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Panic Disorder

  • Author: Mohammed A Memon, MD; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych(UK)  more...
 
Updated: Jan 05, 2015
 

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 are defined as a period of intense fear in which 4 of 13 defined symptoms develop abruptly and peak rapidly less than 10 minutes from symptom onset. (See History.) Although such attacks can occur in other anxiety disorders, these attacks often occur without a discernible predictable precipitant in panic disorder. (See Diagnostic Considerations and Workup.)

To meet the Diagnostic and Statistical Manual of Mental Disorders,Fifth Edition (DSM-5)[1] criteria for panic disorder, panic attacks must be associated with longer than 1 month of subsequent persistent worry about: (1) having another attack or consequences of the attack, or (2) significant maladaptive behavioral changes related to the attack. To make the diagnosis of panic disorder, panic attacks cannot directly or physiologically result from substance use (intoxication or withdrawal), medical conditions, or another psychiatric disorder. (See History.) Other symptoms or signs may include headache, cold hands, diarrhea, insomnia, fatigue, intrusive thoughts, and ruminations. (See Physical Examination.)

Following exclusion of somatic disease, substance use disorders, 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 Examination.)

Consequences of panic disorder

Panic disorder can lead to a significant hindrance in lifestyle. 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 or dependence and suicidality than the general population.[2] However, 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 use disorders, eating disorders, and personality disorders.[3]

For more information, see the Medscape Reference topics Anxiety Disorders; Specific Phobia; Separation Anxiety and School Refusal; and Phobic Disorders.

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Etiology

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 1–beta.[18]

Some authors 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 serotonin 1A (5HT1A) receptors. The 5HT system or one of its subsystems may play a role in the pathophysiology of panic disorder, but further investigation is needed.

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 coeruleus model explains that panic symptoms are due to increased local discharge resulting in adrenergic neuronal stimulation, similar to the more general catecholamine theory. Locus coeruleus activity also affects the hypothalamic-pituitary-adrenal (HPA) 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 cognitive theory suggests that patients with panic disorder have a heightened sensitivity to internal autonomic cues (eg, tachycardia).

Genetic factors

Panic disorder is a common psychiatric disorder that affects 3-5% of the population.[61] Studies of the association between psychiatric illness in first-degree relatives revealed a heredity of approximately 43% for panic disorder.[42] Patients with panic disorder also have a high rate (80%) of having other psychiatric disorders, many of which also have an important genetic basis.

Although panic disorder is a disease with a significant genetic basis, the exact nature of the basis is unclear. The present understanding suggests that panic disorder is a multifactorial condition, with multiple genes creating susceptibility to the condition coupled with influences from the environment.[54] The genetics of panic disorder is poorly understood relative to many psychiatric disorders in which genome-wide association studies (GWAS) have isolated numerous loci associated with susceptibility to disease.

Nonetheless, there are several loci that have been implicated in families with a strong history of panic disorder. Locus 13q22-32 has been linked to panic disorder and bladder conditions in families although the association was not found in families who had isolated panic disorder.[43] A locus at 9q31 was found to be associated with panic disorder (and likely generalized anxiety disorder) for an Icelandic cohort.[44]

In a study that performed a genome scan looking for regions of interest for anxiety disorders broadly defined in 219 US subjects in 19 extended pedigrees, investigators found an association at marker D4S413 on chromosome 4q31-q34, which is located near the NPY1R gene. This gene encodes the neuropeptide Y 1 receptor, and in an animal model, manipulation of this receptor was associated with anxiolysis.[45] A large GWAS that looked mainly at bipolar disorder but also psychosis, panic disorder, and suicidal behavior found an associated locus for panic disorder on 7q21.[47, 52]

Further study has implicated a few genes as likely contributors to panic disorder. Because monoamine oxidase inhibitors (MAOIs) have been used effectively in the treatment of panic disorder, the MAOA (monoamine oxidase A) gene is a logical consideration for contribution to panic disorder. In a study of a German and Italian population, patients with a longer repeat polymorphism in the MAOA promoter region had a higher incidence of panic disorder.[59] In recent years, the use of MAOIs has been in large part supplanted by newer agents.

