pharmacologic treatment of choice for PD and will be a major focus of this article.
To date, three SSRIs are FDA-approved for PD: fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft). The SSRIs are widely promoted, even to the general public (eg, commercial television). Other antidepressants (ie, fluvoxamine, clomipramine, nefazodone, venlafaxine, and mirtazapine) may also be useful for the treatment of PD, but are not FDA-approved for this indication.
Pharmacists are ideally positioned in health care, being one of the most accessible health care professionals to the general public, and are recognized as experts in medication use. Pharmacists are likely to receive questions and/or consultation from patients, physicians, and other health providers regarding pharmacotherapy for PD. Thus, pharmacists should be well informed in this area.
The intended purpose of this continuing education lesson is to equip pharmacists with a general understanding of PD and its pharmacologic treatment.
PD has a lifetime worldwide prevalence of between 1.5% and
3.5%.4
The most common age of onset is in the early- to
mid-20s.5 PD is twice as common in women, and more common in those with a positive family history of panic. An eight times greater chance of developing PD exists for persons who have a first-degree relative with
PD.4,5 Anxiety symptoms early in life and a history of separation anxiety are also risk factors for panic disorder. An increased risk of major depression and agoraphobia (fear of being in a public setting) are associated with
PD.6
Certain comorbidities are associated with PD. These include a higher risk for suicide, agoraphobia, impaired social and marital functioning, use of psychoactive medications, and substance abuse. These patients are also frequent users of emergency medical services and are more likely to be hospitalized for physical problems. The lifetime prevalence of major depression in PD patients is 50% to
60%.6
The exact etiology of PD is unknown. A serotonin dysfunction, or dysregulation, exists in patients with PD and may be involved in the pathogenesis of the
disorder.7 However, the precise nature of serotonin dysfunction in PD is unclear. Clinical trials lend support to the serotonin theory since medications that increase brain serotonin (5-hydroxytryptamine or 5-HT) levels significantly improve symptoms in patients with
PD.8 Serotonin deficiency alone may not fully explain the pathogenesis of PD. Dysregulation of other neurotransmitters, such as gamma-aminobutyric acid (GABA), dopamine, norepinephrine, and cholecystokinin, may also be involved in the pathogenesis of PD. Dysregulation in central GABA activity has been implicated in the development of generalized anxiety. The anticipatory anxiety, worry, and fear associated with individual panic attacks probably contribute to the development of full-blown PD.
The essential feature of PD is the presence of recurrent, unexpected panic attacks followed by at least 1 month of persistent concern about having another attack, worry about the possible implications or consequences of the attacks, or a significant behavioral change related to the
attacks.4 The specific criteria for diagnosing PD as defined by the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), are shown in
Table 1. The panic attacks should not be due to the direct physiologic effects of a substance or a medical condition. The attacks are not better accounted for by another mental disorder, such as a specific or social phobia, obsessive-compulsive disorder, posttraumatic stress disorder, or separation anxiety disorder.
Table 1.
PD is diagnosed into one of two classifications: PD with agoraphobia or PD without agoraphobia. According to the DSM-IV, one essential feature of agoraphobia is anxiety about being in public places or situations from which escape might be difficult or embarrassing, or in which help may not be available during a panic
attack.4 Agoraphobic fears typically involve clusters of situations that include being outside the home alone, being in a crowd or standing in line, being on a bridge, and traveling in a bus, train, or automobile. A second essential feature of agoraphobia, as defined by DSM-IV, is that situations are avoided or endured with marked distress, or with anxiety about having a panic attack or paniclike symptoms. These situations also will often require the presence of a companion.
