Panic disorder and phobias

• A panic attack is a sudden surge of fear with intense physical symptoms that comes out of the blue or is triggered and usually reaches its peak within minutes; on its own it is a normal-ish experience in the population and does not define a disorder.
• Panic disorder is diagnosed when such attacks are recurrent and unexpected, and are followed for at least a month by persistent worry about having more or by a change in behaviour to avoid them. ^[7]
• Agoraphobia, social anxiety disorder and specific phobia are recognised alongside panic disorder: all are fear-based disorders, but each has its own cue (places, social scrutiny, a specific object) and its own avoidance pattern.
• Cardiovascular, respiratory, endocrine and neurological disease must often be excluded, because a first panic attack and a first heart attack can look identical.
• First-line treatment is cognitive behaviour therapy that includes interoceptive and in vivo exposure, plus a selective serotonin reuptake inhibitor (SSRI) such as sertraline started low and titrated; benzodiazepines are not for long-term use. ^[1][2][3][5]

By the end of this page you should be able to:

1. Define a panic attack and distinguish it from panic disorder using the diagnostic criteria. ^[7]
2. Describe agoraphobia, social anxiety disorder (social phobia) and specific phobia, and explain how each presents and is treated. ^[2][3]
3. Explain the fear circuitry thought to underlie panic attacks and the rationale for exposure treatment. ^[4]
4. Recognise the medical and psychiatric conditions that imitate panic disorder and say which tests exclude them. ^[1]
5. Plan treatment for adults following the stepped-care approach of NICE CG113 and NICE CG159, including drug choice, dose titration, monitoring and relapse prevention. ^[1][2]
6. Title the criteria for referral to specialist services and the adaptations needed for children, older adults and pregnancy. ^[1][2]

Panic attacks are not the same as anxiety. They are sudden and dramatic: a person is overwhelmed by fear and physical sensations that peak quickly rather than building slowly. Anxiety in the everyday sense can be an appropriate, proportionate worry that is long-lasting; a panic attack surges. A single unexpected attack is common in the general population and is not an illness. ^[4]

The classification used in this topic is that of DSM-5-TR and ICD-11, which group panic disorder with phobia-related disorders under anxiety disorders. ^[7] Panic disorder can occur with or without agoraphobia. ^[1] The anchor of treatment is the same family of interventions across all of them.

Agoraphobia is intense fear and avoidance of situations from which escape would be difficult or in which help would not be available if a panic attack or a similar incapacitating or embarrassing symptom occurred. Typical situations include using public transport, being in crowds or queues, open spaces, enclosed public places, and being outside the home alone. ^[7]

Social anxiety disorder (social phobia) is marked fear or anxiety about one or more social situations in which the person is exposed to possible scrutiny by others, typically being observed, judged or having to perform, with a fear of acting in a way or showing anxiety symptoms that will be negatively evaluated. ^[2][7]

Specific phobia is fear or anxiety about a specific object or situation that is disproportionate to the actual danger and nearly always provokes immediate fear, persists for at least 6 months and leads to avoidance or severe distress. ^[7]

These descriptions are paraphrases of the diagnostic criteria for these conditions; the wording of DSM-5-TR and ICD-11 is copyrighted and should be read in its original form. ^[7]

A person can have more than one of these disorders. For example, someone with panic disorder may develop agoraphobia, and social anxiety disorder frequently coexists. ^[2] When they overlap, treat the one that is more severe or that the person identifies as the main problem first. ^[1]

Anxiety disorders are the most common mental disorders worldwide. An estimated 5.8% of the global population currently experiences an anxiety disorder, and in 2023 470 million people had one. ^[3] Approximately 1 in 4 people with an anxiety disorder receives treatment. ^[3]

Lifetime prevalence of panic disorder is about 4.7%, while the prevalence of subthreshold panic disorder and of isolated panic attacks (not disorder) is far higher at roughly 22.7% across a lifetime. ^[4] Twelve-month prevalence of anxiety disorders overall ranges from 14.0% to 19.9%. ^[4] Anxiety disorders, chronic pain and mood disorders are leading causes of disability and work impairment. ^[4]

Onset of phobic and panic disorders is usually in late adolescence and the twenties. ^[7] Women are affected more often than men, and panic disorder and phobias typically begin during childhood, adolescence or early adult life. ^[3][7]

Comorbidity is the rule: panic disorder frequently coexists with depression and with substance misuse, including alcohol, nicotine, caffeine and recreational drugs. ^[1][6] Panic disorder is also frequently accompanied by other anxiety disorders, including agoraphobia and specific phobia. ^[1][7]

