eMedicine Specialties > Psychiatry > Adult

Panic Disorder

Colin Y Daniels, MD, Consulting Staff, Department of Psychiatry, Madigan Army MedicalCenter

Updated: Jul 29, 2009

Introduction

Background

Panic disorder is characterized by the spontaneous and unexpected occurrence of panic attacks, the frequency of which can vary from several attacks per day to only a few attacks per year. Panic attacks can occur in other anxiety disorders but occur without discernible predictable precipitant in panic disorder.

To meet the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR)¹ criteria for panic disorder, panic attacks must be associated with more than 1 month of subsequent persistent worry about (1) having another attack, (2) consequences of the attack, or (3) significant behavioral changes related to the attack.

Panic attacks are a period of intense fear in which 4 of 13 defined symptoms develop abruptly and peak rapidly less than 10 minutes from symptom onset. To make the diagnosis of panic disorder, panic attacks cannot directly or physiologically result from substance use, medical conditions, or another psychiatric disorder.

The DSM-IV-TR delineates the following potential symptom manifestations of a panic attack:

• Palpitations, pounding heart, or accelerated heart rate
• Sweating
• Trembling or shaking
• Sense of shortness of breath or smothering
• Feeling of choking
• Chest pain or discomfort
• Nausea or abdominal distress
• Feeling dizzy, unsteady, lightheaded, or faint
• Derealization or depersonalization (feeling detached from oneself)
• Fear of losing control or going crazy
• Fear of dying
• Numbness or tingling sensations
• Chills or hot flashes

Panic disorder is usually qualified with the presence or absence of agoraphobia. Agoraphobia is defined as anxiety toward places or situations in which escape may be difficult or embarrassing. These anxiety-provoking situations are avoided or are endured with anxiety. (Note: Agoraphobia is not a stand-alone disorder; it is a descriptive term [eg, panic disorder with agoraphobia.])

Case study

A 22-year-old single female without past medical history or prior psychiatric care presents to the Emergency Department complaining of a 3 year history of episodic anxiety, increasing over the last 6 months with an acute episode of anxiety this evening. She recollects anxiety attacks beginning around age 19, while working as a waitress after high school. She describes the anxiety episodes as sudden episodes of anxiety with dizziness, abdominal distress, and fear of losing control, which would self resolve after 5-10 minutes in the break room or walk-in refrigerator. The anxiety attacks occurred infrequently (<1 per month initially) and she did not seek any care because she had no medical insurance. 

The woman cites the frequency and severity of these unexpected attacks increasing over the next 3 years. For the past 6 months, she reports experiencing sudden episodes of anxiety 2-3 times per week, which can occur at work or at home, although they occur more frequently at work or when anticipating going to work or other social functions in crowded public places. She describes these episodes now as acute attacks with a sense of impending loss of control, palpitations, shortness of breath, chest tightness, dizziness, and hot flashes. She affirms significant worry about when the next attack will occur and concedes missing work when calling in sick and having her supervisor send her home early due to observed distress. 

The woman denies noting any specific triggers for her anxiety and denies any recreational drug use. She relates limited social alcohol consumption (1-2 times per week with 1-3 regular alcoholic drinks over several hours), which she notes seems to reduce her severity of anxiety attacks. She denies any escalation of alcohol use, tolerance, withdrawal, excessive time spent drinking or recovering, or social or occupational consequences of alcohol use. She denies excessive worry about routine stressors and denies any prior history of traumatic events. She denies any sustained depressed mood, manic symptoms, psychotic symptoms, or interpersonal/relational problems. She denies any suicidal or homicidal ideations, or history of self-injurious behavior and reports future plan to begin study at the local college for business administration if she can control her anxiety and avoid losing her employment.    

Pathophysiology

Many non–mutually exclusive theories and proposed abnormalities/inefficiencies in molecular signal processing in specific neuronal regions or neurotransmitter pathways have recently been investigated to explain panic disorder (from a biologic perspective) in response to the observed efficacy of certain pharmacologic agents for controlling the symptoms or from observations of investigational functional neuroimaging.