The severity and frequency of panic attacks vary from person to person among those diagnosed with PD. Some individuals report attacks that occur regularly over time, whereas others may state that bursts of attacks are followed by variable periods of minimal numbers of attacks or the complete absence of them. The number of symptoms that present with each attack also varies from person to person. Limited-symptom attacks are those accompanied by fewer than four possible symptoms
(Table 2).4 “Full” panic attacks that carry a multitude of symptoms are associated with increased morbidity. A typical panic attack consists of a rapid, increasing intensity of anxiety accompanied by symptoms of heart palpitations, chest pain, shortness of breath, sweating, and
dizziness.4 Frightening fears of going crazy, dying, or losing control often accompany these panic symptoms.
Table 2.
When establishing the diagnosis of PD, physicians must exclude other medical conditions, mental disorders, and physiologic causes that may mimic panic attacks
(Table 3). Medical conditions that can mimic or precipitate panic attacks include hyperthyroidism, hyperparathyroidism, pheochromocytoma, hypoglycemia, vestibular dysfunctions, seizure disorders, and cardiac conditions (eg, mitral valve prolapse, cardiac arrhythmias, supraventricular
tachycardia).4,9 Substances of abuse, especially central nervous system (CNS) stimulants (eg, cocaine, caffeine, LSD, amphetamines), can precipitate panic attacks. Marijuana and withdrawal from CNS depressants (eg, barbiturates, alcohol) can also cause panic attacks.
Table 3
Patients with PD often have an essentially normal physical examination, with the possible exception of sinus tachycardia and moderate systolic blood pressure elevations. Some individuals with PD have shown signs of compensated respiratory alkalosis, demonstrated by a decrease in carbon dioxide and bicarbonate levels with a fairly normal pH on arterial blood gas. The palms may be sweaty, and patients may appear fatigued or exhausted, especially if presenting immediately following a panic attack.
The management of PD involves a combination of psychiatric and psychological techniques. Perhaps the most common nonpharmacologic therapy used in the management of PD is CBT. The elements involved in CBT are quite diverse and involve insight training, continuous panic attack monitoring, anxiety management skills (eg, deep breathing exercises and relaxation techniques), cognitive restructuring, and progressive exposure to panic attack triggers. Graded exposure can reduce anticipatory anxiety and phobic
avoidance.9 These techniques are usually taught by clinical psychologists, behavioral scientists, or other mental health professionals. The response rate to CBT alone is variable, but is in the range of 66% to 78% over 12 to 15
weeks.6 Response rates with CBT may be improved by combining these methods with
pharmacotherapy.6 CBT requires that patients spend considerable time and discipline learning and practicing these exercises, even on a daily basis. Patients must be willing to confront the panic-discomfort.
Other nonpharmacologic strategies used in treating PD include group and family therapy, as well as patient support groups.
Many patients with PD will also benefit from stress reduction or stress management
methods.6,9 Patients should also receive adequate sleep and ample periods of rest and relaxation. Use of anxiety-promoting substances (eg, alcohol, nicotine, caffeine, and CNS stimulants) should be avoided, if possible.
During CBT, patients with PD are often taught to change their thinking patterns in regard to the panic episodes, and are given additional insight to help cope with the attacks. For example, if a patient experiences a panic attack, he or she may confront the attack by proclaiming the following true statement: “This episode may be uncomfortable for now, but it is not dangerous; no one has ever died from a panic attack.” A similar affirmation would be: “Panic attacks never last very long; the discomfort I’m feeling right now will pass in a few moments; then I will be fine
again.”9
The chief objectives of pharmacotherapy are to reduce the number and intensity of panic attacks, reduce the anticipatory anxiety, and treat underlying depression (or other psychiatric comorbidities) associated with PD. Four classes of medications have been shown to be effective in treating PD: SSRIs, benzodiazepines, TCAs, and MAOIs. The choice of medication is determined by several factors, including adverse-effect profile, cost, suicide risk, comorbid conditions, history of past response or failure, or patient preference. There are advantages and disadvantages to each of these four classes of medications. The TCAs carry the risk of both cardiovascular and anticholinergic side effects (e.g., dry mouth, urinary retention, constipation, blurry vision), which are of great concern in the elderly. Although SSRIs can cause sexual side effects, they are devoid of cardiovascular and anticholinergic side effects, and are much safer in overdose, especially relative to TCAs. When rapid control of panic symptoms is necessary, the benzodiazepines offer the advantage of faster symptom resolution. A disadvantage of long-term benzodiazepine use is the possibility of physiological dependence. Therefore, benzodiazepines are contraindicated in patients with a history of substance abuse. The risk of hypertensive crisis and dietary restrictions generally limit the use of MAOIs to patients who have not responded to the other drug therapies. The high cost of the SSRIs compared to generic TCAs and benzodiazepines can also limit the use of the SSRIs in some patients.