Persons who are homozygous for a polymorphism in the COMT gene (catechol-o-methyltransferase), in which a methionine substitutes for a valine at position 158, have been associated with a higher rate of panic disorder than persons who did not carry these polymorphisms.[46] Additionally, it has been suggested that people who were homozygous for this polymorphism also had a poorer response to treatment.[46] A different study of the same polymorphism found an increased benefit of exposure-based therapy for those who had the Val158Met polymorphism.[53]

More recently, studies have isolated additional genes of interest for panic disorder. A polymorphism on the HCRT (hypocretin) gene, in which isoleucine substitutes for valine at position 308 on 17q21.2, has been implicated in increased risk of panic disorder.[48] Additional GWAS have identified the neuropeptide S gene, the amiloride-sensitive cation channel gene, and the adenosine A(2A) genes as candidate genes.[49, 50, 51]

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Epidemiology

Lifetime prevalence estimates for panic disorder in US adults range from 2.0% to 6.0%.[61] The 12-month prevalence in adults is 2.7%, of which 44.8% are classified as “severe” cases.[61]

Panic disorder often coexists with mood disorders, and mood symptoms potentially follow the onset of panic attacks. Lifetime prevalence rates of major depression in panic disorder may be as high as 50-60%.[63] Other psychiatric disorders that occur comorbidly with panic disorder include schizophrenia, obsessive-compulsive disorder, specific phobias, social phobia, and agoraphobia.[60]

There are also medical conditions that apparently share significant comorbidity with panic disorder, such as COPD, irritable bowel syndrome, migraine headache, restless leg syndrome, and fatigue.[20, 21] Cardiovascular disorders (eg, mitral valve prolapse, hypertension, cardiomyopathy, stroke) are also comorbid factors[22] ; panic patients are nearly twice as likely to develop coronary artery disease. Patients with both panic disorder and coronary disease can experience myocardial ischemia during their panic episodes[23, 24] ; thus, panic disorder is also associated with a higher risk of sudden death.[25] In addition, panic disorder is also present in 30% of patients with chest pain and normal findings on angiography, and individuals with panic disorder tend to have lower oxygen consumption and exercise tolerance than does the general population.[26]

Asthma is linked to a 4.5-fold increase in the risk of developing panic disorder, and people with panic disorder are 6 times as likely as those without anxiety disorders to develop asthma.[64] Patients with panic disorder can also have migraine headaches (12.7%), tension headaches (5.5%), and combined migraine and tension headaches (14.2%).[65] The lifetime prevalence of panic disorder in people with epilepsy is 6.6%.[66]

Approximately 10-20% of patients with anxiety disorder abuse alcohol and other drugs, and about 10-40% of alcoholics have a panic-related anxiety disorder.[67]

Pregnant mothers with panic disorder during pregnancy are more likely to have preterm labor and infants of smaller birth-weight for gestational age.[27]

Racial, sexual, and age-related differences

Prevalence data for different racial groups are inconsistent. Symptom manifestations may differ, with black persons more often presenting with somatic symptoms and more likely to seek help in medical rather than psychiatric settings.

Women are 2-3 times more likely to be affected than men. Panic is also more common in women who have never been pregnant and during the postpartum period; it is less common during pregnancy.

Although panic can occur in people at any age, it usually develops between the ages of 18 and 45 years, with an average age of onset of 24 years.[61] Patients with late-onset panic disorder have a tendency toward less use of mental health resources, have lower comorbidity and hypochondriasis, and have better coping behavior.[28]

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Prognosis

Panic disorder is a chronic disorder with a variable course. Appropriate pharmacologic therapy and cognitive-behavioral therapy (CBT), individually or in combination, are effective in more than 85% of cases. Patients with good premorbid functioning and a brief duration of symptoms tend to have a good prognosis.[68] About 10-20% of patients continue to have significant symptoms.[68]

Overall, the long-term prognosis is usually good, with almost 65% of patients with panic disorder achieving remission, typically within 6 months.[29] However, as discussed under History, trigger factors can lead to panic attacks— several of these triggers are associated with poor outcome, including severe illness at the time of the initial assessment, high interpersonal sensitivity, low social class, separation from a parent by death during early life, divorce, and unmarried status.[62]

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]

The suicide rate in individuals with panic disorder is also many times higher than the general population.[2]

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Patient Education

Inform patients that the causes of panic disorder are likely biologic and psychosocial, and that panic symptoms are not life-threatening or uncommon.[55]

Educate patients about their diagnosis and treatment options, as well as about potential adverse effects of not only their treatment medications but also any comorbid substance use such as alcohol consumption and recreational drug use. These psychoactive substances can impact the course of panic disorder. Although 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 about cognitive distortions that may help to amplify anxiety. Teach patients to recognize trigger stimuli so that they can contribute this to their psychological treatment approach.

