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8/11/2017 Panic disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis - UpToDate

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Panic disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and
diagnosis

Author: Peter P Roy-Byrne, MD


Section Editor: Murray B Stein, MD, MPH
Deputy Editor: Richard Hermann, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2017. | This topic last updated: Aug 01, 2017.

INTRODUCTION — Panic attacks and panic disorder are common problems in both primary and psychiatric
specialty care. With the revision of DSM-IV-TR to DSM-5, agoraphobia is diagnosed independently of panic
disorder [1]. Because this is a recent change, most extant pharmacologic treatment data on agoraphobia focuses
on subjects who also have panic attacks.

Panic attacks classically present with spontaneous, discrete episodes of intense fear that begin abruptly and last
for several minutes to an hour. In panic disorder, patients experience recurrent panic attacks, at least some of
which are not triggered or expected, and one month or more of either worry about future attacks/consequences,
or a significant maladaptive change in behavior related to the attacks, such as avoidance of the precipitating
circumstances.

This topic will address the epidemiology, pathogenesis, clinical manifestations, course, assessment, and
diagnosis of panic disorder. The epidemiology, pathogenesis, clinical manifestations, course, and diagnosis of
agoraphobia are discussed separately. The treatment of panic disorder is also discussed separately. (See
"Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis" and
"Pharmacotherapy for panic disorder with or without agoraphobia in adults" and "Psychotherapy for panic
disorder with or without agoraphobia in adults".)

EPIDEMIOLOGY — The 12-month and lifetime prevalence of panic disorder in the United States (US) population
(age 15 to 54 years) was 2.7 percent and 4.7 percent, respectively, in a 2005 nationally representative study [2].
A systematic review of 13 European studies reported a 12-month prevalence rate of panic disorder of 1.8 percent
[3]. The prevalence of panic disorder among primary care patients is approximately twice as high as in the
general population with rates of 4 to 8 percent [4-6]. Panic attacks (which can occur in disorders other than panic
disorder) are much more common than panic disorder, occurring in up to one-third of individuals at some point in
their lifetime [7-9].

The disorder has a median age of onset of 24 years [2] and is approximately twice as common in women as
among men, with a 5 percent lifetime prevalence among women versus 2 percent among men [10]. The
prevalence decreases significantly after age 60 [2].

Comorbidities — The National Comorbidity Study (NCS), which studied a representative sample of US adults
ages 15 to 54, found that 37 percent of patients with panic disorder had a lifetime history of major depression [2].
The NCS found that patients with panic disorder also had elevated rates of social anxiety disorder, generalized
anxiety disorder, and posttraumatic stress disorder. In a separate analysis of NCS data, patients with bipolar
disorder and alcohol abuse had high rates of panic disorder relative to the general population rates [11]. (See
"Generalized anxiety disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course,
assessment, and diagnosis" and "Posttraumatic stress disorder in adults: Epidemiology, pathophysiology, clinical
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manifestations, course, assessment, and diagnosis" and "Unipolar depression in adults: Assessment and
diagnosis" and "Bipolar disorder in adults: Epidemiology and pathogenesis" and "Risky drinking and alcohol use
disorder: Epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis" and "Social
anxiety disorder in adults: Epidemiology, clinical manifestations, and diagnosis".)

PATHOGENESIS — The pathogenesis of panic disorder fits a stress-diathesis model (ie, the combination of an
underlying predisposition interacting with or triggered by life stress). Vulnerability factors include specific genetic
factors, childhood adversity, and several personality traits, including anxiety sensitivity and neuroticism. Current
stressful life events in association with one or more of these vulnerability factors often precipitate development of
panic attacks [12-14].

Genetics — Several lines of research indicate a genetic component to the disorder.

● First-degree relatives of patients with panic disorder have higher rates of panic disorder than relatives of
patients with major depression and relatives of healthy controls [15,16], and rates are even higher if the
panic disorder patient had onset of illness before age 20 [16].