The SSRIs have been found to be effective for PD and are now considered to be first-line
treatment.10 Evidence has shown that fluoxetine, sertraline, and paroxetine are effective in treating
PD.1,3,8,10 There are different theories behind why the SSRIs work for panic. Serotonergic neurons originate in fairly restricted areas of the brain stem and raphe region, but then project widely throughout the CNS. Projections to the frontal cortex may mediate mood, the hypothalamus projections mediate appetite and sleep, and the amygdala projections mediate the anxiety and fear response. Another theory is that the increase in synaptic serotonin leads to a decrease in noradrenergic activity. A diminution of panic symptoms results because noradrenergic hyperactivity may be associated with panic attacks. This theory leads to the belief that norepinephrine reuptake inhibitors like venlafaxine may also be beneficial for
PD.11
While SSRIs are much better tolerated than TCAs and MAOIs, they can produce bothersome side effects such as headaches, nausea, irritability, insomnia, sexual dysfunction, drowsiness, and tremors. SSRIs may also cause an acute increase in anxiety upon initiation. Many of these adverse effects may be attenuated by initiating therapy with lower doses than are usually used for depression. The current recommended starting doses for PD are fluoxetine 10 mg/ day, paroxetine 10 mg/day, and sertraline 25
mg/day.6 The dose is increased as tolerated to target dosages effective for PD
(Table 4). Antipanic effects will generally not be evident before 4 weeks of drug therapy, with continued improvement and full response at 8 to 12 weeks. The optimal duration of SSRI treatment for PD has not yet been determined. The total duration of therapy for PD should be 8 to 12 months before drug discontinuation is
attempted.6
Table 4.
Fluoxetine for PD. Michelson et al conducted a 2-week, single-blind, placebo lead-in study, followed by a 10-week, randomized, placebo-controlled trial comparing fluoxetine 10 mg/day, 20 mg/day, and placebo in 243
patients.1 Patients were required to meet DSM-IV criteria for PD and were excluded if they had an unstable medical illness or other dominant psychiatric diagnoses. After 10 weeks of acute treatment, patients who were markedly or moderately improved were entered in a 24-week continuation phase and were randomly assigned to continue fluoxetine or placebo. Primary efficacy measures in the study were a change in frequency of total panic attacks; Clinical Global Impression (CGI) of improvement; patient record of panic attack frequency, type, and duration; Panic and Phobic Disorder Change Scale; Hamilton Anxiety Rating Scale (HAM-A); Hamilton Depression Rating Scale (HAM-D); and Sheehan Disability Scale. Significant improvement in panic symptoms was seen in the group receiving 20 mg/day of fluoxetine, but not in the 10-mg/day group when compared to placebo. Similarly, anxiety symptoms were reduced significantly in the 20- mg/day group versus placebo, but not in the 10-mg/day group. None of the groups differed significantly in the number of patients who were completely panic-free or free of full panic attacks at the last visit of the acute phase. Improvement in depression was statistically significant in both fluoxetine groups versus placebo. Among the 80 patients who went on to the continuation phase, four receiving placebo and one receiving fluoxetine relapsed. The study concluded that fluoxetine was efficacious in acute treatment for PD, but panic attack frequency was an incomplete measure of clinical response for this disease.
