Background

The DSM defines panic attacks as an abrupt rush of severe fear or distress that peaks within minutes. Four or more specific physical symptoms characterize a panic attack.

Accelerated heart rate, sweating, trembling; sensations of suffocating; choking, chest pain, nausea, or abdominal distress; dizzy, unsteady, shivers, or warmth sensations and paresthesia.

Epidemiology

Compared to the general population, individuals with panic disorder have significantly greater lifelong rates of gastrointestinal, cardiovascular, pulmonary, and other health disorders. Panic disorder is more prevalent in European Americans than Latinos,

Asian Americans, or African Americans; Females are more susceptible than males. Panic disorder often observed more in adolescents and young adults, with individuals under 14 having a less incidence.

Patients share many additional comorbidities with panic disorders, such as social phobia, OCD, COPD, asthma, mitral valve prolapse, irritable bowel syndrome, and hypertension. Pregnant women with panic disorder are likelier to have infants with low birth weight.

Anatomy

Pathophysiology

Many peptides and neurotransmitters in the central nervous system influence physical manifestations significantly. Brain imaging examinations have revealed specific alterations, such as enhanced flow and receptor activation, in specific regions involving the frontal and limbic regions. The amygdala is thought to be the primary source of dysfunction.

Clinical illness and panic disorder are closely connected from a pathophysiological and psychological perspective. Two major hypotheses describe how patients are more susceptible to panic attacks. According to the first theory, susceptible individuals do not have the correct neurochemical mechanisms to control serotonin, so when it is high,

the model of the fear network in the autonomic nervous system is altered. According to the second hypothesis, a lack of endogenous opioids causes separation anxiety and an increased feeling of suffocation.

Etiology

Most theory points to a chemical imbalance as a primary contributor, such as irregularities in serotonin, cortisol, and gamma-aminobutyric acid. An environmental and genetic component is considered to have a role in the etiology of panic disorder. According to a few studies, stressful childhood events might lead to panic disorder among adults.

A newer study suggests neural circuitry plays a more significant part in panic disorder, where some brain sections are hyperexcitable in patients, predisposing them to the illness. According to specific research, genetic factors potentially contribute to the genesis of panic disorder.

First-degree relatives have a 40% likelihood of developing the syndrome if a family member has already been diagnosed. Individuals with panic disorder are also at a high risk of developing other mental health conditions.

Genetics

Prognostic Factors

The prognosis is questionable. It is unusual to have panic disorder without underlying disorders. Even after a symptom-free phase, most individuals will have a recurrence of symptoms.

Treatment adherence is a serious concern, and relapse of symptoms is prevalent. Only roughly 60% of patients reach remission in 6 months.

Chronic illnesses, high interpersonal sensitivity, marital status, belonging to low socioeconomic status, and living alone are all risk factors for poor outcomes. Such individuals are at risk for suicide and premature unfavorable cardiac events.

Clinical History

Physical Examination

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Medication

Future Trends

Media Gallary

References

https://www.ncbi.nlm.nih.gov/books/NBK430973/