Obtain verbal informed consent for psychotropic medications, and document the discussion of the risks and benefits of treatment medications. Promote healthy behaviors, including exercise and good sleep hygiene. Advise patients to avoid anxiogenic substances, such as caffeine, energy drinks, and other OTC stimulants.[55]

Talk to the patient’s family about the importance of minimizing any avoidance behaviors by the patient and ensuring pharmacologic compliance and adherence to therapy appointments. 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-behavioral therapy (CBT) in which the patient learns the coping skills to manage anxiety.

Although dietary modification (eg, 5-hydroxytryptophan or inositol[30] supplementation) may be effective in preventing recurrence, there is much more evidence for the effectiveness of CBT and medications. Herbal supplementation should be deferred until after the patient has discussed it with his or her psychiatrist or primary care provider.

For more information, see Anxiety Center, as well as Anxiety, Panic Attacks, and Hyperventilation.

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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, American Psychiatric Association

Disclosure: Nothing to disclose.

Chief Editor

Iqbal Ahmed, MBBS, FRCPsych(UK) Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Uniformed Services University of the Health Sciences; 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 Psychosomatic Medicine, American Neuropsychiatric Association, American Society of Clinical Psychopharmacology, Royal College of Psychiatrists, American Association for Geriatric Psychiatry, American Psychiatric Association

Disclosure: Nothing to disclose.

Acknowledgements

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.

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

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.

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

Sandra Yerkes, MD Senior Medical Corps Detailer for US Navy, Bureau of Naval Personnel

Disclosure: Nothing to disclose.

References
  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. Fifth Edition. Arlington, VA: American Psychiatric Association; 2013.

  2. Fleet RP, Dupuis G, Marchand A, Burelle D, Arsenault A, Beitman BD. Panic disorder in emergency department chest pain patients: prevalence, comorbidity, suicidal ideation, and physician recognition. Am J Med. Oct 1996. 101(4):371-80. [Medline].

  3. Warshaw MG, Dolan RT, Keller MB. Suicidal behavior in patients with current or past panic disorder: five years of prospective data from the Harvard/Brown Anxiety Research Program. Am J Psychiatry. Nov 2000. 157(11):1876-8. [Medline].

  4. Fleet RP, Martel JP, Lavoie KL, Dupuis G, Beitman BD. Non-fearful panic disorder: a variant of panic in medical patients?. Psychosomatics. Jul-Aug 2000. 41(4):311-20. [Medline].

  5. Dannon PN, Lowengrub K, Amiaz R, Grunhaus L, Kotler M. Comorbid cannabis use and panic disorder: short term and long term follow-up study. Hum Psychopharmacol. Mar 2004. 19(2):97-101. [Medline].

  6. Schifano F, Di Furia L, Forza G, Minicuci N, Bricolo R. MDMA ('ecstasy') consumption in the context of polydrug abuse: a report on 150 patients. Drug Alcohol Depend. Sep 1 1998. 52(1):85-90. [Medline].

  7. González-Berríos N. Sertraline-induced panic attack. Bol Asoc Med P R. Jan-Mar 2009. 101(1):59-60. [Medline].

  8. Dratcu L. Panic, hyperventilation and perpetuation of anxiety. Prog Neuropsychopharmacol Biol Psychiatry. Oct 2000. 24(7):1069-89. [Medline].

  9. Molosh AI, Johnson PL, Fitz SD, Dimicco JA, Herman JP, Shekhar A. Changes in central sodium and not osmolarity or lactate induce panic-like responses in a model of panic disorder. Neuropsychopharmacology. May 2010. 35(6):1333-47. [Medline]. [Full Text].

  10. Esquivel G, Fernández-Torre O, Schruers KR, Wijnhoven LL, Griez EJ. The effects of opioid receptor blockade on experimental panic provocation with CO2. J Psychopharmacol. Nov 2009. 23(8):975-8. [Medline].

  11. Knuts IJ, Cosci F, Esquivel G, Goossens L, van Duinen M, Bareman M, et al. Cigarette smoking and 35% CO(2) induced panic in panic disorder patients. J Affect Disord. Jul 2010. 124(1-2):215-8. [Medline].

  12. Maron E, Hettema JM, Shlik J. Advances in molecular genetics of panic disorder. Mol Psychiatry. Jul 2010. 15(7):681-701. [Medline].