A study conducted by Emmanual et al enrolled 10 patients who met DSM-IV criteria for PD with or without agoraphobia to determine if a once-weekly dosing of fluoxetine was as effective as daily dosing of fluoxetine for
PD.12 Patients initially received 10 or 20 mg daily of fluoxetine and were increased to a maximum of 60 mg/day depending on the response and adverse events. Patients were seen every 2 weeks until they were panic-free. Once patients were panic-free, they were switched to fluoxetine 10 to 60 mg once weekly, and were evaluated every month following the switch. Assessment of outcome was done using the CGI, patient panic diary, HAM-A, and HAM-D. The results showed that only one of 10 patients experienced recurrence of panic attacks 18 months after the switch to weekly dosing of fluoxetine.
Sertraline for PD. A randomized, double-blind, placebo-controlled trial was conducted with 176 patients who met criteria for PD with or without
agoraphobia.8 The trial lasted 10 weeks, with patients in the sertraline group starting at 25 mg/day for the first week, then 50 mg/day, then titrated up to a maximum of 200 mg/day, if needed. Standard subjective and objective measures of panic and anxiety symptoms were performed. Relative to baseline, patients treated with sertraline had a significantly greater reduction in full panic attacks versus placebo at end point. Also, there was a greater reduction in CGI severity scores versus placebo. The average dose of sertraline was 131.4 mg/day. End-point differences in panic-free status did not reach significance. High-end functioning was significantly greater in patients in the sertraline group. No significant difference was seen in the overall incidence of adverse events.
A double-blind, randomized, parallel, flexible-dose study was conducted by Pohl and associates in 168 patients with
PD.13 This study had a 2-week, single-blind, placebo lead-in, followed by a 10-week, double- blind phase. Patients were given 25 mg/day of sertraline for the first week, followed by a flexible titration of 50 to 200 mg/day or placebo. The study was conducted at 10 sites and excluded patients with psychiatric conditions other than PD or a personality disorder. Outcomes were measured using standard panic and anxiety scales. The mean dose of sertraline was 126 mg/day, and by week 4, all sertraline patients were taking at least 50 mg/day. The results showed a 77% decline from baseline in the number of attacks in the sertraline group versus 51% in the placebo group (P < 0.05). The level of anticipatory anxiety decreased in both the sertraline and placebo groups as the study progressed. A higher percentage of patients in the sertraline group had adverse reactions (9% versus 1%).
Paroxetine for PD. A double-blind, randomized, fixed-dose, placebo-controlled study was conducted to determine the efficacy of paroxetine in 278 patients with
PD.14 The study involved 20 centers and had a 2-week, single-blind, placebo lead-in followed by a 10-week phase with patients randomized to receive 10, 20, or 40 mg/day of paroxetine. Of 278 patients, 188 completed the full 10 weeks of treatment. Adverse effects were the most common reason for dropout in both the paroxetine and placebo groups. Patients in the 40-mg/day paroxetine group had significantly greater improvements versus placebo in panic-free status, reduction in full panic attack, and improvement in CGI severity score. During the final 2 weeks, complete response was seen in 86% of the 40-mg/day group, 65.2% of the 20- mg/day group, 67.4% in the 10-mg/day group, and 50% in the placebo group. The number of situational panic attacks in the 40-mg/day group was significantly lower than placebo, and the intensity of full panic attacks was significantly lower by week 10. Improvement in depressive symptoms was significantly greater in the 40-mg/day paroxetine group compared to the remaining groups. The study concluded that paroxetine 40 mg/day was superior to placebo in most outcome measures for PD.
Patients
should appreciate the lag time experienced between the start of drug
therapy and the anticipated therapeutic response.
