PANIC DISORDER

BY DR. FATIMA
TRAINEE RESIDENT
DEPARTMENT OF PSYCHIATRY & BEHAVIORAL SCIENCES
HMC, MTI, PESHAWAR
PANIC ATTACK

 A discrete period in which there is the sudden onset of intense apprehension,

fearfulness, or terror, often associated with feelings of impending doom
 During these attacks symptoms such as shortness of breath, palpitations, chest
pain or discomfort, choking or fear of “going crazy” or feeling of losing control
are present
PANIC DISORDER

 Recurrent panic attacks, which are not secondary to substance misuse, medical
condition or another psychiatric disorder
 Frequency of panic attacks may vary from many attacks a day to very few a year
 Usually there is a persistent worry about having another attack or about
consequences of the attack and significant behavior changes related to the attack
CLINICAL PICTURE

 Symptoms associated with panic attacks in the order of frequency of occurrence

are;
 Palpitations
 Sweating
 Trembling or shaking
 Sense of shortness of breath
 Feeling of choking or difficulties swallowing (Globus hystericus)
 Chest pain or discomfort
CLINICAL PICTURE

 Nausea or abdominal discomfort

 Dizziness or light headedness
 Derealization or depersonalization
 Fear of losing control or going crazy
 Fear of dying (angor animus)
 Numbness or tingling sensations (paresthesia)
 Chills or hot flushes
CLINICAL PICTURE

 Concerns about death from cardiac or respiratory problems may be a focus,

leading to patients often presenting to emergency medical services
 Thoughts of suicide or homicide may be elicited; acute anxiety (particularly when
recurrent) can lead to impulsive acts
EPIDEMIOLOGY

 Life time prevalence:

 1.5 to 3.7% for panic disorder
 7 to 9% for panic attacks
 Women 2-3 times more likely to be affected
 Age of onset has a bimodal distribution
 Highest peak incidence is 15-24 years
 2nd peak of incidence at 45-54 years
 Rare after age 65
EPIDEMIOLOGY

 Other risk factors

 Being widowed divorced or separated
 Living in a city
 Limited education
 Early parental loss
 Physical or sexual abuse
COMORBIDITY
 Agoraphobia (community surveys: 30-50%; psychiatric clinic 75%)
 Depressive disorder up to 68%
 Other anxiety and related disorder up to 50% (e.g. social phobia, OCD)
 Alcohol abuse up to 30%
 Substance abuse 20%
 Bipolar affective disorder 20%
 Medical conditions (e.g. mitral valve prolapse, hypertension, cardiomyopathy, COPD, HVS, IBS,
migraine)
DIFFERENTIAL DIAGNOSIS
 Other anxiety and related disorder
 Substance or alcohol misuse/withdrawal
 Mood disorders
 Endocrine disorders; carcinoid syndrome, Cushing syndrome, hyperthyroidism, hypoglycemia,
hypoparathyroidism, pheochromocytoma
 Hematological; anemia
DIFFERENTIAL DIAGNOSIS

 Cardiac; arrhythmias, atypical chest pain, mitral valve prolapse, MI

 Respiratory; COPD, asthma, HVS
 Neurological; epilepsy especially TLE, vestibular dysfunction
INVESTIGATIONS
 No specific tests for panic disorder
 Tests should be done to rule out other conditions
 FBC
 RFTS
 Serum electrolytes
 Glucose
 TFTs
 ECG
 ECHO
 Serum calcium
 Urinary vanillyl mandelic acid (VMA)/ plasma homovanillic acid (pHVA)
 EEG
 Toxicology
AETIOLOGICAL MODELS

 THE SEROTONERGIC MODEL

 Exaggerated post synaptic receptor response to synaptic serotonin,. Possibly secondary
to receptor sub sensitivity (reduced binding) at 5HT-1A receptor and 5HT transporters,
perhaps secondary to disturbance in serotonin transporter (5-HTTLPR) and promoter
(SLC6A4) genes
AETIOLOGICAL MODELS

 THE NORADRENERGIC MODEL

 Increased adrenergic activity, with hypersensitivity to presynaptic alpha receptors