No single cause has been established. The picture is a biopsychosocial one: genetic liability, temperamental risk (high neuroticism, high anxiety sensitivity), a biological sensitivity to internal bodily signals, and adverse life experiences all contribute. ^[3][4]

Genetic and temperamental factors. Family history raises risk, and twin studies support a polygenic basis. Candidate genes in serotonergic and noradrenergic systems, such as the serotonin transporter and the serotonin 2A receptor genes, have been associated with panic disorder. ^[4] High anxiety sensitivity (fear of bodily sensations) is a well-described cognitive risk factor. ^[7]

Developmental and environmental factors. Abuse, severe loss and other adverse experiences increase risk for anxiety disorders. ^[3] Smoking and substance misuse worsen prognosis and complicate treatment; heavy cannabis use increases risk of psychotic outcomes in some, though the direct causal picture for panic is less clear. ^[6]

Medical and pharmacological triggers. Thyrotoxicosis, pheochromocytoma, arrhythmia, asthma, hypoglycaemia and mitral valve prolapse can produce episodes indistinguishable from panic attacks. Stimulants (cocaine, amphetamines), high-dose caffeine and some medications (for example corticosteroids) can also trigger attacks. ^[1][6][7]

A learning model. Panic disorder is plausibly learned. The first attack is conceptualised as activation of an innate circa-strike defence response to unconditioned internal threats (such as a suffocation alarm). Later, mild bodily sensations are conditioned to the same response, producing anticipatory anxiety and situational avoidance. ^[4]

The current neurobiological model of panic disorder rests on a fear circuit in the brain that detects threat, mounts a response, and normally switches off. In panic disorder that circuit appears to be sensitised and under-controlled. ^[4]

Gorman's neuroanatomical theory, the most cited framework, proposes that panic attacks arise from increased activity of noradrenergic neurons in the locus coeruleus, an arousal relay in the brainstem. Anticipatory anxiety is linked to limbic structures, and phobic avoidance linked to the prefrontal cortex. Treatments fit this picture: SSRIs may dampen amygdala output to subcortical structures, and cognitive behaviour therapy may decondition contextual fear and strengthen the prefrontal inhibition of the amygdala. ^[4]

The central nucleus of the amygdala is a hub in the circuit: it receives viscerosensory input via the thalamus, integrates it, and drives autonomic, endocrine and motor responses (rapid breathing, tachycardia, catecholamine surge) through outputs to the hypothalamus, brainstem and autonomic centres. The periaqueductal gray mediates the innate freeze or flight response; the bed nucleus of the stria terminalis sustains anxiety to uncertain threat and is implicated in agoraphobia. ^[4]

The hippocampus mediates contextual fear learning. It regulates risk assessment and the consolidation of fear memories; damage or dysfunction here disrupts the prediction of aversive events. ^[4]

Neurochemical modulation. Serotonin originating in the dorsal raphe nucleus modulates anxiety and panic, with dysregulated inhibition of dorsal periaqueductal gray linked to spontaneous attacks; GABA deficits and dysfunctional inhibitory circuits lower the threshold for panic. The endogenous opioid system may set the threshold for a suffocation alarm, with dysfunction linked to spontaneous attacks. ^[4]

Respiratory sensitivity. Panic patients appear oversensitive to carbon dioxide and lactate, consistent with an internal suffocation alarm. ^[4] The insula and anterior cingulate cortex detect and evaluate these internal threats. ^[4]

This model explains the time course: a panic attack occurs too fast for cortical thinking to be in charge, and treatments work by raising the threshold and breaking the conditioned loop. The model is imperfect and much of the evidence comes from animal and imaging studies; no blood test or scan diagnoses panic disorder. ^[4][6]

Patients rarely come saying "I have panic disorder". They arrive in casualty with chest pain, or to a GP with breathlessness, or to a neurologist with "dizzy spells". Ask for the full event and its aftermath.

A panic attack is an abrupt surge of intense fear or discomfort that peaks within minutes and includes physical and cognitive symptoms such as the following (paraphrased from DSM-5-TR): palpitations or racing heart, sweating, trembling or shaking, sensations of shortness of breath or smothering, feelings of choking, chest pain or discomfort, nausea or abdominal distress, dizziness or faintness, chills or heat flashes, paraesthesia (numbness or tingling), derealisation or depersonalisation, fear of losing control, fear of dying. ^[7]

Most attacks rise and fall over minutes rather than hours. ^[7] They may occur unexpectedly (out of the blue) or in response to a cue. Between attacks the person is healthy; the anticipatory anxiety, not the attack, causes the impairment.