Bakker et al studied 154 patients with PD and randomly assigned patients to either paroxetine 20 to 60 mg/day, clomipramine 50 to 150 mg/day, placebo, or cognitive therapy for 12
weeks.15 Cognitive therapy consisted of 12 weekly, 45-minute sessions with a psychologist or psychiatrist. Standardized assessments of panic and anxiety symptoms were performed. Of those who completed the study, 36.7% were free of panic attacks on placebo, 53.8% were panic-free with cognitive therapy, 58.6% were panic-free with clomipramine, and 75% were panic-free in the paroxetine group. This study concluded that paroxetine is more effective than placebo in reducing panic attacks, agoraphobia complaints, anxiety, depression, and social dysfunction.
Prior to the SSRIs, the TCAs were the standard drug therapy for PD. Currently, the TCAs are generally considered second-line therapy and are prescribed after a trial of one or more SSRIs has proven
ineffective.6 The TCAs enhance the activity of norepinephrine and serotonin by blocking neuronal reuptake. Because of their lack of specificity on the receptors, TCAs also affect other receptor systems. This is why the TCAs are associated with anticholinergic, cardiovascular, and neurologic adverse effects. The common side effects of the TCAs include orthostatic hypotension, anticholinergic effects, sleep disturbances, increased sweating, weight gain (especially with long-term use), sexual dysfunction, dizziness, fatigue, and weakness. The most problematic side effects of the TCAs are the anticholinergic and cardiovascular side effects. The toxicity with overdose is also a major concern; they should not be given to patients with a history of suicide or suicidal ideation. Thus, the TCAs are now less commonly prescribed for PD.
As with the SSRIs, many patients with PD exhibit a sensitivity to the adverse effects of TCAs at the initiation of therapy. Therefore, low dosages should be administered initially with a gradual upward titration. Starting doses for PD are much lower than doses prescribed for depression or other psychiatric conditions. For example, a common strategy is to initiate imipramine at only 10 mg/day and gradually titrate the dose upward over the following weeks as
tolerated.6 It may take up to 12 weeks of therapy at therapeutic dosages to reach the full clinical effect.
The benzodiazepines produce their antipanic effects within the first week of treatment. Because of this, the benzodiazepines are often used during the initiation phase of drug therapy with SSRIs and
TCAs.6 Later, they can be used to abort recurrent panic attacks. Clonazepam, lorazepam, and alprazolam are the three benzodiazepines used to treat PD, with clonazepam and alprazolam being FDA-approved for this indication. The common side effects of the benzodiazepines include sedation, fatigue, ataxia, slurred speech, memory disturbances, and weakness. There is also an increased risk of falls in the elderly and a higher risk of motor vehicle accidents associated with benzodiazepine use. The major disadvantages of this class are the likelihood of physiologic dependence with chronic use and potential for abuse. These drugs should not be given to patients with a history of substance abuse. Another disadvantage of the benzodiazepines is the serious withdrawal syndrome that can result from abrupt discontinuation. Benzodiazepine withdrawal syndrome is characterized by insomnia, confusion, an increased risk of seizures, and rebound anxiety.
While the MAOIs are sometimes used as last-line therapy, there are few large, well-designed clinical trials that document their efficacy in treating
PD.6 MAOIs have several disadvantages as antipanic therapy. Their substantial side-effect profile, drug interactions, and dietary restrictions place them as last-line medications in PD therapy. The side effects include hypotension, sexual dysfunction, sleep disturbances, myoclonic jerks, edema, weight gain, hypomania, dry mouth, and paresthesia. The biggest risk associated with MAOI usage is the potentially life-threatening hypertensive crisis that can occur secondary to drug interaction or tyramine ingestion. The symptoms associated with hypertensive crisis include a severe headache accompanied by flushing and throbbing and “thumping” of the heart. If these symptoms develop, patients should be counseled to visit an emergency room immediately. It is vitally important that patients taking these medications adhere to a strict low-tyramine diet and also monitor medication intake. The food, drink, and drug restrictions should be started at least 24 hours prior to MAOI therapy and continued for 2 weeks after stopping the MAOI.