  13. Zwanzger P, Eser D, Nothdurfter C, Baghai TC, Möller HJ, Padberg F, et al. Effects of the GABA-reuptake inhibitor tiagabine on panic and anxiety in patients with panic disorder. Pharmacopsychiatry. Nov 2009. 42(6):266-9. [Medline].

  14. Wedekind D, Bandelow B, Broocks A, Hajak G, Rüther E. Salivary, total plasma and plasma free cortisol in panic disorder. J Neural Transm. 2000. 107(7):831-7. [Medline].

  15. Neumeister A, Bain E, Nugent AC, Carson RE, Bonne O, Luckenbaugh DA, et al. Reduced serotonin type 1A receptor binding in panic disorder. J Neurosci. Jan 21 2004. 24(3):589-91. [Medline].

  16. Lonsdorf TB, Rück C, Bergström J, Andersson G, Ohman A, Schalling M, et al. The symptomatic profile of panic disorder is shaped by the 5-HTTLPR polymorphism. Prog Neuropsychopharmacol Biol Psychiatry. Nov 13 2009. 33(8):1479-83. [Medline].

  17. Strug LJ, Suresh R, Fyer AJ, Talati A, Adams PB, Li W, et al. Panic disorder is associated with the serotonin transporter gene (SLC6A4) but not the promoter region (5-HTTLPR). Mol Psychiatry. Feb 2010. 15(2):166-76. [Medline]. [Full Text].

  18. Johnson MR, Lydiard RB, Ballenger JC. Panic disorder. Pathophysiology and drug treatment. Drugs. Mar 1995. 49(3):328-44. [Medline].

  19. Vythilingam M, Anderson ER, Goddard A, Woods SW, Staib LH, Charney DS, et al. Temporal lobe volume in panic disorder--a quantitative magnetic resonance imaging study. Psychiatry Res. Aug 28 2000. 99(2):75-82. [Medline].

  20. Lee HB, Hening WA, Allen RP, et al. Restless legs syndrome is associated with DSM-IV major depressive disorder and panic disorder in the community. J Neuropsychiatry Clin Neurosci. Winter 2008. 20(1):101-5. [Medline].

  21. Kaiya H, Sugaya N, Iwasa R, Tochigi M. Characteristics of fatigue in panic disorder patients. Psychiatry Clin Neurosci. Apr 2008. 62(2):234-7. [Medline].

  22. Chen YH, Hu CJ, Lee HC, Lin HC. An increased risk of stroke among panic disorder patients: a 3-year follow-up study. Can J Psychiatry. Jan 2010. 55(1):43-9. [Medline].

  23. Gomez-Caminero A, Blumentals WA, Russo LJ, Brown RR, Castilla-Puentes R. Does panic disorder increase the risk of coronary heart disease? A cohort study of a national managed care database. Psychosom Med. Sep-Oct 2005. 67(5):688-91. [Medline].

  24. Fleet R, Lespérance F, Arsenault A, et al. Myocardial perfusion study of panic attacks in patients with coronary artery disease. Am J Cardiol. Oct 15 2005. 96(8):1064-8. [Medline].

  25. Sullivan GM, Kent JM, Kleber M, Martinez JM, Yeragani VK, Gorman JM. Effects of hyperventilation on heart rate and QT variability in panic disorder pre- and post-treatment. Psychiatry Res. Jan 30 2004. 125(1):29-39. [Medline].

  26. Schmidt NB, Lerew DR, Santiago H, Trakowski JH, Staab JP. Effects of heart-rate feedback on estimated cardiovascular fitness in patients with panic disorder. Depress Anxiety. 2000. 12(2):59-66. [Medline].

  27. Chen YH, Lin HC, Lee HC. Pregnancy outcomes among women with panic disorder - do panic attacks during pregnancy matter?. J Affect Disord. Jan 2010. 120(1-3):258-62. [Medline].

  28. Katerndahl DA, Talamantes M. A comparison of persons with early-versus late-onset panic attacks. J Clin Psychiatry. Jun 2000. 61(6):422-7. [Medline].

  29. Batelaan NM, de Graaf R, Penninx BW, van Balkom AJ, Vollebergh WA, Beekman AT. The 2-year prognosis of panic episodes in the general population. Psychol Med. Jan 2010. 40(1):147-57. [Medline].

  30. Ashton H. The diagnosis and management of benzodiazepine dependence. Curr Opin Psychiatry. May 2005. 18(3):249-55. [Medline].