A woman in her mid-twenties who repeatedly attends emergency care with chest pain, normal investigations and a feeling of impending doom often has panic disorder. The danger is to send her home with only reassurance once; the opportunity is to identify it early, because a panic attack treated in A&E can limit the development of panic disorder. ^[1]

Agoraphobia. The story centres on places: the person cannot be on a bus, in a queue or in a shopping centre because escape would be hard if an attack came and they fear being embarrassed. The feared outcome is an attack, illness, or being unable to escape; avoidance is wide and predictable. ^[3]

Social anxiety disorder. The story is of being seen and judged: blushing, voice shaking, freezing in meetings, avoiding presentations, drinking before social events to get through. Fear of embarrassment, humiliation or rejection. ^[2][3]

Specific phobia. One well-defined trigger, immediate intense fear, avoidance that can be absolute (flying, needles, animals), and recognition that it is excessive. ^[7]

General and cardiovascular examination must be thorough the first time to exclude coronary, arrhythmic, respiratory or endocrine causes. Repeat if new symptoms appear. Look for pallor, tremor, tachycardia, sweating and hyperventilation. ^[1][7]

Mental state examination. Document anxiety, affect, speech, thought content (especially catastrophic interpretations), perception (derealisation or depersonalisation), cognition and insight. Risk assessment for self-harm, suicide and substance use is obligatory at every contact. ^[1][7]

Hyperventilation can be diagnosed when rapid, deep breathing produces peripheral tingling and circumoral numbness; it can cause tetany if severe. Slow breathing is both a clue and a test of improvement. ^[7]

Panic disorder does not rule out physical disease; it is a diagnosis made after dangerous causes have been considered, and every new or changed symptom deserves re-review. ^[1][6]

No investigation confirms panic disorder or any phobia. Tests are used to exclude organic causes, to arrange safe pharmacological treatment and to monitor. ^[1][6]

For monitoring, NICE recommends short self-completed questionnaires such as the panic subscale of the agoraphobic mobility inventory. ^[1]

Definitions below are paraphrased from DSM-5-TR and should be checked against the original text. ^[7]

Panic disorder. Recurrent, unexpected panic attacks; at least one month afterwards of either persistent concern about further attacks or their consequences, or a maladaptive change in behaviour related to the attacks; and these are not better explained by another medical or psychiatric condition. ^[7]

Agoraphobia. Marked fear or anxiety about two or more of the characteristic situations (public transport, open or enclosed spaces, standing in line or crowds, being outside home alone), almost always provoking immediate fear, leading to avoidance or enduring with intense fear, persisting for at least several months and causing impairment. Its entry criterion is fear of escape difficulty or helplessness rather than of another outcome. ^[7]

Social anxiety disorder. Fear or anxiety about social situations with possible scrutiny, fear of negative evaluation, persisted usually for several months or more, with avoidance or endurance and impairment. ^[7]

Specific phobia. Marked fear, anxiety or avoidance in the presence of a specific object or situation, with immediate fear response, disproportion, persistence over months, and significant distress or impairment. ^[7]

Severity. There is no validated laboratory stage, but Clinically, severe panic disorder is marked by frequent or disabling attacks, extensive avoidance, agoraphobia that restricts life at home, comorbid depression or substance misuse, or suicidal thinking, and by non-response to at least two trials. ^[2]

The management section is adapted to three named guidelines: NICE CG113 (last updated 15 June 2020) for panic disorder, NICE CG159 (last reviewed 21 May 2024) for social anxiety disorder, and the APA Practice Guideline for the Treatment of Patients With Panic Disorder, 2nd edition (2009). ^[1][2][6] For low-resource and non-specialist settings, the WHO mhGAP programme names generalised anxiety disorder and panic disorder as priority conditions. ^[3]

A single panic attack is frightening but self-limiting. ^[1]

• In A&E or general settings, NICE (2004 framework, retained) recommends: ask whether the person is already receiving treatment for panic disorder; perform the minimum investigations needed to exclude acute physical problems; usually do not admit to a medical or psychiatric bed; refer to primary care; give written information about panic attacks and the referral. ^[1]
• Calm environment and explanation. Reassurance is legitimate (it is not a heart attack) combined with an admission that the symptoms were very real.
• Breathing technique. Slow nasal breathing against gently pursed lips, not paper-bag rebreathing.
• Do not routinely tranquilise with benzodiazepines; sedation delays diagnosis and produces a withdrawal-driven rebound. ^[1]

