Prof c tennant PTSD september

ONE YEAR RISK OF PTSD with specific traumas ---Any trauma causing PTSD 1.9 2.9%... PSYCHOLOGICAL SEQUELAE OF TRAUMA PSYCHOLOGICAL SEQUELAE OF TRAUMA • DEPRESSION is far more common tha

Prof Chris Tennant

RNSH- 2005

PTSD: UPDATE

LIFETIME COMMUNITY BASED ESTIMATES of

LIFE TIME PREVALENCE

(Creamer 2001)

LIFE TIME PREVALENCE

OF TRAUMA (in Australia)

Shock (other person) 9.8 12.0

Accident (life threat) 28.3 13.6

Witness (injury etc) 37.8 16.1 Natural disaster 19.9 12.7

ONE YEAR RISK OF PTSD with specific traumas

-Any trauma (causing PTSD) 1.9 2.9%

Prof Chris Tennant

TRAUMA PTSD

PSYCHOLOGICAL SEQUELAE OF

TRAUMA

PSYCHOLOGICAL SEQUELAE OF

TRAUMA

• DEPRESSION is far more common than PTSD.

(Particularly so for Civilian Vs Military Trauma ).

•PTSD is “Relatively” uncommon following trauma.

One year relative risk (Australia]

In Men: 1.9%

In Women: 2.9%

•BRIEF PSYCHOSIS also occurs

e.g East Timor: 1.3%

•EXPLOSIVE ANGER : follows Human Rights Violations

e.g E Timor: 40% (minimum 1 episode per month)

(average 2-3 episodes)

“SYMPTOM RISK” WITH SPECIFIC

TYPES OF TRAUMA

“SYMPTOM RISK” WITH SPECIFIC

TYPES OF TRAUMA

• Acute unpredictable trauma (e.g rape, MVA)

“Reliving” is more common

Dissociation is also common

• Chronic Trauma

Depression, anxiety are more common

Specific effects on sleep

“Administrative” stress – poor global sleep.

Critical incident stress – broken sleep

[nightmares]

VARIANCE IN PTSD SYMPTOMS DUE TO

VARIANCE IN PTSD SYMPTOMS

DUE TO COMBAT

TWIN STUDIES

EXPOSURE SEVERITY AND

VARIANCE IN PTSD in

FIREFIGHTERS

(McFarlane 1988)

(Table 3) (4 months after)

EXPOSURE SEVERITY AND

VARIANCE IN PTSD in

FIREFIGHTERS

(McFarlane 1988)

(Table 3) (4 months after)8%

* Small relation of immediate emotional impact to PTSD

* Trivial relation of “fire stress” exposure to PTSD

* Minimal relation of “fire stress” to emotional impact “distress”

+ (most of the variance due to ‘non trauma’ factors)

** Similar to other studies (8% variance: Tennant and Andrews 1978)

OTHER SUBSTANTIAL VARIABLES INFLUENCING

PTSD

OTHER SUBSTANTIAL VARIABLES INFLUENCING

PTSD

1 Genes

2 Personality

3 Other Psychiatric disorders

4 Other life events

5 Childhood factors

1 Military [ combat exposure ] (Lyon s 1993)

Genes explain 35 - 47% of variance in

combat exposure

2 Civilian population (Male,Female) (Stein 2002)

Genes explain “assaultative” trauma

(but not“non assaultative” trauma)

GENES and TRAUMA

TWIN STUDIES

Variance explained by genes

Avoidance - 30-34%

Re experiencing - 13-30%

GENES and PTSD SYMPTOM CLUSTERS

TWIN STUDIES (True 1993)

RR of conduct disorder in PTSD = 2

RR of antisocial personality in PTSD = 5

Conduct disorder and also correlated with Antisocial personality

•When personality was controlled :

• Combat did not predict PTSD [Gulf war ]

PERSONALITY DISORDER and PTSD

TWIN STUDIES

(Koenen 1999)

1 Genes common to D.D  56% comorbid AD

and PTSD

1 Genes common to A.D  25% comorbid

PTSD

3 Family environment  34% drug

COMORBID DRUGS (AD and DD) and PTSD

TWIN STUDIES

“Re experiencing”  0.4% variance

PROF C TENNANT

PTSD (30% “maximum”) Accounts for significant co morbidity

(Personality Disorder, Anxiety, D & A)

OTHER LIFE EVENTS and

 Genes (35-47%) (Lyons 1993)

 Personality disorder (Koenen 1992)

 FH, D & A, conduct disorder (Koenen 200)

 Earlier life events (King 2000)

 Earlier trauma (Bresalue 1995)

PTSD AND TRAUMA

(HAVE COMMON RISK FACTORS) PTSD AND TRAUMA

(HAVE COMMON RISK FACTORS)

DRUG TREATMENTS OF PTSD

Prof Chris Tennant

DRUG TREATMENT OF PTSD

-Hyper arousal, mood: significant reduction - Re-experiencing, avoidance: less effective.

