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Panic Disorder

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Panic Disorder
Author: Mohammed A Memon, MD; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych (UK) more... Updated: Mar 29, 2011

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. (See Diagnostic Considerations and Workup.) 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. (See History.) 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. (See History.) 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 During the episode, patients have the urge to flee or escape and have a sense of impending doom (as though they are dying from a heart attack or suffocation). Other symptoms may include headache, cold hands, diarrhea, insomnia, fatigue, intrusive thoughts, and ruminations. (See Physical Examination.) 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. (See Epidemiology and History.)
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Following exclusion of somatic disease and other psychiatric disorders, confirmation of the diagnosis of panic disorder with a brief mental status screening examination and initiation of appropriate treatment and referral is time- and cost-effective in patients with this condition, who have high rates of medical resource use. (See Mental Status.)

Consequences of panic disorder

Panic disorder can lead to a significant hindrance in lifestyle. Many people with agoraphobia are unable to travel alone or be in crowds or malls or on public transportation. Individuals with panic disorder also may face problems with employment and depression.[2] In addition, persons with panic disorder have a much higher risk of alcohol abuse and suicidality [2] than the general population does (although some studies suggest that panic disorder itself is not a risk factor for suicide in the absence of other risks, such as affective disorders, substance abuse, eating disorders, and personality disorders).
[3]

Types of panic attacks

Unexpected panic attacks have no known precipitating cue; these 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. A variant of panic disorder unrelated to fear (nonfearful panic disorder [NFPD]) is associated with high rates medical resource use (32-41% of patients with panic disorder seeking treatment for chest pain) and poor prognosis.[4]

Panic triggers
Triggers of panic can include the following: Injury (eg, accidents, surgery) Illness Interpersonal conflict or loss Use of cannabis (can be associated with panic attacks, perhaps because of breath-holding)[5] Use of stimulants, such as caffeine, decongestants, cocaine, and sympathomimetics (eg, amphetamine, MDMA)[6] Certain settings, such as stores and public transportation (especially in patients with agoraphobia) Sertraline, which can induce panic in previously asymptomatic patients [7] The selective serotonin reuptake inhibitor (SSRI) discontinuation syndrome, which can induce symptoms similar to those experienced by panic patients In experimental settings, symptoms can be elicited in people with panic disorder by hyperventilation, inhalation of carbon dioxide,[8] caffeine consumption (as mentioned above), or intravenous infusions of hypertonic sodium lactate or hypertonic saline,[9] cholecystokinin, isoproterenol, flumazenil, or naltrexone.[10] The carbon dioxide inhalation challenge is especially provocative of panic symptoms in smokers.[11] Go to Anxiety Disorders; Anxiety Disorder, Specific Phobia; Anxiety Disorder, Separation Anxiety and School Refusal; and Phobic Disorders for more complete information on these topics.

Etiology
Panic disorder appears to be a genetically inherited neurochemical dysfunction. The condition has moderate
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heritability, with heritability rates estimated to range from 0.3% to 0.6%. Segregation analyses have been inconclusive, and no distinct deoxyribonucleic acid (DNA) linkages are known. However, genetic studies suggest that the chromosomal regions 13q, 14q, 22q, 4q31-q34, and probably 9q31 may be associated with the heritability of panic disorder phenotype.[12]

Etiologic theories
The apparent neurochemical dysfunction behind panic disorder may involve autonomic imbalance, decreased gamma-aminobutyric acid (GABA)-ergic tone,[13] allelic polymorphism of the catechol-O-methyltransferase (COMT) gene, increased adenosine receptor function, increased cortisol,[14] diminished benzodiazepine receptor function, and disturbances in serotonin,[15] serotonin transporter (5-HTTLPR)[16] and promoter (SLC6A4) genes,[17] norepinephrine, dopamine, cholecystokinin, and interleukin 1beta.[18] Some theorize that panic disorder may represent a state of chronic hyperventilation and carbon dioxide receptor hypersensitivity.[8] Some epileptic patients have panic as a manifestation of their seizures. 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 central nervous system (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 corticostriatal-thalamocortical (CSTC) circuitry is 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. The cognitive theory suggests that patients with panic disorder have a heightened sensitivity to internal autonomic cues (eg, tachycardia).