• The serotonergic model suggests an exaggerated or inefficient postsynaptic receptor response to synaptic serotonin, potentially in the signal transduction cascade. Some studies report subsensitivity of 5HT1A receptors. The 5HT system or one of its subsystems may play a role in the pathophysiology of panic disorder, the precise nature of which must be delineated by further investigation.
• The catecholamine model postulates increased sensitivity to or improper processing of adrenergic CNS discharges, with potential hypersensitivity of presynaptic alpha-2 receptors.
• Similarly, the locus ceruleus model explains that panic symptoms are due to increased local discharge resulting in adrenergic neuron stimulation, similar to the more general catecholamine theory. Locus ceruleus activity also affects the hypothalamic-pituitary-adrenal axis, which can respond abnormally to clonidine in patients with panic disorder.
• The lactate model focuses on symptom production by postulated aberrant metabolic activity induced by lactate.
• The false suffocation carbon dioxide hypothesis explains panic phenomena by hypersensitive brainstem receptors.
• The GABA model postulates decreased inhibitory receptor sensitivity, with a resultant excitatory effect.
• The neuroanatomic model suggests that panic attacks are mediated by a "fear network" in the brain that involves the amygdala, hypothalamus, and brainstem centers. More generally, the corticostriatalthalamocortical (CSTC) are believed to mediate worry, interacting with the more fear-specific circuit in the amygdala. The sensation of fear occurs through reciprocal regulatory activity conceptually initiated in the amygdala and projected to the anterior cingulated cortex and/or orbitofrontal cortex. Projections from the amygdala to the hypothalamus then mediate endocrinologic responses to fear. 
• The genetic hypothesis has attempted to refer panic disorder to definable genetic loci, without success to date.

Frequency

United States

Lifetime prevalence estimates range from 1.5-5% for panic disorder and 3-5.6% for panic attacks.

Mortality/Morbidity

Significant comorbidities are associated with panic disorder.

• Panic disorder often coexists with mood disorders, with mood symptoms potentially following the onset of panic attacks. Lifetime prevalence rates of major depression may be as much as 50-60%. These patients may be at higher risk of suicide attempts. Alcohol and other substance use disorders are also frequent sequelae of panic disorder.
• Medical conditions apparently share significant comorbidity with panic disorder. These conditions include cardiovascular disorders (eg, mitral valve prolapse, hypertension, cardiomyopathy) and other disorders (eg, chronic obstructive pulmonary disorder, irritable bowel syndrome, migraine headache).
• Aside from the significant psychological anguish of panic attacks, agoraphobia can result in numerous medical, social, and occupational consequences. These include increased health care use, social withdrawal and restricted role functioning, and decreased work productivity.

Race

Data on prevalence in different racial groups are inconsistent. Symptom manifestations may differ, with African Americans more often presenting with somatic symptoms and more likely seeking help in medical rather than psychiatric settings.

Sex

One-month prevalence estimates for women are 0.7% versus 0.3% for men (ie, women are more likely to be affected than men by a 2- to 3-fold factor).

Age

Panic disorder has a bimodal distribution, with highest incidence in late adolescence and a second peak in the mid 30s.

Clinical

History

A sudden onset of a panic attack reportedly occurs with 4 (or more) of the 13 associated symptoms progressing to a peak within 10 minutes. Triggers and patterns help construct the differential diagnosis.

• Unexpected panic attacks have no known precipitating cue; these panic attacks often support the diagnosis of panic disorder without agoraphobia.
• Situationally bound (cued) panic attacks recur predictably in temporal relationship to the trigger; these panic attacks usually implicate a specific phobia-type diagnosis.
• Situationally predisposed panic attacks are more likely to occur in relation to a given trigger, but they do not always occur. This pattern more likely describes panic disorder with agoraphobia.
• Use of caffeine, alcohol, nicotine, or other substances can trigger or potentiate panic attacks.

Physical

No signs on physical or Mental Status Examination are specific for panic disorder. While the patient may or may not appear anxious at the time of interview, their Mini-Mental Status Examination, including cognitive performance, memory, serial-7, and proverb interpretation, should appear intact and consistent with the patient’s educational level and apparent baseline intellectual functioning. The diagnosis is made primarily by history.