● Twin studies have shown higher concordance for monozygotic compared with dizygotic twins (31 percent
and 0 percent, respectively, in one study) [17]. Twin studies have suggested a heritability of approximately
40 percent with contributions of 10 percent from common familial environment and greater than 50 percent
from individual-specific environmental effects [18].

● The majority of genetic research in panic disorder has focused on linkage and candidate gene studies and
has been hindered by non-replication and sample sizes too small to identify the genes of very small effect
that contribute to this complex disorder [19]. A 2016 meta-analysis suggested that TMEM 132D, the gene for
a transmembrane protein that may be involved in neuronal sprouting and connectivity in brain regions
important for anxiety, is associated with panic disorder [20].

Experts suggest that the underlying genetic factors may differ in various subgroups of patients with panic
disorder (eg, familial versus nonfamilial, early versus late onset), further complicating the search [21]. The
two genome-wide association studies published to date have not been replicated. More recent work has
documented multiple gene expression differences (DNA methylation abnormalities) that might be associated
with panic disorder [22].

Temperament — Anxious temperaments, as measured by high neuroticism scores [23] and anxiety sensitivity
[24], have been shown to be risk factors for development of panic disorder, or may constitute early
manifestations of the disorder. Neuroticism is a personality trait that is associated with poor stress resilience and
often manifests in greater reactivity to life stressors [23]. Anxiety sensitivity is a measure of fear of anxiety
symptoms and catastrophic cognitions regarding bodily sensations (eg, rapid heartbeat may be misinterpreted as
a heart attack). Anxiety sensitivity has been shown to be associated with both genetic and environmental factors
[25-27]. Subjects high in anxiety sensitivity have been shown to be more likely to develop panic disorder after
experiencing stressful life experiences [27].

Panic disorder has also been linked with behavioral inhibition, a temperamental trait [28], that has also been
linked with other anxiety disorders [29]. Offspring of parents with panic disorder who had behavioral inhibition as
children were found to have smaller hippocampi as teens, providing a link between early temperament and
neuroanatomy thought to be involved with panic disorder [30]. It is likely that these various anxious
temperaments are moderating or mediating factors increasing vulnerability to stressful life events (see below).

Childhood adversity — Studies have shown that childhood adversity such as a history of physical or sexual
abuse increases the risk of panic disorder in adult years [31] and may be associated with persistence of non-

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panic anxiety symptoms [32]. Smoking in childhood [33,34], and possibly asthma [35,36], appear to increase the
risk for onset of panic disorder in adulthood.

Life stress — Panic attacks often occur at times of significant life stress. Controlled studies have found that
individuals experiencing panic attacks have a higher frequency of stressful life events than controls, occurring
within the past 12 months and especially within the last month. Events involving loss, threat, or illness are
particularly salient [37].

Neurobiology — Research into underlying neurobiologic factors has gradually shifted from a focus on the
neurotransmitters (serotonin, norepinephrine, and gamma-aminobutyric acid [GABA]) linked with commonly
prescribed anti-panic medications, to proposed neural circuitry closely linked with basic animal models of fear
development (figure 1) [38]. This proposed neuroanatomical model for panic disorder [39] focused on specific
areas in the amygdala or hypothalamus as the potential site of neural triggers for panic attacks, suggesting that
patients may inherit specific brain areas that are hyperexcitable and make the patient susceptible to unprovoked
panic symptoms when exposed to either internal (interoceptive) or external (life event) stressors.

Cognitive researchers have suggested that catastrophic thoughts may also contribute to this susceptibility via the
same neural mechanisms [40]. In this model, the amygdala is a more primary way station that integrates sensory
information via the thalamus and sensory cortex with stored experience via the hippocampus and frontal cortex,
and then generates the panic response via outflow tracts to the locus ceruleus, hypothalamus, periaqueductal
grey (PAG), and parabrachial nucleus [38,41]. More recent reviews have indicated an equally if not more
important role for insula and dorsal anterior cingulate cortex in mediating panic responses [42].