Imaging results
Positron emission tomography (PET) scanning has demonstrated increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients with panic disorder.[15] Magnetic resonance imaging (MRI) has demonstrated smaller temporal lobe volume, despite normal hippocampal volume, in patients with panic disorder.[19]

Epidemiology
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Incidence of panic disorder in the United States

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

Mortality and morbidity 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%. Other medical conditions that apparently share significant comorbidity with panic disorder include chronic obstructive pulmonary disorder, irritable bowel syndrome, migraine headache, obsessive-compulsive disorder, restless leg syndrome,[20] fatigue,[21] specific phobias, social phobia, and agoraphobia. Comorbidities also include cardiovascular disorders (eg, mitral valve prolapse, hypertension, cardiomyopathy, stroke),[22] with panic patients being nearly twice as likely to develop coronary artery disease. Patients with panic disorder who have coronary disease can experience myocardial ischemia during their panic episodes.[23, 24] Panic disorder is also associated with a higher risk of sudden death.[25] However, panic disorder is also present in 30% of patients with chest pain and normal findings on angiography. Panic disorder is found in 5-40% of persons with asthma, 15% of patients with headache, 20% of patients with epilepsy, and 10% of patients in primary care settings. In addition, individuals with panic disorder tend to have lower oxygen consumption and exercise tolerance than does the general population.[26] Individuals with panic disorder have a suicide rate many times higher than the population.[2] The rate of substance abuse (especially stimulants, cocaine, and hallucinogens) in persons with panic disorder is 7-28%, a risk 4-14 times greater than that of the population. In addition, panic disorder is found in 8-15% of individuals in alcohol treatment programs. Pregnant mothers with panic disorder during pregnancy are more likely to have preterm labor and infants of smaller birth-weight for gestational age.[27]

Race predilection in panic disorder

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 predilection in panic disorder

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). Panic is more common in women who have never been pregnant and during the postpartum period, but it is less common during pregnancy.

Age predilection in panic disorder

Although panic can occur in people at any age, it usually develops between the ages of 18 and 45 years. The average age of onset, as with most anxiety disorders, is in the third decade of life. Patients with late-onset panic disorder have a tendency toward less mental health use, lower comorbidity and hypochondriasis, and better coping behavior.[28]

Prognosis
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Long-term prognosis is usually good, with almost 65% of patients with panic disorder achieving remission, typically within 6 months.[29] The risk of coronary artery disease in patients with panic disorder is nearly doubled. In patients with coronary disease, panic can induce myocardial ischemia.[24] The risk of sudden death may also theoretically be increased due to reduced heart rate variability and increased QT interval variability.[25] Appropriate pharmacologic therapy and cognitive-behavioral therapy, individually or in combination, are effective in more than 85% of cases.

Patient Education
Educate patients on potential adverse effects of their treatment medications. Obtain informed consent for psychotropic medications and document the discussion of the risks and benefits of treatment medications. Inform patients that the causes of panic disorder are likely biological and psychosocial. Advise patients to avoid anxiogenic substances, such as caffeine, energy drinks, and other OTC stimulants. In addition, 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. Consider educating patients diagnosed with panic disorder on cognitive distortions that may help to amplify anxiety. Also educate patients about recognizing trigger stimuli so that they can contribute this to their psychological treatment approach. Educate the patients family, if available, on the important issues of minimizing any avoidance behaviors by the patient and ensuring pharmacologic compliance and adherence to therapy appointments. In addition, help the family to understand the nature of the anxiety symptoms and to provide reasonable accommodation (without enabling dysfunctional behaviors or alcohol/prescription drug use). Family members can be particularly important in helping the patient to overcome unrealistic fears and ingrained avoidance behaviors, in the context of ongoing cognitive behavior therapy in which the patient learns the coping skills to manage anxiety. Dietary modification (eg, 5-hydroxytryptophan or inositol[30] supplementation) may be effective in preventing recurrence. Such herbal supplementation should be deferred until after the patient has discussed it with the psychiatrist or primary care provider who is responsible for the follow-up and long-term care of the patient. For patient education information, see eMedicine's Anxiety Center, as well as Anxiety, Panic Attacks, and Hyperventilation.

Contributor Information and Disclosures

Author Mohammed A Memon, MD Chairman and Attending Geriatric Psychiatrist, Department of Psychiatry, Spartanburg Regional Medical Center 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. Coauthor(s) Colin Y Daniels, MD Consulting Staff, Department of Psychiatry, Madigan Army Medical Center

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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. Robert Harwood, MD, MPH, FACEP, FAAEM Senior Physcian, Department of Emergency Medicine, Advocate Christ Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine Robert Harwood, MD, MPH, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Phi Beta Kappa, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Samuel M Keim, MD Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Michael C Plewa, MD Research Coordinator, Consulting Staff, Department of Emergency Medicine, Lucas County Emergency Physicians, Inc, and Mercy Saint Vincent Medical Center Michael C Plewa, MD, is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Physicians for Social Responsibility, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Chief Editor Iqbal Ahmed, MBBS, FRCPsych (UK) Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine Iqbal Ahmed, MBBS, FRCPsych (UK) is a member of the following medical societies: Academy of
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Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, American Psychiatric Association, American Society of Clinical Psychopharmacology, and Royal College of Psychiatrists Disclosure: Nothing to disclose. Additional Contributors 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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