Panic disorder

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Panic disorder
ICD-10 F41.0
ICD-9 300.01, 300.21
DiseasesDB 30913
MedlinePlus 000924

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vatsala Sharma; M.B.B.S[2] Kiran Singh, M.D. [3] Yashasvi Aryaputra[4]

Overview

Panic disorder is a condition characterized by recurring panic attacks with significant behavioral change or at least a month of ongoing worry about having another attack. Panic disorder patients have a series of episodic severe anxiety, known as panic attacks. These attacks typically last 10 minutes, however, they can be of shorter duration. They may vary in intensity and symptoms over a period of time. Symptoms of panic disorder commonly present in the form of rapid heart beat, perspiration, dizziness, dyspnea, tremors, uncontrollable fear or feeling of impending doom. The panic attacks often result in embarrassment and social stigma, ultimately resulting in social isolation. Therefore, most of the individuals with panic disorder also develop agoraphobia. If not treated, somatic symptoms like insomnia and/or anorexia develop, which may eventually result in clinical depression and suicide. So, early, efficient, and affordable treatment options should be encouraged.

Historical Perspective

  • Panic disorder has a long history, dating back to folklores.
  • Greek Mythology includes one of the examples. The term 'Panic' originated from the Greek god, Pan who was responsible for anxiety.[1]
  • In Greek myths, 'Pan' was a man with horns and legs of a goat. His mere appearance was so frightening that it developed irrational fear in people, without any apparent reason. This came to be known as panic attacks or terrors. [1]
  • Fear of meeting Pan once more stopped the travelers from going to the market. In Greek, agora stands for market and this led to the development of a new term 'agoraphobia'. It stands for the fear of public places or large open spaces.[1]
  • In 1621, Burton described different varieties of pathological anxiety. He related the anxiety to delirium, depersonalization, hypochondria, hyperventilation, and phobias.[1]
  • In 1812, Benjamin Rush (father of American psychiatry), described the relation between somatic causes and phobias in his book. He established an association between depression and hypochondriasis. [1]
  • In 1879, Henry Maudsley used the term panic for the first time in psychiatry, and also explained melancholic panic.[2]
  • Sigmund Freud, in the year 1925, described anxiety neurosis. He separated it from neurasthenia and further elaborated anxiety neurosis with a particular clinical presentation.[1]
  • In 1964, Klein proposed three types of panic attacks: situational (related to agoraphobia), spontaneous, and in response to a stimulus (like height, animals, etc.). [1]

Classification

  • Panic disorder was first described in DSM-III, based on Klein's description of panic attacks in 1980.[1] [3]
  • After consistent work on DSM for the next seven years, DSM-III-R described agoraphobia as a consequence of panic disorder in 1987. So, agoraphobia was divided into 'panic disorder with and without agoraphobia'.[1]
  • In 1992, DSM-IV described panic attacks related to other conditions. The criteria for panic disorder was not required to be fulfilled here.[1]
  • The criteria for panic disorder remained the same in the revised version of DSM-IV (DSM-IV-TR), published in 2000.[1]
  • DSM-5 has unlinked panic disorder and agoraphobia. [4]
  • The tenth edition of International Classification of Diseases (ICD-10) describes agoraphobia as a distinct condition that may not occur with panic attacks.[1]

Pathophysiology

  • Multiple factors are associated with the pathophysiology of panic disorder.
  • Imbalance of neurobiological, neuroanatomic, and neurochemical factors lead to the production of this condition.
  • Pathogenesis of Panic Disorder is related to the amygdala, the center for fear processing. MRI studies have further substantiated this finding by showing lesser left and right-sided amygdalar volumes in panic disorder patients as compared to controls. [5][6]
  • There is dysregulation of the prefrontal cortex as well as the subcortical components.[7]
  • The patients with panic disorder have more noradrenergic neuronal activity than controls. [8]
  • Another neurochemical theory proposes that these patients have deficient serotonergic inhibition of neurons in the dorsal periaqueductal gray matter of the midbrain and the rostral ventrolateral medulla. [9]
  • The endogenous opioids buffer the panic attacks in normal subjects and their deficit results in the development of the panic disorder. [9]
  • Panic disorder patients have also been found to have lower occipital cortex GABA levels. Other studies suggest dysfunction of GABA(A) receptors in the pathophysiology of panic disorder. This is further supported by improvement in symptoms by treatment focused on GABA binding site of the GABA(A) and benzodiazepine receptor complex. [10][11]

