5.2 Panic Disorder & Agoraphobia – Comprehensive Study Notes
Distinguishing Anxiety, Panic & Panic Disorder
Anxiety (generalized)
Lower-grade, pervasive, long-lasting; may persist for days.
Onset tends to be gradual; intensity moderate.
Panic
Brief but extremely intense “false alarm.”
Sudden onset, peaks within ; subsides within (rarely > ).
Strong somatic focus: heart, respiration, gastrointestinal, vasomotor sensations.
Panic Disorder (PD)
Characterised by recurrent, unexpected panic attacks plus persistent concern, worry, or behavioural change lasting .
More intense and rapid-onset than Generalised Anxiety Disorder (GAD).
DSM-5 Diagnostic Criteria – Panic Disorder
Criterion A – Recurrent, unexpected panic attacks (see symptom list below).
Criterion B – At least one attack followed by month of either:
Persistent concern/worry about additional attacks or consequences (e.g., “going crazy,” heart attack).
Significant maladaptive behaviour change (e.g., avoiding exercise, unfamiliar places).
Criterion C – Disturbance not due to substance/medication or medical condition (e.g., hyperthyroidism, cardiopulmonary disease).
Criterion D – Not better explained by another mental disorder (social anxiety, specific phobia, OCD, PTSD, separation anxiety, etc.).
Panic Attack – Required Symptom List (≥ 4 of 13)
Abrupt surge can arise from calm or anxious state.
Palpitations / pounding / accelerated heart rate.
Sweating.
Trembling or shaking.
Shortness of breath / smothering.
Feeling of choking.
Chest pain or discomfort.
Nausea or abdominal distress (more common in women during cardiac events).
Dizziness, unsteadiness, light-headedness, or faintness.
Chills or heat sensations.
Paresthesia (numbness/tingling).
Derealisation (unreality) or depersonalisation (detached from self).
Fear of losing control or “going crazy.”
Fear of dying.
Culture-specific symptoms (e.g., tinnitus, neck soreness, uncontrollable screaming) may appear but do not count toward the required four.
DSM-5 Diagnostic Criteria – Agoraphobia (Separate Diagnosis)
Fear/anxiety about situations where escape may be difficult or help unavailable if panic-like symptoms occur.
Must involve ≥ 2 of 5 situation clusters:
Using public transport (cars, buses, trains, ships, planes).
Being in open spaces (parking lots, bridges).
Being in enclosed spaces (shops, cinemas).
Standing in line / being in a crowd.
Being outside home alone.
Situations almost always provoke fear; are actively avoided, endured with distress, or require a companion.
Fear is out of proportion; lasts ≥ ; causes significant distress/impairment.
Not better explained by another disorder or medical condition.
Diagnosed independently of Panic Disorder; if both criteria met, assign both diagnoses.
Epidemiology & Course
Lifetime prevalence of PD: of adults.
Age of onset: typically (can begin late teens).
Course: chronic, disabling; intensity may wax and wane.
12-year study: who recovered later relapsed.
Panic attacks (single episode) far more common: of adults experience ≥ 1, but only develop PD.
First attack often follows major stressor; report negative life event before initial attack (loss, victimisation, etc.).
Gender & Sociocultural Factors
PD ≈ 2 × as prevalent in women as men.
Agoraphobia: severity correlates with female preponderance; severe cases female.
Sociocultural account: avoidance and need for a companion more socially permissible for women; men more likely to “tough it out” or self-medicate (nicotine, alcohol).
Comorbidity & Suicide Risk
of PD patients have ≥ 1 additional disorder:
GAD, Social Anxiety Disorder, Specific Phobia, PTSD.
Major Depression (occurs in of PD cases).
Substance-use disorders (notably smoking, alcohol).
Dependent & Avoidant Personality Disorders.
PD is an independent predictor of suicidal ideation & attempts (Nock et al., , ) even after controlling for comorbidities.
Etiology – Integrated View
Genetic / Temperamental
Trait neuroticism & behavioural inhibition elevate risk.
Brain Circuitry
Amygdala hyperactivation.
Noradrenergic & serotonergic systems implicated:
Locus coeruleus (NE) stimulation → cardiovascular surge.
Serotonin inhibits NE; SSRIs ↑ 5-HT → ↓ NE activity.
GABA (inhibitory) abnormally low in cortex.
Cognitive Theory (Clark)
Hyper-sensitivity to bodily sensations + catastrophic misinterpretation (e.g., “palpitations = heart attack”).
Automatic thoughts fuel vicious cycle → escalating anxiety → full panic.
Learning Theory
Initial attack conditions internal (interoceptive) & external cues → conditioned stimuli.
Generalisation and impaired inhibitory learning slow extinction, promoting anticipatory anxiety and agoraphobic avoidance.
Nocturnal Panic Attacks
Occur in of PD patients.
Abrupt awakening from sleep in panic, typically during Stage 2 / early Stage 3 non-REM (few hours after sleep onset).
Distinct from:
Nightmares (REM).
Night Terrors (children, Stage 3–4, minimal awareness).
Sleep Paralysis (REM–wake transition, immobility).
Associated with greater overall severity, insomnia, frequent awakenings.
Psychological Treatments
Exposure-Based Therapy
Graduated in-vivo exposure to avoided situations.
achieve clinically significant improvement; gains persist ≥ .
Interoceptive (Paresthetic) Exposure
Deliberate induction of feared bodily sensations (e.g., spinning in chair, hyperventilating, running in place) until habituation.
Panic Control Treatment (PCT – CBT variant)
Psychoeducation: adaptive nature of anxiety/panic.
Breathing retraining: slow diaphragmatic breathing.
Cognitive restructuring: identify & challenge catastrophic thoughts.
Exposure to feared situations & sensations.
Outcome: panic-free after weeks; superior to exposure-only; effective for nocturnal panic.
Pharmacological Treatments
Anxiolytics (Benzodiazepines – e.g., Xanax, Klonopin)
Onset: ; useful for acute attacks.
Side-effects: sedation, cognitive/motor impairment, dependency, withdrawal, high relapse → not first-line.
Antidepressants
Tricyclics, SSRIs, SNRIs (e.g., fluoxetine, sertraline).
Advantages: no physiological dependence; treat comorbid depression.
Delayed onset: .
Side-effects: dry mouth, constipation, sexual dysfunction; adherence issues.
SSRIs preferred; relapse still possible when discontinued.
Combined & Novel Approaches
Short-term combination (CBT + medication) may slightly outperform monotherapies; reduces side-effects & drop-outs.
Long-term: reliance on medication alone → higher relapse after discontinuation; CBT fosters durable self-efficacy.
D-cycloserine (DCS) – partial NMDA agonist; shown to enhance exposure-based learning for PD, specific & social phobias.
Remember: Panic Disorder reflects interplay of biological sensitivity, catastrophic cognition, and learned avoidance. Durable recovery usually requires cognitive-behavioural interventions that dismantle the vicious cycle, sometimes augmented—but not replaced—by pharmacotherapy.