• If the patient presents in an acute state of panic, he or she can physically manifest any anticipated sign of an increased sympathetic state. These nonspecific signs may include hypertension, tachycardia, mild tachypnea, and mild tremors. The attack lasts 20-30 minutes from onset—rarely more than an hour. Somatic concerns of death from cardiac or respiratory problems may be a major focus of patients during an attack. Patients may end up in an emergency department.
• The Mental Status Examination may reveal an anxious-appearing person, although this is not required for diagnosis. Speech may reflect anxiety or urgency, or it may sound normal. Mood may be described as similar to "anxious," with congruent affect. Incongruent affect should raise consideration for other diagnostic possibilities. Thought processes should be logical, linear, and goal directed. Thought content is particularly important to specifically assess in order to ensure a patient has no suicidal or homicidal thoughts. Acute anxiety, as a form of acute mental anguish, can lead to unsafe or self-injurious behavior. Abnormalities in thought process or thought content (aside from impulsive suicidal thoughts) should prompt reconsideration of other etiologies. Insight and judgment are usually present and intact.

Causes

Panic disorder has moderate heritability, with heritability rates estimated to range from 0.3-0.6%. Segregation analyses have been inconclusive, and no distinct DNA linkages are known.

Differential Diagnoses

Other Problems to Be Considered

Acute stress/posttraumatic stress disorder
Adrenal dysfunction
Alcohol/sedative-hypnotic withdrawal
Drug intoxication
Generalized anxiety disorder
Hyperthyroidism
Pulmonary disease
Temporal lobe seizure activity
Vestibular dysfunction

Workup

Laboratory Studies

No laboratory parameters are specific for panic disorder. Laboratory evaluation is performed to exclude any of the aforementioned differential diagnoses.

Imaging Studies

No imaging study findings are currently specific for panic disorder, although they are performed to evaluate anatomic evidence of other diagnostic possibilities. Studies may include an EEG to exclude partial complex seizures. Investigational functional neuroimaging is not used in routine clinical practice for diagnosis or for monitoring treatment response.

Procedures

No invasive procedures are required to diagnose panic disorder, although they may be useful in eliminating other differential diagnoses. History, collateral information, and physical/Mental Status Examinations remain the diagnostic cornerstones.

Treatment

Medical Care

Pharmacotherapy, cognitive and behavioral psychotherapy, and other psychological treatment modalities are used to treat panic disorder.

Pharmacotherapy

Selective serotonin reuptake inhibitors (SSRIs) are generally used as first-line agents, followed remotely by tricyclics. Benzodiazepines can achieve long-term control but should be reserved for patients with refractory panic disorder and should generate a psychiatric referral for pharmacologic management review and potentially a psychotherapist for any additional nonpharmacologic treatment options.

Fluoxetine (Prozac) can be used (especially if panic disorder occurs with depression); however, patients may poorly tolerate it initially because it may initially increase anxiety, except at very low starting doses. Fluoxetine has a long half-life, making it a good choice in marginally compliant patients.

Mirtazapine (Remeron)² has a much more sedating effect, generally reducing its potential to aggravate initial anxiety. Remeron acts distinctly as an alpha-2 antagonist, consequently increasing synaptic norepinephrine and serotonin, while also blocking some postsynaptic serotonergic receptors that conceptually mediate excessive anxiety when stimulated with serotonin. Remeron may cause residual morning sedation that often improves with continued therapy and may cause an increase in appetite or weight gain. 

Sedating antidepressants like Paxil, Remeron, and TCAs are usually prescribed only at night before bed to help improve sleep but should include a warning not to operate a motor vehicle or machinery if feeling sedated or directly after the dose. Prozac alters metabolism of cytochrome P-450 2D6–cleared agents; this fact should be considered. Paxil (paroxetine) represents a partially sedating SSRI option that is also available in a controlled release preparation (Paxil CR), which may improve tolerability, but Paxil still inhibits P450 2D6.