Differential Diagnosis

There are some medical and psychiatric conditions with symptomatology mimicking panic disorder- [12][13]

  • Other mental disorders with panic attacks

Epidemiology and Demographics

Prevalence

  • The prevalence of the panic disorder is 2,000-3,000 / 100,000 (2%-3%) of the overall population.
  • 2.7-7.1% of the general population suffers from a lifetime prevalence of panic disorder, means having repeated panic attacks. [3] [13]

Gender

  • Women are twice as likely as men to develop the panic disorder. [14]
  • Similar age at onset of Panic Disorder is observed for men and women. Preceding premorbidity was found to be different for men and women.[15]
  • Men had higher rates of body dysmorphic disorder, cyclothymia, and depersonalization preceding panic disorder. Whereas, women had higher rates of bulimia nervosa. Life stressors played a significant role in precipitating Panic Disorder in women.[15]

Age

  • Anticipation is characterized by the decrease in age at onset and/or the increase in severity of a disorder in successive generations. It helps in exploring the genetic basis of some familial illness.
  • Anticipation is observed in panic disorder and the is responsible for the familial aggregation of this condition. [16]
  • There is an increased risk of panic disorder in relatives of individuals with panic disorder onset at or before the age of 20 years. The age of onset is useful in determining the familial subtypes of panic disorder.[17]

Race

  • Various studies presented with mixed results.
  • A study comparing the White, African American, Asian, and Latino groups found that the White group had higher rates of panic disorder, as compared to the African American, Latino, and Asian groups.[18]

Risk Factors

Several factors can increase the chances of development of Panic Disorder-[19][13]

  • Interpersonal stressors
  • Stressors related to physical well-being

Natural History, Complications, and Prognosis

  • Anxiousness in people with panic disorder begins in childhood due to traumatic life events or distressing family conditions.[20]
  • Family history and genetics play a very important role in the development of panic disorder.
  • Poor prognostic factors are:[21][22][23][24][25]
  • Female gender
  • Comorbid agoraphobia
  • Comorbid depression
  • Comorbid personality disorder
  • Higher oxidative stress index and higher ceruloplasmin level
  • Catastrophic agoraphobic cognitions
  • Panic disorder patients with non-suppression of Dexamethasone Suppression Test (DST)

Diagnostic Criteria

DSM-5 Diagnostic Criteria for Panic Disorder[13]

  • A. Recurrent unexpected panic attacks. A panic attack is an abrupt surge of intense fear or discomfort that reaches a peak within minutes, and during which time four (or more) of these symptoms occur;

Note:The abrupt surge can occur from a calm state or an anxious state.

  • 1. Palpitations
  • 2. Sweating
  • 3. Trembling
  • 4. Shortness of breath
  • 5. Feelings of choking
  • 6. Chest pain or discomfort
  • 7. Nausea or abdominal distress
  • 8. Feeling dizzy, or unsteady
  • 9. Chills or sensation of heat
  • 10. Paresthesias (numbness or tingling sensations)
  • 11. Derealization (feelings of unreality) or depersonalization (being detached from oneself)
  • 12. Fear of losing control
  • 13. Fear of dying

Note: Culture-specific symptoms (e.g., tinnitus, neck soreness, headache, uncontrollable screaming or crying) may occur. Such symptoms should not be included as one of the four required symptoms.

AND

  • B. At least one of the attacks has been followed by a minimum 1 month (or more) duration of one or both:
  • 1. Persistent worries about having another panic attack or the consequences (like losing control).
  • 2. A major maladaptive behavioral change in relation to the attacks (behaviors to avoid having panic attacks)

AND

  • C. The disturbance is not due to the effects of a substance or another medical condition

AND

  • D. The disturbance is not better explained by another mental disorder or due to separation from attachment figures

Treatment

  • Panic Disorder is a potentially disabling condition, but it can be successfully treated.
  • Due to the disturbing symptoms that accompany the panic disorder, it may be mistaken for a life-threatening physical illness.
  • Thorough investigation to rule out the suspected medical condition and early initiation of treatment should be the ultimate goal for managing the panic disorder.
  • Panic disorder can be treated by medications, psychotherapy, or both.
  • A skilled treating team of psychiatrists, psychologists, and social workers is required for this purpose.