Studies have hypothesized that the dorsomedial hypothalamus/perifornical (DMH/PeF) region coordinates rapid
mobilization of behavioral, autonomic, respiratory, and endocrinologic responses to stress [43].

A review of 109 controlled studies examining brain structure, receptor binding/spectroscopy, functional brain
activity at rest, with spontaneous panic, and in response to provocation with pharmacologic agents, emotional
and cognitive tasks [44], provides some support for the model, with studies showing alterations in these various
anatomic regions in panic disorder patients.

Evidence for amygdala involvement is less extensive than for prefrontal, temporal, anterior cingulate, insula, and
hippocampus, suggesting that the human panic response is more complex than animal fear and likely to involve
a broader set of neural circuits and processes.

Neurotransmitter-focused studies over the decade of 2005 to 2015 have largely implicated alterations in the
GABA-benzodiazepine receptor [45-48] and serotonin receptor systems [49,50]. Studies have linked fear
conditioning models with the “spontaneous” aspect of human panic by showing that panic disorder patients have
increased fear generalization, ie, impaired cue discrimination, using a startle response paradigm [51]. This
overgeneralization has been linked to increasing activity in the ventromedial prefrontal cortex [52].

CLINICAL MANIFESTATIONS — Panic attacks typically present with spontaneous, discrete episodes of intense
fear that begin abruptly and last for several minutes to an hour. In panic disorder, patients experience recurrent
panic attacks, at least some of which are not triggered or expected, and one month or more of either worry about
future attacks/consequences, or a significant maladaptive change in behavior related to the attacks, such as
avoidance of the precipitating circumstances or of situations where they would be unable to escape or obtain
help were they to panic. Patients may present with autonomic symptoms of a panic attack such as chest pain or
shortness of breath.

Patients may less commonly present with panic attacks but not otherwise endorse fear or anxiety – so-called
"non fearful" panic attacks [53]. The absence of subjectively experienced fear in some patients may make
recognition of panic more difficult.
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Panic attacks may occur in other anxiety disorders, where they are specifically triggered by the occurrence or
recollections of feared objects or situations (eg, trauma, phobic exposure or in obsessive compulsive disorder,
contamination).

Somatic features and utilization of medical services — Somatic symptoms of panic disorder, especially
cardiorespiratory, gastrointestinal and otoneurologic symptoms [54], often predominate in patients’ clinical
presentations, though the rate is similar to that seen in both depression and other anxiety disorders. This causes
many patients to seek health care from a general medical rather than mental health clinician [55], and the
dramatic and paroxysmal nature of panic may result in more emergency room visits. Patients with continuing,
frightening symptoms of panic disorder are often unsatisfied following a negative general medical work-up and
repeatedly seek medical care [56].

This often results in high medical utilization, including excess medical visits [57,58], unnecessary medications,
and costly and unnecessary testing to rule out medical illness, eg, cardiac testing for unexplained chest pain [59]
and dyspnea, pulmonary function testing for unexplained dyspnea, endoscopy for unexplained abdominal pain or
diarrhea, and MRI scanning for unexplained dizziness. This extensive use of resources often precedes the
diagnosis of panic disorder by as long as 10 years [60].

Agoraphobia — Patients with panic attacks can develop agoraphobia; ie, anxiety about and avoidance of
situations where help may not be available or where it may be difficult to leave the situation in the event of
developing panic-like symptoms or other incapacitating or embarrassing symptoms [1]. With the transition from
DSM-IV-TR to DSM-5, agoraphobia was reclassified as a separate disorder diagnosed independently of panic
disorder. The epidemiology, clinical manifestations, course, and diagnosis of agoraphobia are discussed
separately. (See "Agoraphobia in adults: Epidemiology, pathogenesis, clinical manifestations, course, and
diagnosis".)

