Panic Disorder.

🧠 What Is Panic Disorder? (The Brain Mechanism of Acute Panic)

Panic Disorder is an emotional disorder defined by “sudden fear without real danger” (a false alarm fear response). The body and brain react as if facing a severe threat even when the situation is safe. Symptoms typically peak within minutes: the person may feel as if having a heart attack, unable to breathe, faint, with numb/tingling hands and feet, hot or cold flashes, and a sense of “about to die or go crazy.” These are direct effects of a rapid surge in the sympathetic nervous system and the HPA axis (hypothalamic–pituitary–adrenal), releasing adrenaline and cortisol beyond what is needed.
Under DSM-5-TR (APA, 2022), diagnosis requires recurrent, unexpected panic attacks followed by ≥1 month of persistent concern about additional attacks and/or maladaptive avoidance, with medical/substance causes ruled out.

At the neural level, studies from Harvard and Yale show hyper-reactivity of the amygdala (threat detection), while the prefrontal cortex (PFC) and anterior cingulate cortex (ACC)—which normally inhibit fear—show reduced activity. The “fear-brake” therefore fails, producing a false-alarm cascade. The brain misinterprets bodily signals (e.g., stress-related palpitations or dizziness) as “I’m dying.” This is Clark’s (1986) theory of catastrophic misinterpretation of bodily sensations, later supported by neuroimaging and modern computational models. This mechanism explains why CBT’s interoceptive exposure teaches patients that bodily sensations are not dangerous, helping to dismantle the panic cycle.

Psychologically, Panic Disorder often evolves into a “fear of fear” loop: vigilance toward one’s bodily sensations (e.g., feeling the heart speed up) triggers fear of another attack, which in turn releases more adrenaline and provokes the very symptoms feared—thereby reinforcing the loop. Over time, this can lead to Agoraphobia—fear of places perceived as hard to escape or get help (metros, malls, elevators)—resulting in avoidance of leaving home. The DSM-5-TR separates Panic Disorder and Agoraphobia to reflect that not all patients have situational fears, though the two frequently co-occur. Most effective treatments include Cognitive Behavioral Therapy (CBT)—especially interoceptive exposure—and SSRIs/SNRIs, which rebalance serotonin and norepinephrine for longer-term stabilization.

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📋 DSM-5-TR Criteria (Concise, High-Yield)

A. Recurrent unexpected panic attacks (abrupt surge of intense fear/discomfort peaking within minutes) with ≥4 of 13 symptoms: palpitations, sweating, trembling, shortness of breath/smothering, choking sensations, chest pain, nausea/abdominal distress, dizziness/lightheadedness, paresthesias (numb/tingling), chills/hot flushes, derealization/depersonalization, fear of losing control/“going crazy,” fear of dying.
B. ≥1 month of (i) persistent concern/worry about additional attacks or their consequences, and/or (ii) maladaptive behavioral changes to avoid attacks.
C. Not better explained by a substance/medical condition or another mental disorder (e.g., social anxiety, specific phobia, OCD, PTSD).

Note: DSM-5/5-TR includes a “Panic Attack” specifier that can be added to other diagnoses (e.g., Major Depressive Disorder with panic attacks).
NCBI

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📈 Epidemiology & Course

Onset is typically late adolescence to early adulthood; more common in women; tends to be relapsing if untreated. NIMH emphasizes that attacks often occur “out of the blue” with prominent physical symptoms, leading many patients to ED visits and misattributions to cardiac or other acute medical problems—further reinforcing fear of bodily sensations.
National Institute of Mental Health

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🧬 Pathophysiology (Core Points)

Neuroimaging indicates abnormalities in the amygdala–insula–ACC (the salience network) with reduced top-down control from the PFC, yielding hypersensitive threat/bodily-signal detection plus impaired emotion regulation. Heightened interoceptive sensitivity promotes catastrophic misinterpretation of “normal” sensations (palpitations, rapid breathing, dizziness). This is central to Clark/Barlow models and the target of modern CBT (interoceptive exposure). (Synthesized from contemporary neurobiological reviews and CBT evidence.)
ScienceDirect

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🔍 Key Differentials to Exclude

• Medical emergencies: myocardial ischemia/arrhythmias, asthma exacerbation, pulmonary embolism, hyperthyroidism, hypoglycemia, vestibular disorders, etc.
  