Medications

  • SSRIs like paroxetine, escitalopram, citalopram, etc. are used for maintenance therapy. [26][27]
  • MAOIs are usually avoided because of the associated life-threatening side effects like serotonin syndrome, hypertensive crisis, and other drug interactions.
  • TCAs like Imipramine is associated with anticholinergic side effects, so avoided in the elderly.
  • Both SSRIs are TCAs are effective in treatment but SSRIs are better tolerated and so they are preferred.[28]
  • These are used for a short duration to control the acute phase of illness or given until the SSRIs have achieved the therapeutic action.
  • Long-term use is not advised because of the chances of developing dependence and drug-seeking behavior.

Psychotherapy

  • There are multiple treatment options available like- Exposure to somatic cues, cognitive behavior therapy (CBT), and relaxation therapy for panic disorder. When combined, these management options provide the best results.
  • Exposure to somatic cues and CBT, when combined resulted in about an 85% response rate. [29]
  • Relaxation technique resulted in greater reductions in the anxiety associated with panic attacks but was found to be related to higher drop-out rates. [29]
  • CBT can also be administered in the form of group therapy. It is found to be equally effective as compared to pharmacotherapy in some studies.[30]
  • CBT comprises of: [30]
  • Education and corrective information
  • Cognitive therapy
  • Training in diaphragmatic breathing
  • Interoceptive exposure

Other treatment modalities

  • Regular aerobic exercise alone has been associated with clinical improvement in patients with panic disorder but it is lesser effective than pharmacotherapy. [31]
  • Internet-based self-help programs plus minimal therapist contact can be equally efficacious as traditional individual CBT. [32]
  • Both for short and long-term treatment of panic disorder with or without agoraphobia, Virtual Reality Exposure (VRE) has been found to be effective.[33]