Substance use — Panic disorder prevalence is modestly increased in subjects with alcohol use disorders, as
are a variety of other anxiety and mood disorders [61]. Evidence suggests that this association is due to both
“self medication” as well as a progressive anxiogenic effect of alcohol over time [62]. Patients may use alcohol or
sedative hypnotics in desperation to control symptoms of panic disorder. These agents have a short-lived
anxiolytic action, but are subsequently associated with rebound exacerbation of anxiety and panic attacks when
blood levels decline. This effect may not just be short term but result in progressive worsening of the course of
panic and anxiety over time [63]. (See "Risky drinking and alcohol use disorder: Epidemiology, pathogenesis,
clinical manifestations, course, assessment, and diagnosis".)

Medical comorbidity — Medical illnesses and mood and anxiety disorders all may increase risk of multiple
medical disorders. The burden of symptoms and number of comorbid diagnoses may be the most important
factors increasing risk. Nonetheless, both community-based and clinic-based studies have shown that
respondents with panic disorder may have a higher prevalence of other medical disorders compared with
controls including:

● Asthma [64,65]
● Coronary artery disease [66]
● Hypertension [67]
● Ulcer [68]
● Interstitial cystitis [69]
● Migraine headaches [70,71]

A longitudinal cohort analysis over 3.9 years of a nationwide Taiwanese database involving more than 43,000
individuals found an association between sleep apnea and a subsequent diagnosis of panic disorder (hazard

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ratio 2.17; 95% CI 1.68-2.81) [72].

The previously reported association between mitral valve prolapse and panic disorder [73] has been questioned
because of inconsistent results and methodologic limitations in the supporting research, including flawed
diagnostic criteria for mitral valve prolapse, which resulted in over-diagnosis of this condition [74]. (See "Mitral
valve prolapse syndrome".)

Mitral valve prolapse may be encountered in patients with panic disorder, but is unlikely to be the cause of the
panic symptoms; in such instances, the panic disorder should be treated. (See "Pharmacotherapy for panic
disorder with or without agoraphobia in adults" and "Psychotherapy for panic disorder with or without
agoraphobia in adults".)

Data suggest that a history of panic attacks is associated with an increased risk of mortality due to vascular
causes [75] and there was a trend toward an increased risk for stroke. The risk for coronary heart disease was
intermediate for women reporting limited-symptom panic episodes. Panic disorder also worsens the course of
asthma [65].

COURSE — Panic disorder is a recurrent or chronic disease in the majority of cases. A review of 16 studies of
panic disorder diagnosed with modern psychiatric criteria found that most patients had improvement in panic
symptoms over a period of 15 to 60 months, but few experienced complete resolution of the disorder [76]. A
large community-based study of panic disorder followed over a two-year course found that remission occurred in
64 percent of subjects with time to remission of 5.7 months [77]. However, remission had not occurred in one
year in 43 percent of those with panic disorder. Panic attacks recurred in 21 percent of those who had achieved
remission [77].

Predictors of remission in the community-based trial were female gender, absence of ongoing life stressors, low
initial frequency of attacks, and sub-threshold panic [77]. Other studies have found comorbid major depression,
agoraphobia, and personality disorders to predict a poorer outcome in patients with panic disorder [76].

Panic disorder reduces the quality of life and function in affected patients and their families. Decrements in
familial, social, and vocational functioning occur to a degree comparable to that seen with major depression
[78,79]. In one study, the number of disability days taken by patients with anxiety disorders was significantly
greater than in those with diabetes, cardiac disease, or renal disease [80].

Both infrequent panic attacks and panic disorder are associated with higher medical utilization, in large part
resulting from frightening physical symptoms such as chest pain, palpitations or dizziness, and increased
functional impairment [57,58,78].