Citalopram (Celexa) and escitalopram (Lexapro) are likely to cause fewer hepatic enzyme interactions and may be appropriate initial choices for patients with complicated medical regimens or those who are concerned about drug interactions. Escitalopram also appears particularly well tolerated in preliminary studies, although it may be restricted from some formularies due to the large difference in cost with Celexa without a commensurate improvement in efficacy or tolerability for many patients. Sertraline (Zoloft) represents a similar SSRI option with a slightly different pharmacodynamic profile, including sigma receptor effects, although it has some P450 3A4 interactions.

Benzodiazepines act quickly but carry the liability of physiologic and psychologic dependence. Benzodiazepines can be reasonably used as an initial adjunct while SSRIs are titrated to an effective dose. Benzodiazepines then can be tapered over 4-12 weeks while the SSRI is continued. This approach can improve short-term tolerability, although it may increase the risk of sedation and requires warnings not to operate motor vehicles after taking benzodiazepines or if feeling sedated.

Alprazolam (Xanax) has been widely used for panic disorder, but it is currently discouraged because of its higher dependence potential; alprazolam has a short half-life, which makes it particularly prone to rebound anxiety and psychological dependence. Clonazepam (Klonopin) has become a favored replacement because it has a longer half-life and empirically elicits fewer withdrawal reactions upon discontinuation.

Cognitive and behavioral psychotherapy

Cognitive and behavioral psychotherapy can be used alone or in addition to pharmacotherapy. The combination approach yields superior results for most patients compared to either single modality.

Cognitive therapy helps patients understand how automatic thoughts and false beliefs/distortions lead to exaggerated emotional responses, such as anxiety, and can lead to secondary behavioral consequences. Specific patterns of cognitive distortions (twisted thoughts) tend to respond best to specific techniques described in cognitive behavior therapy books (eg, The Feeling Good Handbook by David Burns, MD). While intended for use in conjunction with therapy, patients can purchase these books and complete the course themselves.

Behavioral therapy involves sequentially greater exposure of the patient to anxiety-provoking stimuli; over time, the patient becomes desensitized to the experience. Relaxation techniques also help control patients' levels of anxiety. Respiratory training can help control hyperventilation during panic attacks and help patients control anxiety with controlled breathing. Other forms of psychological treatment, including psychodynamic psychotherapy for specific issues, are available but exceed the scope of this article.

• Prehospital care
  • Reassure and calm the patient.
  • Transport the patient to a medical treatment facility to exclude medical causes for the first attack or when suspected on subsequent attacks.
• Emergency Department care
  • Acute panic disorder is best treated with benzodiazepines. The natural history of panic attacks is spontaneous remission of panic symptoms with anxiety about recurrence during the episode.
  • Prompt use of benzodiazepines can ease the uncomfortable anxiety associated with the attack and can provide the patient with definitive confidence that treatment can control the symptoms. This is particularly helpful for preventing subsequent visits to emergency services while longer-term therapy is helping the patient gain control.
  • Consultation with a psychiatrist is helpful to initiate longer-term therapy and to provide follow-up planning. Longer-term therapy currently consists of SSRIs, often with additional psychotherapeutic techniques.

Medication

Benzodiazepine therapy should be provided if acute symptoms are still present at the time of the interview or if significant apprehension about future attacks remains. If necessary, benzodiazepines are continued for a brief period (<2 wk if prescribed on a scheduled basis).

Clonazepam has become the benzodiazepine of choice for outpatient use. Selecting patients for whom benzodiazepine therapy will be helpful rests on the clinician's judgment of a patient's ability to control his or her symptoms in their native environment, until the next psychiatric appointment, or until an SSRI begins to control the symptoms (about 2 wk, although sometimes much longer as the SSRI may require dose escalation). Alprazolam (Xanax) has been reviewed in the literature, although its use is currently discouraged because of its higher potential to elicit dependency.

Some patients may benefit from a standing dose of a benzodiazepine, whereas others do better with an as-needed (prn) dosing regimen. Longer-term control should be attempted with SSRIs if appropriate follow-up care (including the PCM) is available. SSRIs are usually well tolerated, and appropriate follow-up care merely consists of meeting with the patient in 2 weeks to assess treatment efficacy and to deal with temporary symptom exacerbations right after beginning SSRIs and ensuring the patient has no emergence of suicidal thoughts. Serotonergic drugs may contain warnings about potential increases in suicidal thoughts, particularly in those younger than age 25 years, but this is generally NOT associated with an increase in completed suicides compared with patients who receive no treatment. Potential suicide risk should be assessed routinely for every patient, whether they take SSRI treatment or not.