 THE GABA MODEL

 Decreased inhibitory receptor sensitivity (impaired GABA neuronal response to BZDs)
with resultant excitatory effect
AETIOLOGICAL MODELS

 THE CHOLECYSTOKININ-PENTAGASTRIN MODEL

 Pentagastrin induces panic in dose-dependent fashion in patients with panic disorder.
Gene studies also implicate CCK gene polymorphisms in panic disorder

 THE LACTATE MODEL

 Postulated aberrant metabolic activity induced by lactate, from studies involving
exercise induced panic attacks (replicated by IV lactate infusion)
AETIOLOGICAL MODELS

 THE FALSE SUFFOCATION CO2 HYPOTHESIS

 Explains panic phenomena by hypersensitive brainstem receptors. Panic disorder
occurs more frequently in individuals with raised pCO2 e.g. during sleep, during the
premenstrual period and due to respiratory disorders

 THE COGNITIVE THEORY

 Postulates that panic disorder is due to a heightened sensitivity to internal autonomic
cues such as tachycardia
AETIOLOGICAL MODELS

 THE NEUROANATOMICAL MODEL

 Panic attacks are mediated by an overactive fear network in the brain that involves the
amygdala, hippocampus, periaqueductal grey matter, locus coeruleus, thalamus,
cingulate and orbitofrontal areas
 Fear is originated in the amygdala and projected to the anterior cingulate cortex and
orbitofrontal cortex
 Other projections from amygdala to the hypothalamus mediate endocrine responses
AETIOLOGICAL MODELS

 THE GENETIC HYPOTHESIS

 Panic disorder has moderate heritability of around 25-50% (from family and twin studies)
 Vulnerability is genetically determined and is multifactorial, but critical stressors are required to
develop clinical symptoms
 Replicated linkages have been found with chromosomes 13q, 22q, 7p and 9q31
AETIOLOGICAL MODELS

 Candidate genes include ADOR2A, 10832/T, CCK and those coding for 5HT-1A, 5HT-
2A, COMT, NPY1R, MAO-A, HCRT and linked to the CRH gene
 Recent large GWAS has identified the neuropeptide S gene, the amiloride-sensitive
cation channel gene and the adenosine A(2A) genes as candidate genes, with 4q21 and
7p being considered the strongest candidate regions for panic and fear associated
anxiety disorder loci
MANAGEMENT

 PHARMACOLOGICAL:
 SSRIs: Citalopram, Escitalopram, Paroxetine and sertraline are all licensed for panic
disorder and recommended as first line by NICE
 Alternative antidepressants: SNRIs, TCAs, MAOIs and RIMAs
 Benzodiazepine: not recommended by NICE. Should be used with caution but may be
effective for severe, frequent, incapacitating symptoms
 Limited benefit: little evidence for buspirone, bupropion, mirtazapine, inositol,
reboxetine, antipsychotics, anticonvulsants and propranolol
MANAGEMENT

 PHARMACOLOGICAL:
 Second line treatment: consider changing to a different class agent, addition of BDZ,
trial of bupropion, or for severe symptoms, an SGA
 If successful: continue treatment for 12 to 18 months before discontinuation (gradually
tapering off dose over 2-4 months)
 Do not confuse withdrawal effects (10-20% of patients) with re-emerging of symptoms
(50-70% of patients)
 If symptoms recur, continue for 1 year before considering second trial discontinuation
MANAGEMENT

 PSYCHOLOGICAL
 CBT
 Psychodynamic psychotherapy

 Treatment of comorbidity
COURSE

 Most patient seeking treatment have already experienced chronic symptoms for
10-15 years
 Untreated, the disorder runs a chronic course
 With treatment, functional recovery is seen in 25-75% after the first 1-2 years,
falling to 10-30% after 5 years. Long term around 50% will experience only mild
symptoms
COURSE

 Poor response associated with;

 Severe initial symptoms
 Marked agoraphobia
 Low socio-economic status
 Less education
 Long duration of untreated symptoms
 Restricted social networks (including loss of a parent, divorce, remaining unmarried)
 Presence of personality disorder
THANK YOU