Suicide attempts — Most studies have shown a higher likelihood of suicide attempts among people with panic
disorder compared with the general population [81-83]. A 2006 analysis of data from the National Comorbidity
Survey found that panic disorder was associated with suicide attempts in the prior 12 months, controlling for
sociodemographic and clinical factors, including comorbid major depression, substance abuse, and childhood
abuse [81]. The Netherlands Mental Health Survey found that a diagnosis of one or more anxiety disorders,
including panic disorder, was associated with a higher rate of subsequent suicidal ideation and suicide attempts
after controlling for sociodemographic factors and psychiatric comorbidity [82]. The study also found that
individuals with co-occurring anxiety and mood disorders had a higher likelihood of suicide attempts compared
with those with a mood disorder alone [82]. (See "Suicidal ideation and behavior in adults".)

ASSESSMENT

History and physical examination — A complete psychiatric examination, including a medical history, thorough
physical and neurologic examination, and standard laboratory testing (thyroid function tests, complete blood

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count, and a chemistry panel) are needed to rule out organic causes of the symptoms and establish an accurate
diagnosis of panic disorder. A thorough evaluation may also provide reassurance to patients worried about the
medical implications of their symptoms. Additional testing (eg, an electrocardiogram or Holter monitoring) may be
indicated based on age, family, and medical history.

Information should be elicited about current life stress, separations, recent deaths, patient concerns and fears,
interpersonal problems, recent substance abuse, and use of medications. The patient should be asked about
avoidance patterns that have developed since the onset of panic attacks. Family members may provide valuable
information overlooked or neglected by the patient.

Rating scales — Clinician-administered and patient self-assessment instruments can be useful for monitoring
changes in severity of panic disorder, for example, in response to treatment. The gold standard instrument for the
disorder is the Panic Disorder Severity Scale (PDSS) [84]. Each of seven items covers a key clinical aspect of
the syndrome (attack frequency, attack intensity, anticipatory anxiety, phobic avoidance, avoidance of internal
bodily sensations, relationship impairment, work impairment). A 0 to 4 severity rating for each item is anchored
with an unambiguous behavioral descriptor. It is psychometrically sound with excellent reliability and validity [85],
and was used in a seminal multi center collaborative study of panic disorder treatment [86].

DIAGNOSIS

DSM-5 diagnostic criteria

Panic attack — A panic attack is not a mental disorder. Panic attacks occur in the context of panic disorder,
with other anxiety disorders, and with other mental disorders (eg, depressive disorders, posttraumatic stress
disorder, substance use disorders) and some medical conditions. When the presence of a panic attack is
identified in conjunction with a mental disorder other than panic disorder, it should be noted as a specifier (eg,
"posttraumatic stress disorder with panic attacks").

DSM-5 diagnostic criteria for a panic attack are described below [1].

An abrupt surge* of intense fear or intense discomfort that reaches a peak within minutes, and during which time
four or more of the following 13 symptoms occur:

● Palpitations, pounding heart, or accelerated heart rate


● Sweating
● Trembling or shaking
● Sensations of shortness of breath or smothering
● Feelings of choking
● Chest pain or discomfort
● Nausea or abdominal distress
● Feeling dizzy, unsteady, light-headed, or faint
● Chills or heat sensations
● Paresthesias (numbness or tingling sensations)
● Derealization (feelings of unreality) or depersonalization (being detached from oneself)
● Fear of losing control or "going crazy"
● Fear of dying

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

Note: Culture-specific symptoms (eg, tinnitus, neck soreness, headache, uncontrollable screaming or crying)
may be seen. Such symptoms should not count as one of the four required symptoms.
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The diagnosis of agoraphobia is discussed separately. (See "Agoraphobia in adults: Epidemiology, pathogenesis,
clinical manifestations, course, and diagnosis".)

Panic disorder — DSM-5 diagnostic criteria for panic disorder are described below [1].

● A. Recurrent unexpected panic attacks

● B. At least one of the attacks has been followed by a month or more of one or both of the following:

• 1. Persistent concern or worry about additional panic attacks or their consequences (eg, losing control,
having a heart attack, "going crazy").