Other antidepressants that have an effect on the serotonergic system have been used, especially when SSRIs have been ineffective or poorly tolerated. Prior to SSRIs, the tricyclics and the monoamine oxidase inhibitors (MAOIs) were used much more commonly. More recently, venlafaxine (Effexor) and mirtazapine (Remeron) have been used, which act on both serotonin and norepinephrine. Beta-blockers, clonidine, calcium channel blockers, atypical antipsychotics (Abilify, Zyprexa, Seroquel, Risperdal, Geodon), buspirone, and anticonvulsants such as divalproex (Depakote) and gabapentin (Neurontin) have also been used as adjunctive agents in patients with refractory panic disorder, although these uses have not been approved by the US Food and Drug Administration.

Intermediate-acting benzodiazepines

By binding to specific receptor-sites, these agents appear to potentiate the effects of gamma-aminobutyrate (GABA) and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. These agents are effective on standing-dose and prn schedules.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively intermediate half-life. By increasing action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.

Dosing

Adult

0.5-1 mg IV/IM or 1-2 mg PO bid/tid
Elderly: Begin with half dose

Pediatric

Not established

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, narcotic analgesics, phenothiazines, barbiturates, and MAOIs

Contraindications

Documented hypersensitivity; end-stage COPD with tenuous respiratory function (could impact oxygenation/ventilation by lowering respiratory rate, even if tachypneic); advanced hepatic synthetic failure (decreases first-pass metabolism and prolongs half-life); history of addiction to alcohol/sedative-hypnotics (can initiate cravings/relapse, use with caution); acute narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Clonazepam (Klonopin)

Facilitates inhibitory GABA neurotransmission and other inhibitory transmitters. Relatively longer half-life (approx 36 h)

Dosing

Adult

0.5-2 mg PO bid/tid

Pediatric

Not established

Interactions

Phenytoin and barbiturates may reduce effects; coadministration of CNS depressants increases toxicity similar to lorazepam

Contraindications

Documented hypersensitivity; severe liver disease; acute narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in chronic respiratory disease or impaired renal function; withdrawal symptoms can result from abrupt discontinuation

Selective serotonin reuptake inhibitors

First-line agents for long-term management of anxiety disorders, with control gradually achieved over a 2- to 4-wk course, depending on required dosage increases.

All commonly used SSRIs appear to have a role in the treatment of panic disorder. Fluoxetine is covered herein because it has a very long half-life. This makes it well suited for patients who have difficulty remembering to take all of their medications each day. The longer half-life also minimizes the risk and severity of SSRI withdrawal that can occur when patients exhaust or abruptly discontinue their SSRI.

Fluoxetine (Prozac)

Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in reuptake of norepinephrine or dopamine.

Dosing

Adult

20-60 mg PO qd; consider starting at 10 mg without benzodiazepine coverage (for 1-2 wk) or 20 mg with coverage

Pediatric

Not established

Interactions

Phenobarbital and phenytoin may decrease effects; cimetidine may increase toxicity; because of its effects on cytochrome P-450 (especially 2D6) enzyme systems and on protein binding, can increase blood levels of antipsychotics, anticonvulsants, other antidepressants, beta-blockers, type 1C antiarrhythmics, and warfarin (Coumadin); serotonin syndrome may occur when used with other serotonergic agents such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, nefazodone, or other SSRIs, but especially with MAOIs

Contraindications

Documented hypersensitivity; concurrently taking MAOIs or took them in the last 2 wk.

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating therapy; Prozac has a long half-life and requires a longer wash-out period (typically 4-6 wk).

Paroxetine (Paxil)

Alternative sedating SSRI. Potent selective inhibitor of neuronal serotonin reuptake. Also has weak effect on norepinephrine and dopamine neuronal reuptake. For maintenance dosing, make dosage adjustments to maintain patient on lowest effective dosage, and periodically reassess patient to determine need for continued treatment.

