Transcript Post-Traumatic Stress Disorder
Post-Traumatic Stress Disorder
Nimalee Kanakkahewa Specialty Registrar September 2010
Reaction to severe stress, and adjustment disorders
This category differs from others in that it includes disorders identifiable on the basis of not only symptoms and course but also the existence of one or other of two causative influences: • an exceptionally stressful life event producing an acute stress reaction • significant life change leading to continued unpleasant circumstances that result in an adjustment disorder
Aetiologically defined disorders in the classificatory systems
• • • PTSD (DSM-IV, ICD-10) Adjustment disorder (DSM-IV, ICD-10) Acute stress reaction (ICD-10) Acute stress disorder (DSM-IV)
A little bit of history
• • • First appeared in the classificatory systems in 1980 in the DSM-III Initially described as a disorder secondary to a traumatic experience ‘outside the range of human experience’.
Downgraded to more appropriate definition in the DSM-IIIR. Similar to the ICD-10: ‘(event) of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in almost anyone.’
Characteristic symptoms of post-traumatic stress disorder adapted from DSM-IV
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Re-experiencing phenomena (at least one required)
Recurrent and intrusive distressing recollections - Recurrent distressing dreams Acting or feeling as if the events are recurring Intense psychological distress to cues - Physiological reactivity to cues
Avoidance and numbing (at least three required)
- Avoidance of thoughts, feelings, and Conversations - Greatly reduced interest in related activities Detachment or estrangement feelings - Sense of a foreshortened future Avoidance of reminders Psychogenic amnesia Restricted range of affect
Increased arousal (at least two required)
- Difficulty sleeping - Difficulty concentrating - Exaggerated startle response Irritability or outbursts of anger Hypervigilance
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Traumatic events
Common stressors of moderate impact (precede PTSD in 5-20%) – Diagnosis of life-threatening illness in self or loved one.
– Sudden death of loved one.
– Involvement in fire/flood/small scale natural disaster • Common high impact stressors (precede in > 20%) – Being mugged/ threatened with a weapon – Domestic violence – Rape – Childhood sexual/physical abuse • Uncommon high impact stressors – Combat – War atrocities – Large scale natural disasters.
Diagnostic criteria ICD-10
• • • Delayed and/or protracted response to a stressful event (as described before) Develops within 6 months of the stressful event.
Repetitive, intrusive recollection or re-enactment of event.
• • • Emotional numbing and detachment.
Avoidance.
Hypervigilance and hyperarousal.
(last 3 not essential for diagnosis)
Diagnostic criteria DSM-IV
Criterion A: stressor
The person has been exposed to a traumatic event in which both of the following have been present: 1.
2.
The person has experienced, witnessed, or been confronted with an event or events that involve actual or threatened death or serious injury, or a threat to the physical integrity of oneself or others.
The person's response involved intense fear, helplessness, or horror. Note: in children, it may be expressed instead by disorganized or agitated behavior.
Criterion B: intrusive recollection
The traumatic event is persistently re-experienced in at least one of the following ways: 1.
Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: in young children, repetitive play may occur in which themes or aspects of the trauma are expressed.
2.
3.
4.
5.
Recurrent distressing dreams of the event. Note: in children, there may be frightening dreams without recognizable content Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur upon awakening or when intoxicated). Note: in children, trauma-specific reenactment may occur.
Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.
Physiologic reactivity upon exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event
Diagnostic criteria DSM-IV
Criterion C: avoidant/numbing
Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following: 1. Efforts to avoid thoughts, feelings, or conversations associated with the trauma 2. Efforts to avoid activities, places, or people that arouse recollections of the trauma 3. Inability to recall an important aspect of the trauma 4. Markedly diminished interest or participation in significant activities 5. Feeling of detachment or estrangement from others 6. Restricted range of affect (e.g., unable to have loving feelings) 7. Sense of foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)
Criterion D: hyper-arousal
Persistent symptoms of increasing arousal (not present before the trauma), indicated by at least two of the following: 1. Difficulty falling or staying asleep 2. Irritability or outbursts of anger 3. Difficulty concentrating 4. Hyper-vigilance 5. Exaggerated startle response
Diagnostic criteria DSM-IV
Criterion E: duration
Duration of the disturbance (symptoms in B, C, and D) is more than one month.