• 2. A significant maladaptive change in behavior related to the attacks (eg, behaviors designed to avoid
having panic attacks, such as avoidance of exercise or unfamiliar situations).

● C. The disturbance is not attributable to the physiological effects of a substance (eg, medication or illicit
drug) or another medical condition (eg, hyperthyroidism, cardiopulmonary disorders).

● D. The disturbance is not better explained by another mental disorder. As examples, the panic attacks do
not occur only in response to:

• Feared social situations, as in social anxiety disorder

• Circumscribed phobic objects or situations, as in specific phobia

• Obsessions, as in obsessive-compulsive disorder

• Reminders of traumatic events, as in posttraumatic stress disorder

• Separation from attachment figures, as in separation anxiety disorder

Differential diagnosis — The presentation of panic disorder can overlap with manifestations of other psychiatric
disorders and mimic a number of general medical conditions.

Somatic symptom disorder — Patients with both panic disorder and somatic symptom disorder present with
multiple physical symptoms. Many patients with somatic symptom disorder also have comorbid panic attacks or
disorder. In one study, for example, 32 of 78 women (41 percent) with somatic symptom disorder also met criteria
for panic disorder [87]. However, somatic symptom preoccupation is more enduring with somatic symptom
disorder and more episodic with panic disorder. (see "Somatization: Epidemiology, pathogenesis, clinical
features, medical evaluation, and diagnosis")

Identifying patients with concurrent somatic symptom disorder requires questions regarding the existence of
chronic somatization symptoms since adolescence, family history of females with somatic symptom disorder,
family history of males with antisocial personality disorder or substance abuse problems, chaotic family histories,
childhood sexual or physical abuse or emotional neglect, abuse of prescription drugs, poor stress resilience and
coping, and abuse of street drugs or alcohol.

Illness anxiety disorder — Illness anxiety disorder is defined in DSM-5 as individuals with high health
anxiety without somatic symptoms unless their health anxiety is better explained by a primary anxiety disorder
such as panic disorder. Many patients with panic disorder develop anxiety and fears of having a serious medical
illness such as HIV or cancer but can be differentiated from patients with illness anxiety by also having multiple
somatic symptoms such as tachycardia, chest pain and shortness of breath.

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Treatment of panic disorder in patients with milder forms of somatization frequently leads to remission of both
physical symptoms and the tendency to have illness anxiety. In contrast, treatment of panic disorder in those with
somatic symptom disorder may only lead to a 30 to 40 percent reduction in somatic symptoms because of the
development of chronic social stressors and maladaptive patterns of coping with stress.

Other mental disorders — To meet criteria for panic disorder, symptoms of panic attacks must be
distinguished from panic-like symptoms that occur as part of other mental disorders. At least some of the panic
attacks should be spontaneous and should not be limited to a specific situation, such as heights as in
acrophobia, or to other specific circumstances as described in Criterion D above. (See 'Panic disorder' above.)

Substance abuse — Overuse of caffeine as well as abuse of stimulant drugs such as cocaine and
amphetamines can precipitate panic attacks. In addition, withdrawal from sedative hypnotics, alcohol, and
opiates can also precipitate panic attacks. (See "Benefits and risks of caffeine and caffeinated beverages",
section on 'Psychiatric' and "Cocaine use disorder in adults: Epidemiology, pharmacology, clinical manifestations,
medical consequences, and diagnosis" and "Prescription drug misuse: Epidemiology, prevention, identification,
and management", section on 'Stimulants'.)