Dosing

Adult

10-40 mg PO qhs

Pediatric

Not established

Interactions

Phenobarbital and phenytoin may decrease effects; cimetidine may increase toxicity; because of its effects on cytochrome P-450 enzyme systems and on protein binding, can increase blood levels of antipsychotics, anticonvulsants, other antidepressants, beta-blockers, type 1C antiarrhythmics, and warfarin (Coumadin); serotonin syndrome may occur when used with other serotonergic agents such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, nefazodone, or other SSRIs, but especially with MAOIs; inhibits CYP450 2D6

Contraindications

Documented hypersensitivity; concurrent administration with MAOIs or administering within 14 d of discontinuing an MAOI

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in history of seizures, mania, renal disease, and cardiac disease.

Follow-up

Further Inpatient Care

Inpatient care is rarely considered for uncomplicated panic disorder. Patients may get admitted if they display any evidence of dangerous behavior, safety concerns, report suicidal or homicidal ideation as may occur in context of acute anxiety, fear of anxiety or its consequences. Patients may require hospitalization for intoxication or withdrawal from sedative/hypnotics such as alcohol or Xanax, which sometimes get ingested or abused in attempts to medicate or manage the anxiety. Patients may also get hospitalized if they become so incapacitated by their anxiety that they are unable to adhere to outpatient care.

Further Outpatient Care

• Initial follow-up care should occur within 2 weeks because SSRIs can cause an initial exacerbation of panic symptoms. For this reason, begin with the lowest dose with the understanding that the dose must be increased at the initial follow-up visit.
• Providing a few doses of a benzodiazepine as needed (prn) can enhance patient confidence and compliance. Total tablet dispensing should remain limited to ensure patients understand they have a limited supply and that this medicine represents a temporary or emergency use option and reaffirm the importance of longer term management with SSRI medication and psychotherapeutic techniques (eg, cognitive behavior therapy). Avoid benzodiazepine prescriptions in patients with a known history of substance misuse or alcoholism.
• Assess potential suicide risk at all appointments.
• Ensure continuing treatment of any concurrent substance use disorders.

Prognosis

Prognosis is excellent with adherence to medical management.

Patient Education

• Educate patients on potential adverse effects of their treatment medications.
• Obtain informed consent for psychotropic medications.
• Document the discussion of the risks and benefits of treatment medications.
• Inform patients that causes are likely biological and psychosocial.
• Advise patients to avoid anxiogenic substances such as caffeine, energy drinks, other OTC stimulants or recreational drugs.
• Consider educating patients diagnosed with panic disorder on cognitive distortions that may help amplify anxiety. Also educate patients about recognizing trigger stimuli so they can contribute this to their psychological treatment approach.
• Discuss alcohol consumption and any recreational drug use because these psychoactive substances can impact the course of panic disorder. While some substances may seem to avert the anguish of an acute attack, they often compromise the long-term treatment plan.
• Educate the patient’s family, if available, on the important issues of minimizing any avoidance behaviors from the patient, ensuring adherence to therapy appointments and pharmacologic compliance, and understanding the nature of the anxiety symptoms with reasonable accommodation without enabling dysfunctional behaviors or alcohol/prescription drug use. Family members can be particularly helpful in helping the patient overcome unrealistic fears and ingrained avoidance behaviors, in context of ongoing cognitive behavior therapy where the patient has learned coping skills to manage the anxiety.
• National Institute of Mental Health, Panic Disorder
• MedlinePlus, Panic Disorder
• MayoClinic, Panic attacks and panic disorder
• For excellent patient education resources, visit eMedicine's Anxiety Center. Also, see eMedicine's patient education articles Anxiety, Panic Attacks, and Hyperventilation.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize an underlying medical etiology
• Failure to document informed consent for medications
• Failure to document warnings to patients about the potential adverse effects (eg, sedation or suicidal ideation) of treatment medications
• Failure to assess suicide risk and ensure safety plan in case these thoughts occur

References

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Press; 2000.