Criterion F: functional significance
The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
• • •
Specify if:
Acute: if duration of symptoms is less than three months Chronic: if duration of symptoms is three months or more With or Without delay onset: Onset of symptoms at least six months after the stressor
•
ICD-10 vs DSM-IV
Clinical picture is defined more specifically in the DSM-IV • There is a minimum duration of 1 month to qualify for diagnosis in the DSM-IV.
• Distress and functional impairment are part of the DSM-IV criteria.
• There are acute and chronic specifiers.
• Syndrome can develop after 6 months of exposure. The ICD-10 accords a ‘probable’ diagnosis after 6 months. However delayed onset is very rare outside military samples.
(As a result of these references the concordance between the diagnosis of PTSD using the two sets of criteria is only 35% - Andrews et al 1999)
Epidemiology
• • • • Rates of lifetime trauma exposure are 50-90% Lifetime rates of PTSD 5-10% (Alonso et al Acta Psychiatra Scand 2004) 12 month rates 2-5% ( Kessler et al Arch Gen Psych 2005) Risk factors: – Female sex – Past and family psychiatric history – History of childhood trauma – Neuroticism
Co-morbidity
High co-morbidity rates in PTSD, up to 80% have another psychiatric diagnosis, majority following onset of PTSD. Depression and anxiety disorders Alcohol and other substance misuse/dependency.
Controversy Some have criticised the very existence of PTSD, arguing that it is a Western social construct; others acknowledge its existence but are concerned by probable overdiagnosis(e.g. Tyrer, 2005).
- Bisson JI, Advances in Psychiatric Treatment (2007), vol. 13,
119–126
Differential diagnosis
• • • • • Acute polymorphic psychosis (can be temporally related to acute stressor) Adjustment disorders Acute stress reactions Depressive and anxiety disorders Dissociative and depersonalisation disorders Distinctive clinical picture and longitudinal time course usually differentiates it from the above.
Aetiology- Genetics
• Genetic contributions to increased risk of traumatic events – Childhood adjustment, neuroticism, externalizing, personality variables. • Genetic risk of developing PTSD on exposure to traumatic events – From twin studies: approximately 30% of variance in susceptibility can be attributed to genetic factors – These genetic influences overlap with those for depression, GAD and substance abuse. – :.
Aetiology- Genetics
Candidate genes •
SLC6A4 (Sodium- and chloride-dependent members of the solute carrier family 6 - an integral membrane protein that transports the neurotransmitter serotonin from synaptic spaces into presynaptic neurons)
, locus 5 HTTLPR. Insertion deletion polymorphism in the promoter region • DRD2
(encodes the D2 subtype of the dopamine receptor)
and DAT
(Dopamine Transporter gene)
have been other candidates with less convincing evidence.
Prevalence of post-hurricane PTSD by SLC6A4 genotype, level of social support, and level of hurricane exposure in adults exposed to 2004 Florida Hurricanes. Kilpatrick et al 2007
Aetiology- Psychological factors
• Emotional processing theory: The pathological fear of memories of the traumatic event leads to avoidance, resulting in an increase of re-experiencing and arousal symptoms, which reinforce and increase fear.
People are reluctant to be in fear provoking situations because they fear that anxiety will persist until they escape, that stimuli present an unrealistic threat of causing harm, and that consequences are particularly aversive, such as going crazy or losing control.
Victims also develop views of themselves as incapable of self-protection (from future traumatic events) and normal functioning (because of an inability to control symptoms).
Aetiology – psychological factors
Aetiology- Psychological factors
•
Memory encoding:
Implicit memories of experiences are over time coded into explicit autobiographical memories.
Failure to do this means that the trauma memory persists in the emotionally charged implicit state leading to re-experiencing phenomena.
Aetiology- Neurobiology
• HPA axis: reduced basal cortisol with exaggerated cortisol suppression with dexamethasone.
• Neurotransmitters: – Increased CRF
( corticotropin-releasing factor)
, NA and endogenous opioids: increased sympathetic drive and numbing – Decreased 5-HT1A: anxiogenic • Brain structure: – Reduced hippocampal volume in brain imaging (vulnerability factor) Hippocampus – important in conscious memory formation Hippocampal lesions have been associated with a stronger fear response.