  31. Johnson PL, Truitt W, Fitz SD, et al. A key role for orexin in panic anxiety. Nat Med. Jan 2010. 16(1):111-5. [Medline]. [Full Text].

  32. Chen YH, Chen SF, Lin HC, Lee HC. Healthcare utilization patterns before and after contact with psychiatrist care for panic disorder. J Affect Disord. Dec 2009. 119(1-3):172-6. [Medline].

  33. Cloos JM. The treatment of panic disorder. Curr Opin Psychiatry. Jan 2005. 18(1):45-50. [Medline].

  34. Rosenberg NK, Mellergård M, Rosenberg R, Beck P, Ottosson JO. Characteristics of panic disorder patients responding to placebo. Acta Psychiatr Scand Suppl. 1991. 365:33-8. [Medline].

  35. 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].

  36. {Best Evidence} Furukawa TA, Watanabe N, Churchill R. Psychotherapy plus antidepressant for panic disorder with or without agoraphobia: systematic review. Br J Psychiatry. Apr 2006. 188:305-12. [Medline].

  37. Sánchez-Meca J, Rosa-Alcázar AI, Marín-Martínez F, Gómez-Conesa A. Psychological treatment of panic disorder with or without agoraphobia: a meta-analysis. Clin Psychol Rev. Feb 2010. 30(1):37-50. [Medline].

  38. Palatnik A, Frolov K, Fux M, Benjamin J. Double-blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder. J Clin Psychopharmacol. Jun 2001. 21(3):335-9. [Medline].

  39. Strohle A, Graetz B, Scheel M, et al. The acute antipanic and anxiolytic activity of aerobic exercise in patients with panic disorder and healthy control subjects. J Psychiatr Res. Aug 2009. 43(12):1013-7. [Medline].

  40. Bowen R, Baetz M, D'Arcy C. Self-rated importance of religion predicts one-year outcome of patients with panic disorder. Depress Anxiety. 2006. 23(5):266-73. [Medline].

  41. Advocat J, Lindsay J. Internet-based trials and the creation of health consumers. Soc Sci Med. Feb 2010. 70(3):485-92. [Medline].

  42. Hettema JM, Neale MC, Kendler KS. A review and meta-analysis of the genetic epidemiology of anxiety disorders. Am J Psychiatry. 2001 Oct. 158(10):1568-78. [Medline].

  43. Weissman MM, Fyer AJ, Haghighi F, et al. Potential panic disorder syndrome: clinical and genetic linkage analysis. Am J Med Genet. 2000. 96:24-35. [Medline].

  44. Thorgeirsson TE, Oskarsson H, Desnica N, et al. Anxiety with panic disorder linked to chromosome 9q in Iceland. Am J Hum Genet. 2003. 72:1221-30. [Medline].

  45. Kaab B, Gelernter J, Woods SW, Goddard A, Page GP, Elston RC. Genome scan for loci predisposing to anxiety disorders using a novel multivariate approach: strong evidence for a chromosome 4 risk locus. Am J Hum Genet. 2006. 78:543-53. [Medline].

  46. Woo J-M, Yoon K-S, Yu B-H. Catechol O-methyltransferase genetic polymorphism in panic disorder. Am J Psychiat. 2002. 159:1785-7. [Medline].

  47. Cheng R, Juo SH, Loth JE, et al. Genome-wide linkage scan in a large bipolar disorder sample from the National Institute of Mental Health genetics initiative suggests putative loci for bipolar disorder, psychosis, suicide, and panic disorder. Molec Psychiat. 2006. 11:252-60. [Medline].

  48. Annerbrink K, Westberg L, Olsson M, et al. Panic disorder is associated with the Val308Iso polymorphism in the hypocretin receptor gene. Psychiatr Genet. 2011 Apr. 21(2):85-9. [Medline].

  49. Domschke K, Reif A, Weber H, et al. Neuropeptide S receptor gene -- converging evidence for a role in panic disorder. Mol Psychiatry. 2011 Sep. 16(9):938-48. [Medline].

  50. Gregersen N, Dahl HA, Buttenschon HN, et al. A genome-wide study of panic disorder suggests the amiloride-sensitive cation channel 1 as a candidate gene. Eur J Hum Genet. 2012 Jan. 20(1):84-90. [Medline].

