Stress and Memory: 2
Dr. Sarah N. Garfinkel
Brighton and Sussex Medical School
Applied Cognitive Psychology
Post Traumatic Stress Disorder (PTSD)
Vietnam veteran with PTSD related the
following memory:
.
I was a body bagger (responsible for picking up
dead bodies). We were going out in a chopper,
picking up bodies. We had overlooked a
marine who had been killed. By the time we
went out to get him he had been dead for a
week. I went to pick him up, and my arm went
right through him. I was standing there,
holding his heart, guts, and insides in my hand
Bremner and Brett, 1997
PTSD: Symptom Clusters
• Intrusion—memories of the trauma or “flashbacks” that
occur unexpectedly; these may include nightmares or
physical reactions such as a racing heart
• Avoidance—avoiding people, places, thoughts, or
activities that bring back memories of the trauma; this
may involve feeling numb or emotionless, withdrawing
from family and friends, or “self-medicating” by abusing
alcohol or other drugs
• Hyperarousal—feeling “on guard” or irritable, having
sleep problems, having difficulty concentrating, feeling
overly alert and being easily startled, having sudden
outbursts of anger
PTSD prevalence
• Statistics regarding this illness indicate that
approximately 7%-8% of people in the United
States will likely develop PTSD in their lifetime,
with the lifetime prevalence in combat veterans
and rape victims ranging from 10% to as high as
30%.
• Institute of Psychiatry in London: “Studies of atrisk groups e.g. combat veterans, victims of
natural disasters or criminal violence have yielded
prevalence rates ranging form 3% to 58%”.
Outline
• Memory for the original trauma
– Stability over time?
– Relationship between memory change and PTSD
symptoms
• Is a lack of memory for the trauma protective?
• Treat or prevent PTSD by interventions that
specifically target memory?
• Altered neurocircuitry in PTSD
– Predisposing factor vs. acquired sign?
– Can this altered neurocircuitry contribute to the
maintenance of fear memories?
Memory and PTSD
• The person experienced, witnessed, or was
confronted with an event or events that involved
actual or threatened death or serious injury, or a
threat to the physical integrity of self
• The person’s response involved intense fear,
helplessness or horror
Assessed retrospectively: Memory for the
trauma & memory for acute response to
trauma
Memory for traumatic events
• Stable and indelible vs. subject to alteration and
distortion?
“Indelible” conditioned fear responses (LeDoux, 1996; McGaugh
2003; Pitman 1989)
Reconsolidation (Nader, Schafe, LeDoux
2000a; Schiller, Monfils, Raio, Johnson,
LeDoux, Phelps 2010)
Severity of Trauma
PTSD
Interaction with vulnerability
factors [genetics, childhood abuse,
etc]
Trauma
PTSD
Interaction with vulnerability
factors [genetics, childhood abuse,
etc]
Perceived severity of
Trauma
Memory amplification and PTSD: World
Trade Center
• 2641 disaster restoration workers
during or after 9/11.
• T1 & T2 [1 year later].
• [CAPS]: re-experiencing,
avoidance/numbing & hyperarousal.
•
• WTC Exposure Questionnaire: 11
exposure variables examined:
Witnessed people jumping
from towers
Saw human remains
Concern about someone at
WTC
Knew
someone
injured
someone
•
Memory
change score:
Number of exposureKnew
variables endorsed
T2 – killed
Attended funerals / memorial
services
Assisted people affected by
attack
Displaced from residence
Evacuated for safety
Perceived life danger
Disturbed by smell
Number exposed T1
Traumatic endorsements between T1 and T2
Percentage of people
70
60
50
40
30
Increased
Decreased
No Change
20
10
0
Amplification of memory for two specific items (‘seeing bodies’ &
‘perceived life threat’) was associated with CAPS increase over time.
Tsunami
PTSD symptomatology
Increased recall of threat
intensity associated with
increase in / lack of
improvement in IES-R symptom
score
Heir et al., 2009
Memory amplification
Nature of Traumatic Memory
• Traumatic memory does not remain stable
over time
• Increase in propensity to endorse traumatic
items predicts PTSD
• Memory amplification: Unclear whether this is
increasing or decreasing in accuracy
Does amnesia for the traumatic event play
a protective role?
• Traumatic events involving
traumatic brain injury are
associated
with
reduced
prevalence of PTSD > Amnesia
of the traumatic event may play
a protective role (Mayou et al.,
1993; Sbordone & Liter, 1995)
• TBI and PTSD not mutually
exclusive (Bryant & Harvey,
1998; Ohry et al., 1996).
• >> These studies lack
systematic investigation
of memory for the event
• Purpose: Direct assessment of
the relationship between
explicit memory of the
traumatic event and
subsequent development of
PTSD in participants who had
experienced TBI
120 subjects injured primarily in
traffic accidents (90%).
Initial evaluation took place within
24 hours after injury, during
hospitalization. Also, follow up 7-10
days, 4 weeks and 6 months.
55%
45%
6% met diagnostic criteria for
PTSD at 6 months
% with PTSD at 6 months
23% met
diagnostic criteria
for PTSD at 6
months
25
*
20
15
10
5
0
No memory
Memory
Question…
If lack of memory for the traumatic event is
“protective”, can:
a) the memory be weakened and
b) is a weakened memory protective
against subsequent PTSD development?