– Increased amygdala activity with decreased medial prefrontal and anterior cingulate activation (amygdala- non-conscious processing of emotionally charged memories such as autonomic aspects of the classic fear response (overactivity)
Aetiology – neurobiology contd ..
• Hippocampal dysfunction prevents adequate memory processing while increased activity in noradrenergic innervation of the amygdala increase arousal and facilitates the automatic encoding and recall of traumatic memories
Treatment
• • Acute, intermediate, chronic.
Psychological and pharmacological
Treatment options- Psychological
• • • Trauma focused CBT EMDR (Eye movement desensitization and reprocessing) Group trauma focused CBT Essentially help individual reprocess and integrate the traumatic memories. Bisson et al Cochrane review 2005
EMDR
based on the theory that bilateral stimulation (mostly in the form of eye movements) Allows the processing of traumatic memories (while the patient focuses on specific images, negative sensations and associated cognitions) bilateral stimulation is applied to desensitise the individual to these memories more positive sensations and cognitions are introduced
-Rikus H. Coetzee and Stephen Regel ,
Advances in Psychiatric Treatment (2005) 11: 347-354
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Group trauma focused CBT
Group psychotherapy has its origins in psycho-dynamic models of pathology and it developed before the practice of CBT was first outlined by Aaron Beck and colleagues ( Beck 1979 ). Importantly, group psychotherapy views the interactions between the group members as the vehicle of change. In CBT groups, it has traditionally been assumed that the cognitive–behavioural model taught to the group is more of an ‘active ingredient’ than the relationships between the group members ( Bieling 2006 ).
• In comparison to individual trauma focused CBT, the weight of research investigating trauma-focused CBT delivered in group format is very small. Nevertheless, group trauma-focused CBT was more efficacious in the evidence available (one study of a small sample) than the equivalent waiting list/usual care interventions in reducing symptoms of PTSD.
-Whitfield G, Advances in Psychiatric Treatment (2010) 16: 219-227
Treatment options- pharmacological
• • SSRIs and SNRIs have the best evidence base Paroxetine ,Sertraline, Mirtazepine.
60% respond but only 20-30% reach full remission. Cochrane reviews, NICE, Berger et al 2009.
Targeting treatment : NICE guidelines*
Early interventions: - Watchful waiting - Do not debrief, either single session or multiple. No evidence of efficacy, some evidence of harm.
Established illness -Trauma focused CBT -Medication as second line treatment
Prognosis
25% of patients continue to experience long term symptoms.
Brewin and Holmes 2003.
Acute stress reactions and disorders
Clinical features and criteria ICD-10 Acute stress reaction
• • • Exceptional stressor leading to a rapid onset of symptoms.
Mixed and usually changing picture- ‘daze’, depression, anger, anxiety with none predominant.
Rapid resolution after removal of stress or symptoms diminish with 24-48 hours if stress persists, minimal symptoms in 3 days.
ICD-10 vs DSM-IV
• DSM-IV has a category for acute stress disorder which is diagnostically very similar to PTSD but lasts at least 48 hours but no more than 4 weeks.
Treament
• • Supportive- for acute stress reaction.
Similar to PTSD for acute stress disorder.
Adjustment disorders
Clinical features and criteria (ICD-10)
• • • • Development of an adjustment reaction within one month of experiencing a stressful event.
Does not usually last more than 6 months (with exception of prolonged depressive reaction) Focus on premorbid personality and vulnerability Types – Brief depressive reaction (transient mild, no more than 1 month) – – Prolonged depressive reaction (mild, no more than 2 years) Mixed anxiety and depressive reaction – – Predominant disturbance of other emotions.
Predominant disturbance of conduct – Mixed disturbanance of emotions and conduct.
ICD-10 vs DSM-IV
• • • • DSM-IV allows the onset of syndrome to be within 3 months of stressor.
Syndrome does not persist for more than 6 months after stressor disappears If total length of syndrome is greater than 6 months- chronic adjustment disorder.
Similar subtypes.
Treatment
• • • • Not the clearest of categories Psychosocial support Brief psychological interventions.
80% have recovered in 5 years time, most with complete remission.