UNDERSTANDING PTSD

PTSD
a.
b.
c.
d.
e.

Fear Response
Failure of Fear Extinction
Memory
Anxiety
Memory Encoding

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PTSD
PTSD is a disorder associated with changes in neural
circuitry involving frontal and limbic systems
Altered metabolism in such structures are
correlated to PTSD.
It is an anxiety disorder caused by the onset of an
extreme stressor
combat, childhood physical and sexual abuse,
MVAs, rape and natural disasters.
Perceptual induced symptom activation in PTSD is
associated with an emotionally determined motor
preparation, ie: subcortically initiated rather than
cortically controlled memory mechanisms determine
the central pattern (Fancati, Vermetten & Bremner, 2007).
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 Symptoms are intrusiveness, flashbacks, hyper

vigilance, sleep disturbance, physiological
hyper-responsivity and numbing of emotions
7.8% of the population exhibits symptoms of
traumatic events (Bremner & Charney,1994).

fMRI has allowed to uncover some of the

neural networks involved in the
pathophysiology of PTSD
specifically reduced brain activation of the mPFC
and increased activation in the Amygdala
alterations in functional activity were also found
in the hippocampus, parahippocampus,
orbitofrontal cortex (OFC) and thalamus.
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 Correspondingly, studies of the

neurobiological mechanisms related to
stress show alteration in:
Fear response mechanism
Behavioral sensitization
Failure of extinction of fear (Charney et al., 1993).

Also, significant deficits in memory are

shown correlated with specific brain
structures and functional pathways (Bremner et
al., 1993, 1995b).
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a. FEAR RESPONSE - PTSD

Fear Response
Adaptation to danger is normal and crucial for
survival. The alteration referred to as diagnostic
criteria for PTSD resides in the overgeneralization
of danger cues; continuous perceiving nonthreatening situations as dangerous
Frequent recall is a part of the diagnostic criteria for
PTSD as per the DSM-IV classification for psychiatric
disorders.

Traumatic memories can be elicited via sensory

and cognitive stimuli that are paired with the
traumatic event that was experienced.
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 Structures involved in the fear response

mechanism in humans
sensory cortex, dorsal thalamus, lateral and central
nucleus of the Amygdala and the mPFC/Anterior
Cingulate Cortex (Rauch et al., 2003; Woodward et al.,
2005; Yamasue et al., 2003).

Neurochemical systems that are functional within

and communicate between these structures
Glutamate, N-methyl-D-aspartate acid (NMDA)
receptors and voltage-gated calcium channels
The central nucleus of the Amygdala is the main
output center for the response to fearful stimuli,
mediating autonomic, behavioral and endocrine
responses related to fear (Charney, 2004).
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Data trajectory: the lateral Amygdala transfers

information to the central nucleus after
receiving it via 2 main pathways:
Short subcortical pathway
dorsal thalamus directly to the lateral Amygdala.

Longer cortical pathway

through cortices involving cognition and
assessment of the fearful situation and its context.
The Hippocampus can also send contextual data
about a stimulus to the lateral Amygdala, given its
memory related role.
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b. FAILURE OF FEAR EXTINCTION PTSD

Failure of Fear Extinction

Fear extinction is linked to conditioning of fear
The neural mechanisms dealing with the extinction of
fear greatly overlap with fear acquisition.

The main structures involved in the extinction of

fear are
the mPFC and the Amygdala (Quirk & Gehlert, 2003).

NMDA receptors and voltage-gated calcium

channels are essential neurochemicals to the
process of extinction (Charney, 2004).
GABA, norepinephrine and dopamine are also
involved in extinction processes (Quirk & Gehlert,
2003; Southwick et al., 1999; Pezze & Feldon, 2004).
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 Normally, during a fearful response of the

Amygdala the mPFC is activated and
modulates the initial response to the threat
Fear is contained and managed that way.

If prefrontal activation is absent or lessened,

the Amygdala does not receive sufficient
inhibitory feedback
resulting in autonomic arousal and exaggerated
responses.

The feedback loop between the Amygdala and

the mPFC is mediated by GABA inter-neurons
(Nutt & Malizia, 2004).
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c. MEMORY - PTSD

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Memory
Memory deficits in PTSD have significant
associations with reduction in hippocampal volume,
where spatial and episodic memory, stress and
emotional regulation, and novelty processing take
place (Geuze et al., 2005).
Smaller hippocampal volumes (5 26% reduction)
have been shown in patients exhibiting combat
trauma, physical and sexual abuse and childhood sex
abuse found in different areas within the structures,
depending on the trauma (Bremner, 2003; Geuze et al.,
2005)
Reduction in hippocampal volume is mostly due to neurotoxicity
caused by elevated glucocorticoids, reduced BDNF and inhibition of
regeneration of damaged brain tissue (Bremner, 2002, 2003).
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 PTSD patients often show difficulty to

intentionally retrieve a complete memory of the
traumatic event
fragmented, poorly organized and difficulty to
recalling exact temporal order of events (Foa & Riggs,
1993; Amir et al., 1998)

High frequency of involuntarily triggered intrusive

memories and vivid re-experiencing.

