Cbt: Panic

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Time Parameters of Panic

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1) Panic Attack peaks within 10 minutes or less 2) Usually doesn’t last for more than 30 min

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Physical Sxs of Panic

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1) need 4 or more

2) Shortness of breath

3) Dizziness/lightheaded

4) Palpitations/tachycardia (heart racing)

5) Sweating

6) Choking

7) Parasthesias (numbness, often around mouth andextremities)

8) Nausea/abdominal distress 9) Depersonalization/derealization

9) Hot flushes/chills

10) Chest pain/discomfort

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· Cognitive Sxs of Panic

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1) Fear of dying

2) Fear of going crazy

3) Fear of doing something uncontrolled

4) Urge to flee

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DSM Criteria for Panic D/O

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1) recurrent, unexpected panic attacks

2) at least one of the attacks has been followedby

a) persistent worry about having more attacks ortheir consequences (i.e. a panic attack might give me a heart attack)

b) a significant change in behavior (aka agoraphobia)

c) not attributable to a medical condition

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Hx of Panic D/O

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1960s: 1st recognized and differentiated from other anxiety disorders

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Panic DO Rule Outs

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for women: thyroid disorder

mid-older age: heart disease

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PD and Agoraphobia Comorbidity

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1) 1/3-1/2 of PD has Agoraphobia

2) in clinical settings, majority are comorbid

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Agoraphobia (Define)

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fear or avoidance of a range of situations fromwhich escape might be difficult (or embarrassing) or in which help may not beavailable in the event of having an unexpected or situationally-predisposedpanic attack or panic-like sxs

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Impairment in PD

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Substance abuse

1) Suicide attempts (more common when comorbid wdepression

2) Social, Marital, Vocatinoal fx

3) Physical and emotional health problems(somatically preoccupied)

4) Use of med and psych care

5) Work absenteeism (2x higher than other pts) 6) More impairment than chronic/terminal medicalpts

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Nocturnal Panic Attacks

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1) Occurs in app 50% of individuals w PD

2) Tend to occur between 1-4 hours after onset ofsleep, during transition into slow-wave sleep (delta, low BP, HR, respiration)

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Prevalence Community Samples:

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22% of general population (in the absence ofanxiety d/o)

lifetime prevalence: 1.5-3.5%

12-month prevalence ranges from .5-1.5%

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Prevalence Clinical Samples:

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1) 10% referred for mental health have PD

2) 10-30 presenting at general medical clinics

3) 60% of those presenting to cardiology clinics!! 4) vast majority present w agoraphobia

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Women

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1) 1.3 times more frequently among individuals without agoraphobia

2) 3-4 times more frequent agoraphobia w PD among women

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Cultural Groups

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1) Epidemiological studies: similar rate of PD inEA,AA,HA groups

2) Clinical Samples: AA under-represented, tend tohave a later age of onset, may use different coping strateiges (i.e. substanceuse)

OTHER NAMES

3) Brain fag: West Africa

4) Ghost sickness-Navajo

5) Shenjing shuaruo and shenkui-China

6) Sore Neck Syndrome-Cambodia (cultural belief ofoverload of wind is fatal, main fear is too much wind)

7) “attaq de nerviosa”--Latin American

(followed by cursing, falling to the floor ormemory loss, less cultural stigma, more support)

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Typical Onset

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1) early twenties (may occur late adolescence or inmid-thirties)

2) few ppl under 16 or over 45

3) agoraphobia typically occurs within the firstyear following a PA

4) linked to recent stress, life-change (going tocollege, loss etc.)

5) chronic condition (*can also be triggered by weed)

6) waxes and wanes over individual’s lifetime (ifnot treated)

7) episodic and continuous courses have beenreported in a minority of cases

8) higher rates of recovery reported in individualswithout agoraphobia (agoraphobia maintains panic)

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Genetic/Bio Factors(**see Sanderson article**)

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1) genetic studies

2) lab provocation models

3) respiratory

4) moderate genetic loading BUT non-specific biovulnerability (i.e. gene for reacting to stress but not specifically w panic)

5) 8x more likely in first-degree relatives

6) 50-75 do not have an affected family member

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Hyperventilation Theories

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1) dysfunctional suffocation monitorfalsesuffocation alarm -->hyperventilation

2) fear of having a panic attack --> physicalsxs --> increasefear --> hyperventilation --> panicattack (Cognitive Model)

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NeurotransmitterTheories

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1) Dysregulation in the noradrenergic, serotonergic and benzodiazepine systems

