Panic Disorder

Panic Disorder

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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.)

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.

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 cingulate 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 (e.g., tachycardia).

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]}

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 comorbidity 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 (e.g., 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]

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]

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]

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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Mohammed A Memon, MD Psychiatrist/Geriatric Psychiatrist, Carolina Center for Behavioral Health; Assistant Professor of Psychiatry, Virginia Commonwealth University School of Medicine

Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, American Psychiatric Association