General medical conditions — The possibility of organic etiologies should be considered prior to making the
diagnosis of panic disorder. A number of conditions can mimic symptoms of panic attacks including:

● Angina (see "Outpatient evaluation of the adult with chest pain", section on 'Myocardial ischemia')

● Arrhythmias (see "Outpatient evaluation of the adult with chest pain", section on 'Myocardial ischemia')

● Chronic obstructive pulmonary disease (see "Approach to the adult with interstitial lung disease: Diagnostic
testing")

● Temporal lobe epilepsy (see "Localization-related (focal) epilepsy: Causes and clinical features")

● Pulmonary embolus (see "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with
suspected acute pulmonary embolism")

● Asthma (see "Diagnosis of asthma in adolescents and adults")

● Hyperthyroidism (see "Diagnosis of hyperthyroidism")

● Pheochromocytoma (see "Clinical presentation and diagnosis of pheochromocytoma")

● Treatment side effects, eg, hypoglycemia in patients with diabetes, toxic serum aminophylline concentrations
in patients with asthma (see "Hypoglycemia in adults without diabetes mellitus: Diagnostic approach" and
"Theophylline use in asthma")

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries
and regions around the world are provided separately. (See "Society guideline links: Anxiety disorders in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and
“Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10th to 12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
“patient info” and the keyword(s) of interest.)

● Basics topics (see "Patient education: Panic disorder (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Panic attacks are characterized by an abrupt surge of intense fear or intense discomfort that reaches a peak
within minutes, and the abrupt development of specific somatic, cognitive, and affective symptoms. In panic
disorder, panic attacks lead to persistent concern or anxiety about possible recurrence and/or resulting
changes in behavior, such as agoraphobia, hypochondriacal concerns, and high medical utilization. (See
'Clinical manifestations' above and "Agoraphobia in adults: Epidemiology, pathogenesis, clinical
manifestations, course, and diagnosis", section on 'Clinical manifestations'.)

● The biological basis of panic disorder is not yet known, but functional imaging and other translational studies
strongly suggest the involvement of fear circuitry (including the amygdala) in its pathogenesis. (See
'Pathogenesis' above.)

● Somatic symptoms of panic disorder often predominate in patients’ clinical presentations. Cardiac
symptoms, (eg, chest pain and tachycardia) are common, as are neurologic (eg, headaches and dizziness)
and gastrointestinal (eg, epigastric pain) symptoms. (See 'Somatic features and utilization of medical
services' above.)

● Patients with panic attacks can develop agoraphobia, ie, anxiety about and avoidance of situations where
help may not be available or where it may be difficult to leave the situation in the event of developing panic-
like symptoms or other incapacitating or embarrassing symptoms [1]. With revision of the DSM from the
fourth to fifth edition, agoraphobia is diagnosed independently of panic disorder. Agoraphobia and its co-
occurrence with panic disorder are discussed separately. (See "Agoraphobia in adults: Epidemiology,
pathogenesis, clinical manifestations, course, and diagnosis".)

● Panic disorder is a recurrent or chronic disease in the majority of cases. Predictors of remission include
female gender, absence of ongoing life stressors, low initial frequency of attacks, and sub-threshold panic.
(See 'Course' above.)

● Prior to making a diagnosis of panic disorder, organic etiologies for symptoms of panic should be
considered. Medical conditions that can mimic panic attacks include angina, arrhythmias, asthma, chronic
obstructive pulmonary disease, pulmonary embolus, thyroid disease and, very rarely, temporal lobe epilepsy
or pheochromocytoma. Substances that may trigger or worsen panic disorder include excessive caffeine use
or the use of other stimulants, including certain drugs of abuse. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT — We are saddened by the death of Wayne Katon, MD, who passed away in March
2015. UpToDate wishes to acknowledge Dr. Katon's past work as an author for this topic. UpToDate also wishes
to acknowledge Paul Ciechanowski, who contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.

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GRAPHICS

Neural circuitry of panic attacks

Original figure modified for this publication. Roy-Byrne, P, Craske, MG, Stein, MB. Panic
disorder. Lancet 2006; 368:1023. Illustration used with the permission of Elsevier Inc. All
rights reserved.

Graphic 58548 Version 1.0

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