eMedicine Specialties > Psychiatry > Adult

Panic Disorder

Author: Colin Y Daniels, MD, Consulting Staff, Department of Psychiatry, Madigan Army MedicalCenter
Contributor Information and Disclosures

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.

• Search for CME/CE on This Topic »

• Anxiety Disorder, Panic Disorder (Pediatrics: Developmental and Behavioral)
• Panic Disorders (Emergency Medicine)
• Toxicity, Selective Serotonin Reuptake Inhibitor (Emergency Medicine)
• Menopause and Mood Disorders (Psychiatry)

• Anxiety Symptoms
• Anxiety Center
• Anxiety Overview
• Anxiety Causes
• Anxiety Treatment
• Hyperventilation Overview
• Panic Attacks Overview

• Lifestyle Intervention Shows Promise for Panic Disorder
• "Safe" Lead Levels Linked to Depression, Panic in Young Adults
• Brain Function Differs Markedly for Patients With PTSD and Comorbidities vs PTSD Alone

• Psychiatric Comorbidities and Schizophrenia
• Brief Intervention for Anxiety in Primary Care Patients
• Health Consequences of Illegal Drug Use

• Anxiety Disorders Resource Center