2) Proposed on the basis of tx response to antidepressants and benzodiazepines

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Evolutionary Models of Panic

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1) Fear is an unconditioned response to a dangerous situation

2) Sensitivity to certain stimuli or conditions (heights, trapped in closed spaces, open spaces etc.) all adaptive to fear

3) triggers the Fight or flight response

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Comorbid Conditions

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1) 50% will have a comorbid conditions (usually a reactive depression)

2) Depression (25%)

3) Anxiety D/O (16% GAD, 15% SAD, 15% SP)

4) Personality (25-65 Dependant, ?, Hystrionic)

5) Alcohol or other substance use (15%)

6) Comorbid conditions improve w tx of PD

7) Mitrovalve Prolapse (open flap in heart)

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Differenctial Dx

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1) Endocrine/Hormonal

2) Neurological/Muscular

3) Aural (i.e. vertigo, Meunier’s disease)

4) Hematic (anemia)

5) Cardiac conditions (i.e. arrhythmias) supraventricular, tachycardia)

6) Respiratory (asthma)

7) Drug-related (withdrawal from CNS depressants alcohol,barbituates, CNS stimulants)

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Differential Anxiety Disorders

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1) SAD: only in social or performance situations

2) Specific phobia

3) OCD: only when exposed to the stimulus that isthe context

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CBT Model of Panic

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1) adaptive nature of fears in primitive environmentsgone awry

2) interoceptive stimuli become perceived asfearful via classical conditioning or cog misappraisal (i.e. “I’m having aheart attack” or “I’m going crazy”) --> PA

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Cognitive Model of Panic

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1) Misinterpretation of arousal leads to PA

2) Anticipatory anxiety about having future attacks

3) Anxiety and avoidance of an increasing number situationsthat are associated with the risk of anxiety or somatic arousal

**misappraisal iskey**

ex: Internal/External Trigger (sweating) --> Perceived Threat (I’m going to have a PA) --> Anxiety --> catastrophic misinterpretation (I’m going to die) moresxs --> PA

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Behavioral Model of Panic

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1) Mowrer’s 2 stage Theory

2) Dev of fear: classical conditioning

3) Maintenance of fear: operant conditioning(avoidance -->relief,reinforcing)

4) Generalization

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Cognitive Biases in PD

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1) Initial misinterpretation (overestimating negoutcomes) focused on the likelihood of having a panic attack ( ex: I’m going to havea PA instead of, I walked up the stairs, that’s why I’m sweating)

2) Second level (catastrophic thinking) focuses onthe catastrophic misinterpreations: I’m going to die

3) Underestimation of ability to cope

4) Self-criticism for having panic

5) Assume never get better (hopelessness, depression)

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Consensus Statement by NIH of EST (9/27/91)

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1) TCA-tricyclic

2) MAOIs

3) High potency benzodiazepines (small, potentbenzo) contraindicated for CBT

4) CBT

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Pharmacotherapys

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80-90% of ppl w meds or CBT alone will getbetter!

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Probs w Meds:

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1) substantial proportion respond eitherincompletely or not at all

2) lead to side-effects and or withdrawal

3) high dropout and relapse rate

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CBT Txs

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1) David Barlow: Panic Control Tx (mainly behavioral)

2) David Clark: Cognitive Therapy

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Is CBT effective?

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1) 75-90% response rate

2) reduce all sxs of PD and agoraphobia

3) 50-70 percent of pt with mild agora fx as wellas normal controls following tx

4) 85-100 % of pt are completely panic free

5) as effective or more effective than meds(depending on study)

6) effective even w comorbid conditions

7) comorbid onditions improve w tx of PD

8) pts w moderate to severe agoraphobia respondless well than those w mild agoraphobia but continue to improve over time,especially when family members of friends are involved in tx

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Do components of CBT Differ in Efficacy?

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1) Exposure and Cognitive restructuring is MOREEFFECTIVE than applied relaxation (acutely and at 2 year follow-up in 2 out of3 studies)

2) Combined tx didn’t enhance gains

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Do effects of CBT last?

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1) 75-85% of pt are panic free at follow-up (6 mo --> 2 yr)

2) does seem to taper off after 2 years (60% in one study from 83%)

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Mechanisms of Change in CBT

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1) AT change over the course of CBT

2) Changes in cognitions are correlated w sxreducation (cognitive change must come before) 3) Disconfirmation of appraisals appears to be themechanism of change in exposure