Small effect on hyper arousal, re-experiencing.

nightmares, [problems with hypotension and rebound hypertension on ceasing] (Prazosin, Propananol,

Clonidine)

outcomes Prevention of PTSD? No evidence for

Prof Chris Tennant

SSRI’s were most commonly studied

 Greater in combat PTSD than civilian PTSD

(probably due to chronic/repetetive trauma or chronicity of PTSD itself).

 Severity of PTSD symptoms correlates with memory problems.

 Not due to comorbid depression or alcohol.

 What is cause, and what is effect?

UNDERLYING NEUROBIOLOGY AND

COGNITIVE BEHAVIOURAL

TREATMENTS

COGNITIVE BEHAVIOURAL

TREATMENTS

Traumatic Event is paired with a ‘neutral’ stimulus (reminders, recollection)

and Cognitive and Behavioural

Avoidance

“New learning” (extinction) is the basis of CBT.

Prof Chris Tennant

COGNITIVE BEHAVIOUR THERAPIES COGNITIVE BEHAVIOUR THERAPIES

1 COGNITIVE THERAPY

Socratic questioning and challenge maladaptive beliefs.

Efficiency : most studies show some benefit.

2 EXPOSURE THERAPY

Exposure allows emotional reprocessing/re-learning.

Efficiency: clinically most effective treatment.

3 (Combined) CBT

Efficiency: consistently clinically effective.

4 EMDR

Efficiency: Clinically effective (exposure)

[ Value of Eye Movement is uncertain ]

5 COPING SKILLS (Stress treatment ,Assertiveness training Relaxation

exercise, Sleep hygiene).

Efficiency: No evidence.

MDMA (ECSTASY) ASSISTED

“EXPOSURE”

MDMA (ECSTASY) ASSISTED

“EXPOSURE”

(+ 90 minute follow up at 24 hours)

3 weeks of weekly follow up.

CAPS PTSD scale scores (baseline 79)

EFFECTS OF MDMA (ECSTACY) EFFECTS OF MDMA (ECSTACY)

1) Increases in Serotonin Improved

EFFECTS OF MDMA (ECSTACY) EFFECTS OF MDMA (ECSTACY)

2) INCREASES IN DOPAMINE AND NORADRENALINE

Increases: Alertness/ Arousal

- (Improves recall; “Optimal Arousal Zone”)

3)INCREASES IN ALPHA RECEPTOR ACTIVITY

Increases: Relaxation

- (Improved mental alertness)

4) OXYTOCIN AT HYPOTHALAMUS

Increases: Oxytocin

- (Improves empathy, closeness)

Prof Chris Tennant

OTHER ADJUNCTS TO THERAPY ?

 D-CYCLOSERINE Enhances learning

(Agonist at NMDA receptors (i.e extinction)

i.e glutaminergic activity)

*Strong Animal Research

*Strong Human Research:

only in social anxiety/phobia.

 CORTICOSTEROIDS “Reduces Avoidance” in PTSD

(No positive long term effects however)

• Stress Education: No value

• Very early CBT: No preventative effects

IN THE MILITARY

• Trauma Risk Management (TRIM (UK)

(Symptom identification, structural interview and

subject encouraged to access psychological help) Minimal effects

• Battlemind (USA)

(Normalises reactions to trauma i.e education).

Minimal effects

HIPPOCAMPUS AND HPA (GLUCOCORTICOIDS) IN PTSD

HIPPOCAMPUS AND HPA (GLUCOCORTICOIDS) IN PTSD

I Animal Experimental Studies

I Stressors

II Glucocorticoids All Correlate

III Hippocampus Loss

IV Memory Deficits

HUMAN STUDIES OF PTSD AND

Have poorer Hippocampal blood flow.

(During memory tasks) (Not at rest).

Hippocampal changes are associated with memory problems +

Hippocampal Memory Problems are of ‘Retention’ (not “Acquisition”)

Have reduced N-Acetyl Aspartate

(Which is a marker of neuronal integrity).

These changes are not observed in kids with PTSD.

PREFRONTAL CORTEX AND CATECHOLAMINES

IN PTSD (Function is ‘Acquisition and Learning’ i.e

working memory).

PREFRONTAL CORTEX AND CATECHOLAMINES

IN PTSD (Function is ‘Acquisition and Learning’ i.e

working memory).

• Stress  Glucocorticoid and Catecholamine Released in the PFC

• G/C and C/A  Reduced Working memory

 Reduced Executive function  Reduced Emotional

ARE COGNITIVE CHANGES AND BRAIN CHANGES A CAUSE OR EFFECT OF

Are these impairments a risk factor for PTSD*?

* MZ Twins Discordant for Combat trauma or PTSD

– Had similar verbal memory impairments

– Had similar (smaller) Hippocampi

So poorer Neurocognitive function is risk factor for PTSD

Seems both cause and effect (i.e “Downward

Spiral”).