References

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  2. Nardi, Antonio Egidio; Freire, Rafael Christophe R. (2016). "The Panic Disorder Concept: A Historical Perspective": 1–8. doi:10.1007/978-3-319-12538-1_1.
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  6. Massana, Guillem; Serra-Grabulosa, Josep Maria; Salgado-Pineda, Pilar; Gastó, Cristòbal; Junqué, Carme; Massana, Joan; Mercader, José Maria; Gómez, Beatriz; Tobeña, Adolf; Salamero, Manel (2003). "Amygdalar atrophy in panic disorder patients detected by volumetric magnetic resonance imaging". NeuroImage. 19 (1): 80–90. doi:10.1016/S1053-8119(03)00036-3. ISSN 1053-8119.
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  10. Goddard, Andrew W.; Mason, Graeme F.; Almai, Ahmad; Rothman, Douglas L.; Behar, Kevin L.; Petroff, Ognen A. C.; Charney, Dennis S.; Krystal, John H. (2001). "Reductions in Occipital Cortex GABA Levels in Panic Disorder Detected With 1H-Magnetic Resonance Spectroscopy". Archives of General Psychiatry. 58 (6): 556. doi:10.1001/archpsyc.58.6.556. ISSN 0003-990X.
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  12. Edlund, Matthew J.; McNamara, M.Eileen; Millman, Richard P. (1991). "Sleep apnea and panic attacks". Comprehensive Psychiatry. 32 (2): 130–132. doi:10.1016/0010-440X(91)90004-V. ISSN 0010-440X.
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  16. Battaglia, Marco; Bertella, Silvana; Bajo, Sonia; Binaghi, Flora; Bellodi, Laura (1998). "Anticipation of Age at Onset in Panic Disorder". American Journal of Psychiatry. 155 (5): 590–595. doi:10.1176/ajp.155.5.590. ISSN 0002-953X.
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  18. Asnaani, Anu; Gutner, Cassidy A.; Hinton, Devon E.; Hofmann, Stefan G. (2009). "Panic Disorder, Panic Attacks and Panic Attack Symptoms across Race-Ethnic Groups: Results of the Collaborative Psychiatric Epidemiology Studies". CNS Neuroscience & Therapeutics. 15 (3): 249–254. doi:10.1111/j.1755-5949.2009.00092.x. ISSN 1755-5930.
  19. Roy-Byrne, Peter P; Craske, Michelle G; Stein, Murray B (2006). "Panic disorder". The Lancet. 368 (9540): 1023–1032. doi:10.1016/S0140-6736(06)69418-X. ISSN 0140-6736.
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  21. . doi:10.1007/BF00452785. Missing or empty |title= (help)
  22. Liebowitz MR (1997). "Panic disorder as a chronic illness". J Clin Psychiatry. 58 Suppl 13: 5–8. PMID 9402913.
  23. Ersoy, Mehmet Akif; Selek, Salih; Celik, Hakim; Erel, Ozcan; Kaya, Mehmet Cemal; Savas, Haluk A.; Herken, Hasan (2009). "Role of Oxidative and Antioxidative Parameters in Etiopathogenesis and Prognosis of Panic Disorder". International Journal of Neuroscience. 118 (7): 1025–1037. doi:10.1080/00207450701769026. ISSN 0020-7454.
  24. Keijsers, Ger P.J.; Hoogduin, Cees A.L.; Schaap, Cas P.D.R. (1994). "Prognostic factors in the behavioral treatment of panic disorder with and without agoraphobia". Behavior Therapy. 25 (4): 689–708. doi:10.1016/S0005-7894(05)80204-7. ISSN 0005-7894.
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  27. Ballenger, James C.; Wheadon, David E.; Steiner, Martin; Bushnell, William; Gergel, Ivan P. (1998). "Double-Blind, Fixed-Dose, Placebo-Controlled Study of Paroxetine in the Treatment of Panic Disorder". American Journal of Psychiatry. 155 (1): 36–42. doi:10.1176/ajp.155.1.36. ISSN 0002-953X.
  28. Bakker, A.; Van Balkom, A. J. L. M.; Spinhoven, P. (2002). "SSRIs vs. TCAs in the treatment of panic disorder: a meta-analysis". Acta Psychiatrica Scandinavica. 106 (3): 163–167. doi:10.1034/j.1600-0447.2002.02255.x. ISSN 0001-690X.
  29. 29.0 29.1 Barlow, David H.; Craske, Michelle G.; Cerny, Jerome A.; Klosko, Janet S. (1989). "Behavioral treatment of panic disorder". Behavior Therapy. 20 (2): 261–282. doi:10.1016/S0005-7894(89)80073-5. ISSN 0005-7894.
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  31. Broocks, Andreas; Bandelow, Borwin; Pekrun, Gunda; George, Annette; Meyer, Tim; Bartmann, Uwe; Hillmer-Vogel, Ursula; Rüther, Eckart (1998). "Comparison of Aerobic Exercise, Clomipramine, and Placebo in the Treatment of Panic Disorder". American Journal of Psychiatry. 155 (5): 603–609. doi:10.1176/ajp.155.5.603. ISSN 0002-953X.
  32. Carlbring, Per; Nilsson-Ihrfelt, Elisabeth; Waara, Johan; Kollenstam, Cecilia; Buhrman, Monica; Kaldo, Viktor; Söderberg, Marie; Ekselius, Lisa; Andersson, Gerhard (2005). "Treatment of panic disorder: live therapy vs. self-help via the Internet". Behaviour Research and Therapy. 43 (10): 1321–1333. doi:10.1016/j.brat.2004.10.002. ISSN 0005-7967.
  33. Botella, C.; García-Palacios, A.; Villa, H.; Baños, R. M.; Quero, S.; Alcañiz, M.; Riva, G. (2007). "Virtual reality exposure in the treatment of panic disorder and agoraphobia: A controlled study". Clinical Psychology & Psychotherapy. 14 (3): 164–175. doi:10.1002/cpp.524. ISSN 1063-3995.

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