Re-experiencing is mainly about sensory

impressions, rather than thoughts, involving all
sensorial modalities (Ehlers & Steil, 1995)
Sensory impressions are experienced as if they were
happening right now, and emotions, including physical
reaction and motor response, are the same as the
original emotions.
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 Original emotions and sensory impressions

are re-experienced even if the person later
acquires new data contradicting the original
impression.
Affect without recollect are physiological
sensations associated with the original
event without a recollection of the event.
Re-experiencing triggered by cues that were
temporarily associated with the event,
without semantic relationship.
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d. ANXIETY - PTSD

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Anxiety
Anxiety is a result of appraisals relating to
impending threat
PTSD is a disorder whereby the problem resides in the
memory of an event that has already passed.

PTSD persists when trauma is processed in a way

that produces a sense of serious current threat,
due to individual differences in appraisal of
trauma and in the nature of memory of event,
and links to other autobiographical memory.
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 Persistent PTSD is due to processing and

encoding trauma in a way that causes a sense
of current threat by excessively negative
appraisals of the trauma and a corrupt
autobiographical memory exhibiting poor
elaboration and contextualization, strong
associative memory and strong perceptual
priming
Change in the negative appraisal and the trauma
memory are usually prevented by a series of
problematic albeit well-intended behavior and
cognitive strategies.
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 Most patients with persistent PTSD experience

a range of negative emotions, from the
possibility of a loss leading to anxiety to the
certainty of a loss leading to depression.
Appraisals concerning
danger lead to fear
unfairness to anger
personal responsibility to guilt
violation of self to shame
loss to sadness
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e. MEMORY ENCODING - PTSD

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Memory Encoding
Intrusion characteristics and patterns of retrieval found in
persistent PTSD are due to the way the trauma is encoded
and laid down in memory (Brewin et al, 1996).
There are two routes to retrieve autobiographical data:
1. High-order meaning-based retrieval strategies (first day at
school, first car, etc.)
2. Directly triggered by stimuli associated with event (smell,
music, imagery, etc.).

Normal processing selects and incorporates

autobiographical events into an autobiographical memory
knowledge base organized by themes and time periods
(Conway, Pleydell-Pearce, 1997). This elaboration
enhances the first retrieval route and inhibits the second
When autobiographical memory enters into consciousness,
both specific data and general data about the life period are
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comprised, and abstract data about the type of event.

 Main problem is that trauma memory is poorly

elaborated and inadequately integrated into context RE
time, place, subsequent and previous data and other
biographical memories (Siegel, 1995)
This explains problematic intentional recall arising from
the lack of context in time thus producing the perception
of current threat.

Strong sensory association to traumatic material

increase chance of emotional response to associated
stimuli (Reemtsma, 1997)
where footsteps and subsequent knocking sounds once
heard by a captured person may become problematic cues
to emotional response.

Associative learning helps the organism in making

predictions: what will happen next?. In PTSD, distinct
stimuli present shortly or during traumatic event
become associated with the default prediction of
severe danger to self.
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 Retrieval from associative memory is cue-driven

and unintentional
whereby the person is not always aware of the
triggers for the re-experiencing , or of the link to the
emotion reaction taking place.

Failure to spot the origin of the re-experiencing

symptoms makes it hard for patient to learn that
there is no present danger when exposed to
(unidentified) triggers.
Strong perceptual priming is like an implicit
memory for stimuli temporarily associated with
the event, ie: reduced perceptual threshold for
the stimuli.
Cues able to trigger the trauma memory are
more likely to be noticed.
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 Implicit memory traces are not well discriminated

from other memory traces (Baddeley, 1997)
whereby a vague physical similarity would suffice to
perceive stimuli as similar (poor stimulus
discrimination).

Reciprocal relationship between the nature of the

trauma memory and the appraisals of trauma and
sequelae
A recall is always biased by appraisals, selectively
retrieving data that is consistent with these appraisals,
preventing the recalling of aspects contradicting
appraisals and thus preventing change in appraisals.
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Encoding Trauma Memory...

The nature of the trauma memory depends on
the quality of the encoding (Krystal et al., 1995;
Schacter et al., 1997; Siegel, 1995).

Conceptual vs. data-driven encoding (Roediger,

1990) suggest that persistent PTSD is data-driven
because the degree of conceptual processing
determines nature of memory and ability to
retrieve data from it
Lacking conceptual memory will cause strong
perceptual priming for accompanying stimuli.

Unorganized memories observed in persistent

PTSD indicates a lack of perspective and
dissociation that explains the fragmentation of
traumatic memories (Spiegel, 1991).
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Bad Memory Encoding...

Impact of high arousal and fear on trauma
memory includes cognitive and biological
pathways
very high levels of cortisol during extreme stress
interfere with memory encoding of event, thus
impairing intentional recall (Newcomer et al., 1999).

Like a cupboard, filled up quickly and in a

disorganized way, that does not allow fully closing
the door, and then things fall out at unpredictable
times.
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CONSONANCE CLINIC LLC

UNDERSTANDING PTSD

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