Step 1 is recognition, assessment and education, with active monitoring for less severe cases. Education about the nature of panic attacks is itself therapeutic. ^[1]

Step 2 (mild to moderate disorder) offers low-intensity interventions: individual non-facilitated or facilitated self-help, often based on CBT principles, support groups, exercise as part of general health and education about prescribed medicines. ^[1]

Step 3 (moderate to severe disorder, with or without agoraphobia) considers referral for cognitive behaviour therapy or an antidepressant when the disorder is long-standing or the person has not benefited from or has declined psychological intervention. ^[1]

Steps 4 and 5 move to specialist mental health teams with complex case management, comorbidity treatment and alternative or augmented therapy. In most instances, referral is appropriate if two treatment trials have not produced significant improvement. ^[1]

CBT is the psychological treatment with the strongest evidence for panic disorder and phobias. ^[1][2][3]

Panic disorder (NICE CG113).

• CBT should be delivered only by suitably trained and supervised people closely following empirically grounded protocols. ^[1]
• 7 to 14 hours of CBT in total is the optimal range; break points exist for briefer (about 7 hours, integrated with self-help) or intensive shorter courses. ^[1]
• For most people, weekly sessions of 1 to 2 hours, completed within a maximum of 4 months. ^[1]
• The content includes cognitive restructuring (understanding catastrophic misinterpretation of bodily sensations), interoceptive exposure (provoking sensations deliberately to show they are not dangerous), behavioural experiments, and in vivo exposure to feared places and situations; and relapse prevention. ^[1][4]

Social anxiety disorder (NICE CG159).

• Individual CBT specifically developed for social anxiety disorder is first-line; group CBT is less cost-effective and is not routinely offered in preference. ^[2]
• The Clark and Wells model runs to up to 14 sessions of 90 minutes over about 4 months; the Heimberg model runs 15 sessions of 60 minutes plus one 90-minute exposure session. ^[2]
• Supported self-help continues up to 9 sessions over 3 to 4 months when it is more acceptable. ^[2]

Specific phobias. Exposure therapy is the core, with systematic desensitisation or one-session flooding and cognitive restructuring; high-intensity, focused formats can be delivered in one to a few sessions. NICE specifically advises against routine computerised CBT for specific phobias in adults. ^[2]

The rationale for exposure is central. Avoidance keeps panic going because it prevents the prediction error that disconfirms catastrophic belief; exposure produces habituation and new safe learning. The fear-circuit models support this: prefrontal inhibition of the amygdala is strengthened by repeated, non-catastrophic experience. ^[4]

Panic disorder (NICE CG113).

• Antidepressants are the only pharmacological intervention recommended for longer-term management. ^[1]
• SSRIs are first-line. At the 2020 amendment of CG113, the SSRIs and SNRI licensed for panic disorder were escitalopram, sertraline, citalopram, paroxetine and venlafaxine. ^[1]
• Benzodiazepines, sedating antihistamines and antipsychotics should not be prescribed for panic disorder. ^[1]
• Start at the bottom of the range and titrate slowly; transient increased anxiety at the start is expected and explained. ^[1]
• If an SSRI is unsuitable or no improvement is seen after 12 weeks, consider imipramine or clomipramine (tricyclics), taking into account overdose risk, side-effect profile and interactions. ^[1]
• If there is no improvement after 12 weeks, offer an alternative class antidepressant or another form of therapy. ^[1]
• Where there is partial response, add a high-intensity psychological intervention. ^[1]

Dose example. A US product label for sertraline recommends 25 mg once daily initially in panic disorder, then 50 mg after one week, with titration in weekly increments and a therapeutic range of 50 to 200 mg once daily, maximum 200 mg. ^[5] This is one labelled example; prescribers must follow the product label and local formulary for each agent. ^[1][5]

Social anxiety disorder (NICE CG159).

• SSRI first-line, specifically escitalopram or sertraline when the person chooses or declines psychological intervention. ^[2]
• Alternatives if no response or poor tolerability: fluvoxamine or paroxetine, or SNRI venlafaxine. Phenelzine or moclobemide are reserved for later. ^[2]
• Benzodiazepines, tricyclics, anticonvulsants and antipsychotics are not routinely offered; St John's wort and over-the-counter anxiety preparations are avoided. ^[2]

Social phobia and "beta-blockers". Beta-blockers are not recommended for generalised panic or social anxiety disorder in its broad form, but they are used pragmatically for performance situations (public speaking, examination nerves) at small single doses on an as-needed basis; evidence for this comes only from clinical experience, not from NICE guidance. ^{[6] [3]}

Monitoring and duration.