  
• Substances/medications: high caffeine, stimulants/amphetamines, benzodiazepine/alcohol withdrawal.
  
  
• Psychiatric: Social Anxiety (situation-bound), Specific Phobia (specific trigger), OCD (obsession-driven), PTSD (trauma-triggered), GAD (chronic worry without abrupt panic peaks).
  Guidelines (NICE/AAFP) stress appropriate medical and substance screening before initiating psychotherapy/pharmacotherapy.
  NICE
  

🧭 Evidence-Based Treatment

1) CBT (First-line)
Core components: psychoeducation, cognitive restructuring, interoceptive exposure, in-vivo exposure.

• Interoceptive exposure: safely evoke bodily sensations (e.g., stair sprints to raise heart rate/dizziness) to disconfirm catastrophic beliefs and reduce fear of sensations.
  
  
• In-vivo exposure: graded confrontation of avoided situations (driving, elevators, enclosed spaces, bridges).
  
  
• Breathing/relaxation skills are useful adjuncts but do not replace exposure.
  NIMH/NICE and clinical reviews: CBT shows moderate–large effects and lower relapse than medication after discontinuation.
  National Institute of Mental Health
  
  

2) Medication (alone or combined with CBT, depending on severity/access)

• SSRIs (e.g., sertraline, paroxetine, escitalopram) and SNRIs (e.g., venlafaxine XR) are first-line. Start low, titrate gradually; assess at 4–6 weeks; continue 6–12 months after remission to reduce relapse.
  
  
• Benzodiazepines (e.g., clonazepam, alprazolam) may be used short-term for acute/severe cases while awaiting SSRI/SNRI or CBT effects, but not recommended long-term due to dependence/tolerance/withdrawal and potential interference with exposure learning.
  
  
• Minimize stimulants/caffeine, and treat comorbidities (depression, insomnia, substance use).
  Aligned with NICE CG113 and AAFP practice summaries.
  NICE
  
  

3) Stepped-Care Approach
Begin with education and guided self-help CBT / digital CBT → if insufficient, move to high-intensity CBT or SSRI/SNRI → specialist referral for complex/treatment-resistant cases. Target remission, not merely fewer attacks.
NICE

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🧑‍⚕️ What Patients Can Do (Adjuncts—not a substitute for care)

• Map the panic cycle (trigger–thought–bodily sensation–behavior) for CBT work.
  
  
• Practice interoceptive exercises safely (with guidance), e.g., spin in a chair 30–60s to induce dizziness and observe it fade—evidence that it isn’t dangerous.
  
  
• Sleep/caffeine/alcohol: follow sleep hygiene; reduce caffeine/energy drinks; avoid alcohol “self-medication.”
  
  
• Gradually drop safety behaviors that maintain the disorder via a stepwise exposure plan with a therapist.
  (From NIMH/NICE/CBT principles.)
  National Institute of Mental Health
  

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📚 Key References

• American Psychiatric Association. DSM-5-TR. APA Publishing, 2022.
• Clark, D.M. (1986). A cognitive approach to panic. Behaviour Research and Therapy.
• Etkin, A., & Wager, T.D. (2007). Functional neuroimaging of anxiety: a meta-analysis. American Journal of Psychiatry.
• National Institute of Mental Health (NIMH). Panic Disorder. 2023.
• NICE Guideline CG113 (2019). Generalised anxiety disorder and panic disorder in adults.
• Gorman, J.M., et al. (2000). Neuroanatomical hypotheses of panic disorder revisited. American Journal of Psychiatry.
• DSM-5-TR, APA (2022): panic criteria/specifier and diagnostic principles.
• NCBI

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