Interfering with the trauma memory
• Increased epinephrine is thought to mediate enhanced
memory for emotional events
Trauma
Excess
epinephrine
PTSD symptoms
Strong emotional
memory and
fear conditioning
Young & Breslau, 2004
•Searing in of memory adrenergically mediated → Blocking (e.g. β – adrenergic blocker
propranolol) interferes with memory formation.
CAPS Score
Propranolol
Placebo
One-Month
Pitman et al., (2002)
Propranolol
Placebo
Three-Month
Skin Conductance
SC (sd)
t=2.0, p=.03
Physiologic responses during personal script-driven imagery of the traumatic
event that occurred 3 months earlier
Placebo
Propranolol
Findings not replicated (Stein et al., 2007). Administration time? 48 hours max vs. 1-6
used by Pitman
Interim Summary
• Memory amplification over time is associated
with PTSD symptoms
• Blocking memory for the original trauma has a
“protective” effect against getting PTSD
– Amnesia following TBI
– Drugs following trauma (impair memory
consolidation)
Question…
Does the trauma memory activate different parts of
the brain in PTSD patients?
Symptom provocation studies
Show traumatic reminders
to patients with PTSD, and
investigate whether
different patterns of brain
activity are observed.
Hyperactive Amygdala
• Amygdala is an area in the brain that underlies
fear processing and expression
• Amygdala hyper-responsivity in PTSD
has been reported during the
presentation of personalized
traumatic narratives (Shin et al., 2004)
and cues (Driessen et al., 2004)
combat sounds (Liberzon et al., 1999)
combat photographs (Hendler et al.,
2003) and trauma-related words
(Protopopescu et al., 2005).
Patients with PTSD from
9/11 viewing pictures from
the attack (Silbersweig)
mPFC
• Involved in inhibitory control , underactive in PTSD
patients (Lanius, Bluhm, Lanius, & Pain, 2005).
• PTSD pathophysiology, specifically as failures of
midline prefrontal regions to inhibit subcortical limbic,
especially amygdala, reactivity (e.g., Milad, Rauch,
Pitman, & Quirk, 2006)
Question…
Are brain alterations associated with PTSD 1)Pre-existing
vulnerability factors or 2) acquired signs?
TRAUMA
Brain Differences
PTSD
PTSD
Brain Differences
Hippocampus
• Area involved in learning and memory and
particularly implicated in rich recollective
autobiographical memories (Addis et al.,
2004).
Hippocampal Volume: Reduced in
PTSD
• Bremner et al., (1995) Vietnam veterans with (n = 26) and
without PTSD (N = 22). PTSD subjects had 8% smaller right
hippocampus volume & poorer performance on verbal
memory measurements (Wechsler Memory Scale).
• Bremner et al., (2003): 22 female adult survivors of childhood
abuse with PTSD (N = 10) or without PTSD (N = 12). PTSD had
15% smaller hippocampal volume than abuse subjects
without PTSD. No difference in memory measures.
• Stein et al., (1997) assessed hippocamal vulume in 21 female
adult survivors of severe childhood sexual abuse and 21
control subjects, and also administered cognitive tests (e.g.
CVLT). Abuse subjects had 5% smaller left hippocampus size,
but no differences or correlations were found on cognitive
performance.
-Exposure to severe stress can damage the hippocampus.
- Human studies show smaller hippocampal volume in individuals
with PTSD.
Nature Neuroscience 5, 1242 - 1247 (2002)
Published online: 15 October 2002; | doi:10.1038/nn958
Smaller hippocampal volume predicts pathologic
vulnerability to psychological trauma
Mark W. Gilbertson1, 2, Martha E. Shenton2, 3, 4, Aleksandra Ciszewski4, Kiyoto Kasai4,
Natasha B. Lasko1, 2, 5, Scott P. Orr1, 2, 5 & Roger K. Pitman2, 5
Does this represent:
1) neurotoxic effect of trauma
2) a pre-existing condition that renders the brain more vulnerable to the
development of pathological stress responses?
PTSD+
PTSD-
Trauma-Exposed
Combat Veterans
with PTSD
Combat Veterans
without PTSD
Trauma-UnExposed
Co-twin
Co-twin
A
B
C
Replication of previous research
Neurotoxicity Effect
Pre-existing Vulnerability
PTSD +
Exposed
Un-Exposed
PTSD -
PTSD Severity
Combat Un-Exposed
Combat Exposed
Hippocampus: Conclusions
• Smaller hippocampus in veterans with PTSD
• Smaller hippocampus in PTSD represents a
pre-existing, familial vulnerability factor rather
than neurotoxic product of trauma and PTSD
development
Triad of Structures:
Amygdala
Fear
mPFC
Hippocampus
Inhibition
Memory
Question…
Does altered neurocircuitry in PTSD patients
contribute to the maintenance of fear memories?
CS + E
CS +
?
Impaired safety memories
• PTSD patients are not able to retain safety
information (e.g. impaired extinction recall
Milad et al., 2009).
– > Can lead to the maintenance of fear memories
• This is a consequence of getting PTSD, and not
a predisposing factor (Milad et al., 2008)
Summary
• Memory for the original trauma
– Not stable over time
– Increased memory change predicts PTSD
• Lack of memory for the trauma is protective against
subsequent PTSD
• Preliminary evidence that PTSD can be treated via
interventions that specifically target memory
• Altered neurocircuitry in PTSD
– Triad: Amygdala, mPFC and Hippocampus
– Smaller hippocampus is a predisposing factor
– Altered neurocircuitry can lead to the maintenance of fear
memories
Thank you.
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