Serious drug interactions can occur when MAOIs are used with the following drugs: meperidine, dextromethorphan, sympathomimetic amines (e.g., pseudoephedrine), and SSRIs. These medications should always be avoided in patients receiving MAOI therapy. The MAOIs should be reserved for patients who are refractory to other drug therapy for PD. In this class, phenelzine has been the most studied and prescribed for PD. The starting dose of phenelzine is 15 mg/day every 3 to 4 days, with the dosage increased until 60 mg/day is reached. A dose of less than 45 mg/day is rarely effective, and the maximum dosage is 90 mg/day. The adverse effect of orthostatic hypotension can be lessened if phenelzine is administered after meals. As with the TCAs and SSRIs, the antipanic effects are delayed; MAOI effects are seen in 3 to 5 weeks, with maximal response in 6 to 10 weeks.
Some patients who are started on an MAOI are switching from other types of antidepressants. If this is the case, 2 weeks should lapse before beginning an MAOI, due to the potential for drug interaction. Fluoxetine must be stopped 5 weeks prior to initiating an MAOI.
Role of the Pharmacist
Some patients may be apprehensive about taking medications to treat PD.9 Some may fear that they will become addicted,
that they will have a worsening of their panic symptoms, or that they will
experience unwanted adverse effects from the medication. All of these can
potentially contribute to noncompliance. To prevent this, pharmacists should
reassure and educate patients appropriately. Patients should appreciate the
lag time experienced between the start of drug therapy and the anticipated
therapeutic response. Patients must be taught to remain compliant and tolerant during this time period, which may last up to 12 weeks. Pharmacists
should also explain the rationale for initiating treatment with lower doses
(e.g., to avoid anxiogenic, CNS excitatory, or adverse gastrointestinal side
effects). Both male and female patients receiving SSRIs should be counseled about the potential for sexual dysfunction and encouraged to
discuss this with their physicians. Unless otherwise directed by the physician, SSRIs should be dosed initially in the morning, since they are
sometimes associated with insomnia. Other medications that increase central serotonin levels (e.g., antimigraine therapy, St. John’s wort) should be used only with great caution in patients receiving SSRI therapy to avoid the serotonin
syndrome.16 This syndrome consists of a constellation of nonspecific symptoms, such as headache, sweating, dizziness, and
agitation, and is related to excessive CNS accumulation of serotonin.
Because of the coexistence of suicidal ideation, depression, and PD, pharmacists should dispense no more than a 1-month supply of TCAs, since these agents can be lethal during intentional overdose. Patients with significant cardiovascular disease, prostate disease, or urinary retention must be monitored closely since TCAs can exacerbate these conditions. Patients should be made aware of the need to taper benzodiazepines when discontinuing them. Patients should not decrease, increase, or abruptly stop benzodiazepine therapy without first consulting their physician. If an MAOI is being prescribed, counseling the patient about the dietary restrictions and potential drug interactions is important. Because caffeine, over-the-counter stimulants, nicotine, alcohol, and drugs of abuse can precipitate panic attacks, patients should also be counseled to avoid these substances. Finally, the pharmacist can assist patients in finding qualified therapists, psychiatrists, patient support groups, and patient education materials on the topic of PD. The following resource list may be
helpful.
• Anxiety Disorders of America
What Is Panic Disorder?
11900 Parklawn Drive
Suite 100
Rockville, MD 20852
www.adaa.org
• American Psychiatric
Association
Let’s Talk Facts About Panic Disorder
1400 K St., NW
Washington, DC 20005
Fax on demand: 202-682-6000
www.psych.org
• National Institute of Mental Health
Understanding Panic Disorder
888-8-ANXIETY or
301-443-4513
www.nimh.nih.gov
• Journal of the American Medical Association (JAMA) JAMA Patient Pages-Panic Disorder
May 17, 2000-Vol. 283, No. 19
www.ama-assn.org/consumer.htm
Acknowledgment
The authors wish to recognize and thank Anne
Deitzel, an Ohio Northern University College of Pharmacy student, for her contribution in preparing this article.
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