• Review efficacy and side effects within 2 weeks, then at 4, 6 and 12 weeks; continue 8- to 12-weekly if treatment continues. ^[1]
• If improved, continue for at least 6 months after the optimal dose is reached, then taper. ^[1]
• Stop gradually over an extended period and warn about discontinuation symptoms (dizziness, paraesthesia, gastrointestinal upset, headache, sweating, anxiety, sleep disturbance). ^[1]
• For adults under 30, warn of increased suicidal thinking and self-harm risk, see weekly in the first month and within one week of prescribing. ^[1][2]
• For people aged 30 and above who are not assessed as suicide risk, see within 1 to 2 weeks of first prescribing. ^[2]
• Consider the increased bleeding risk on SSRIs, especially with NSAIDs, aspirin or anticoagulants. ^[1]

Combination treatment is reasonable for partial response: CBT plus medication. ^[1][2]

Specialist referral (NICE CG113). Offer referral after two trials without significant improvement, and to manage complex comorbidity, agoraphobia with marked impairment, self-neglect, risk of self-harm or substance misuse. ^[1]

• Education and accurate information about panic attacks so the person stops attributing them to catastrophe. ^[1]
• Supported self-help, exercise and graduated daily activity. ^[1][3]
• Identify and reduce maintaining factors, such as excessive caffeine, stimulants and avoidance. ^[1][6]
• Support groups and bibliotherapy as adjuncts. ^[1]

Children and adolescents. For social anxiety disorder, first-line CBT (individual or group, 8 to 12 sessions of 45 or 90 minutes) and involving parents. Pharmacological treatment is not routinely offered. ^[2] Panic disorder in children is managed with age-adapted CBT; sertraline is only licensed for paediatric obsessive-compulsive disorder under US labelling, so medication in under-18s should be under specialist care. ^{[5] [1]}

Older adults. Start lower and titrate slowly, and consider side effects carefully, including hyponatraemia and QT prolongation, and interactions with other medicines. ^[5][6]

Pregnancy and breastfeeding. Treat severe illness rather than stop treatment abruptly. Psychological interventions first if feasible; if medication is needed, SSRIs such as sertraline are used after multidisciplinary discussion, with awareness of neonatal withdrawal and bleeding risk. Benzodiazepines are avoided. ^[1][6]

Non-specialists can recognise panic and phobia with the WHO mhGAP approach: assess, ensure safety, provide psychoeducation and a low-dose SSRI where available, and refer when possible. ^[3] CBT-based self-help and problem solving (PM+) and Doing What Matters materials are available from WHO at no cost. ^[3] Where ECG and laboratory monitoring are unavailable, use clinical monitoring, a single cheap SSRI at the lowest effective dose (often sertraline where available), gradual titration and urgent referral for suspected serotonin syndrome or cardiac symptoms. ^[1][5]

• Chronic panic and phobia with avoidance; restriction of life, agoraphobia, not leaving home.
• Depression and other anxiety disorders.
• Substance misuse, particularly alcohol and benzodiazepine reliance, which worsens outcome.
• Suicide risk from secondary depression and from panic-driven hopelessness; monitor.
• Medically: unnecessary investigations and presentations; iatrogenic harm from recurrent urgent attendances.
• Tachyphylaxis, withdrawal and relapse on stopping treatment if it is too early. ^[1]

With adequate treatment, many people recover completely. NICE targets complete relief of symptoms (remission) because it predicts better functioning and lower relapse. ^[1] SSRI and CBT trials are assessed over a three-month horizon, and relapses are more likely after premature discontinuation. ^[1][5]

There is no universal screening instrument for panic disorder; diagnosis relies on consulting skills and a careful history. ^[1]

• Early recognition after a first attack in A&E limits the development of disorder. ^[1]
• Treat comorbidities and substance misuse.
• Avoid unnecessary combined anxiolytic and sedative prescribing; benzodiazepine avoidance from the outset reduces long-term harm. ^[1]
• Physical health promotion matters because anxiety increases cardiovascular and other diseases. ^[3]

• Generalised anxiety disorder (GCO not yet verified)
• Depression and other mood disorders
• Psychosis and substance use
• Chest pain and palpitations (differential)
• Hyperventilation and respiratory physiology