2. Croom KF, Perry CM, Plosker GL. Mirtazapine: a review of its use in major depression and other psychiatric disorders. CNS Drugs. 2009;23(5):427-52. [Medline].

3. American Psychiatric Association. Practice guideline for the treatment of patients with panic disorder. Work Group on Panic Disorder. American Psychiatric Association. Am J Psychiatry. May 1998;155(5 Suppl):1-34. [Medline].

4. Bandelow B, Behnke K, Lenoir S, et al. Sertraline versus paroxetine in the treatment of panic disorder: an acute, double-blind noninferiority comparison. J Clin Psychiatry. Mar 2004;65(3):405-13. [Medline].

5. Bohni MK, Spindler H, Arendt M, Hougaard E, Rosenberg NK. A randomized study of massed three-week cognitive behavioural therapy schedule for panic disorder. Acta Psychiatr Scand. Mar 10 2009;[Medline].

6. Fogel BS, Schiffer RB, Rao SM, eds. Neuropsychiatry. ed. Baltimore, Md: Williams & Wilkins; 1996:263-8.

7. Hales RE, Yudofsky SC, Talbott JA, eds. APA Textbook of Psychiatry. 3^rd ed. Washington, DC: American Psychiatric Press; 1999.

8. Kaplan HI, Sadock BJ, eds. Synopsis of Psychiatry. Behavioral Sciences/Clinical Psychiatry. 8^th ed. Baltimore, Md: Williams & Wilkins; 1997:594-603.

9. Kim YW, Lee SH, Choi TK, Suh SY, Kim B, Kim CM, et al. Effectiveness of mindfulness-based cognitive therapy as an adjuvant to pharmacotherapy in patients with panic disorder or generalized anxiety disorder. Depress Anxiety. 2009;26(7):601-6. [Medline].

10. Kushner MG, Sletten S, Donahue C, Thuras P, Maurer E, Schneider A, et al. Cognitive-behavioral therapy for panic disorder in patients being treated for alcohol dependence: Moderating effects of alcohol outcome expectancies. Addict Behav. Jun-Jul 2009;34(6-7):554-60. [Medline].

11. Marcks BA, Weisberg RB, Keller MB. Psychiatric treatment received by primary care patients with panic disorder with and without agoraphobia. Psychiatr Serv. Jun 2009;60(6):823-30. [Medline].

12. Pfeiffer PN, Ganoczy D, Ilgen M, Zivin K, Valenstein M. Comorbid anxiety as a suicide risk factor among depressed veterans. Depress Anxiety. Jun 18 2009;[Medline].

13. Pollack MH, Simon NM, Worthington JJ, et al. Combined paroxetine and clonazepam treatment strategies compared to paroxetine monotherapy for panic disorder. J Psychopharmacol. Sep 2003;17(3):276-82. [Medline].

14. Sadock BJ, Sadock VA, Kaplan HI. Kaplan and Sadock's Comprehensive Textbook of Psychiatry. Baltimore, Md: Williams & Wilkins; 2000:1445-90.

15. Stahl SM, Gergel I, Li D. Escitalopram in the treatment of panic disorder: a randomized, double-blind, placebo-controlled trial. J Clin Psychiatry. Nov 2003;64(11):1322-7. [Medline].

16. Stahl's Essential Psychopharmacology, Neuroscientific Basis and Practical Applications. 3rd Ed. New York: Cambridge University Press; 2008.

17. Swoboda H, Amering M, Windhaber J, Katschnig H. The long-term course of panic disorder--an 11 year follow-up. J Anxiety Disord. 2003;17(2):223-32. [Medline].

Keywords

anxiety attack, panic attack, mood disorder, agoraphobia, phobia, anxiety disorder, anxiety provocation, acute anxiety, panic, panic disorder

Contributor Information and Disclosures

Author

Colin Y Daniels, MD, Consulting Staff, Department of Psychiatry, Madigan Army MedicalCenter
Colin Y Daniels, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.

Medical Editor

Mohammed A Memon, MD, Medical Director of Geriatric Psychiatry, Department of Psychiatry, Spartanburg Regional Hospital System
Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

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Managing Editor

Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Sandra Yerkes to the development and writing of this article.

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