  51. Hohoff C, Mullings EL, Heatherley SV, et al. Adenosine A(2A) receptor gene: evidence for association of risk variants with panic disorder and anxious personality. J Psychiatr Res. 2010 Oct. 44(14):930-7. [Medline].

  52. Logue MW, Bauver SR, Knowles JA, et al. Multivariate analysis of anxiety disorders yields further evidence of linkage to chromosomes 4q21 and 7p in panic disorder families. Am J Med Genet B Neuropsychiatr Genet. 2012 Apr. 159B(3):274-80. [Medline].

  53. Lonsdorf TB, Ruck C, Bergstrom J, et al. The COMTval158met polymorphism is associated with symptom relief during exposure-based cognitive-behavioral treatment in panic disorder. BMC Psychiatry. 2010 Nov 26. 10:99. [Medline].

  54. Schumacher J, Kristensen AS, Wendland JR, Nothen MM, Mors O, McMahon FJ. The genetics of panic disorder. J Med Genet. 2011 Jun. 48(6):361-8. [Medline].

  55. American Psychiatric Association. Practice guideline for the treatment of patients with panic disorder. 2nd ed. Washington, DC: American Psychiatric Association; 2009.

  56. National Collaborating Centre for Mental Health, National Collaborating Centre for Primary Care. Generalised anxiety disorder and panic disorder (with or without agoraphobia) in adults. Management in primary, secondary and community care. London, UK: National Institute for Health and Clinical Excellence; 2011.

  57. US Food and Drug Administration. Celexa (citalopram hydrobromide) - Drug safety communication: revised recommendations, potential risk of abnormal heart rhythms [press release]. March 28, 2012. [Full Text].

  58. Roberson-Nay R, Kendler KS. Panic disorder and its subtypes: a comprehensive analysis of panic symptom heterogeneity using epidemiological and treatment seeking samples. Psychol Med. 2011 Nov. 41(11):2411-21. [Medline].

  59. Deckert J, Catalano M, Syagailo YV, et al. Excess of high activity monoamine oxidase A gene promoter alleles in female patients with panic disorder. Hum Mol Genet. 1999 Apr. 8(4):621-4. [Medline].

  60. Buckley PF, Miller BJ, Lehrer DS, Castle DJ. Psychiatric comorbidities and schizophrenia. Schizophr Bull. 2009 Mar. 35(2):383-402. [Medline].

  61. National Institute of Mental Health. Panic disorder among adults. [Full Text].

  62. Noyes R Jr, Clancy J, Woodman C, et al. Environmental factors related to the outcome of panic disorder. A seven-year follow-up study. J Nerv Ment Dis. 1993 Sep. 181(9):529-38. [Medline].

  63. Noyes R Jr, Hoehn-Saric R. Panic disorder and agoraphobia. In: Noyes R Jr, Hoehn-Saric R, eds. The Anxiety Disorders. Cambridge, England: Cambridge University Press. 1998. 86-157.

  64. Hasler G, Gergen PJ, Kleinbaum DG, et al. Asthma and panic in young adults: a 20-year prospective community study. Am J Respir Crit Care Med. 2005. 171:1224-30. [Medline].

  65. Beghi E, Allais G, Cortelli P, et al. Headache and anxiety-depressive disorder comorbidity: the HADAS study. Neurol Sci. 2007 May. 28 suppl 2:28 suppl 2. [Medline].

  66. Tellez-Zenteno JF, Patten SB, Jette N, Williams J, Wiebe S. Psychiatric comorbidity in epilepsy: a population-based analysis. Epilepsia. 2007 Dec. 48(12):2336-44. [Medline].

  67. Cox BJ, Norton GR, Swinson RP, Endler NS. Substance abuse and panic-related anxiety: a critical review. Behav Res Ther. 1990. 28(5):385-93. [Medline].

  68. Kaplan HI, Sadock BJ. Panic disorder and agoraphobia. In: Millet KC, ed. Kaplan and Sadock's Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. 8th ed. Baltimore, Md: Williams & Wilkins; 1998. 594-603.

  69. Johnson J, Weissman MM, Klerman GL. Panic disorder, comorbidity, and suicide attempts. Arch Gen Psychiatry. 1990 Sep. 47(9):805-8. [Medline].

  70. Fleet RP, Marchand A, Dupuis G, Kaczorowski J, Beitman BD. Comparing emergency department and psychiatric setting patients with panic disorder. Psychosomatics. 1998 Nov-Dec. 39(6):512-8. [Medline].

 
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