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PTSD :PENCIL2: B+B2 LECTURE 8 - Coggle Diagram
PTSD
:PENCIL2:
B+B2 LECTURE 8
PTSD
“Soldier’s Heart”, “Shell Shock” (1918, after WWI), “Battle Fatigue” (1945, after WWII), “Delayed Stress”
The term ‘PTSD’ came about in the 60s/70s, after the Vietnam war.
Defined by Patient Report (which leads to suspicion, soldiers accused of cowardice, or coming up with ‘excuses’ to not return to the front line)
PTSD originally defined in DSM III – 1980
Medical diagnosis led to search for biological markers
Greater understanding led to wider diagnoses in general population
Challenge for modern neuroscience to advance medical understanding and facilitate treatment
fMRI Studies
Identify a Neural Pain Network
Many areas overlap with those in Major Depressive Disorder
These areas also overlap with those in PTSD.
Shin et al. (2001)
8 Vietnam war veterans with PTSD vs. 8 Vietnam war veterans without PTSD
Subjects counted the number of combat words, negative words and neutral words.
Results showed a diminished response to negative words in rostral (closest to the nose) anterior cingulate cortex (ACC)
ACC mediates / controls response to negative stimuli in the healthy brain.
ACC responds differently in PTSD than it would do in depression, where hypoactivity (reduced activation) would be found in the DLPFC.
BUT...
small sample and there was also activity in other parts of the brain.
Meta-analysis of PTSD
Compared fMRI studies of PTSD, Social Anxiety, Phobias and Fear.
Established Brain activations to each condition.
PTSD showed HYPOACTIVITY in ventromedial prefrontal (also called OFC) and Cingulate.
Demonstrates PTSD is different to other anxiety disorders - different brain signature.
Amygdala and PTSD
PTSD veterans, combat veterans and controls scanned with PET.
Played white noise and combat sounds.
PTSD veterans showed a greater stress and skin response (Galvanic Skin Conductance Response) to combat noise than to white noise.
PTSD veterans showed a greater response to combat noise in left amygdala (around 3 times higher skin conductance reading for comba noises in PTSD victims compared to white noise condition)
Biomarker for PTSD
Etkin et al. (2019)
Resting-state fMRI study of PTSD patients and controls (just sit in the scanner - no task given to patients)
Resting state should show brain areas that are active in synchrony.
Reports rsfMRI connectivity of brain networks and cognitive testing.
Results show PTSD patients with poor verbal memory and weak connectivity in the ventral attention network had poorer CBT treatment response.
Shows neural and cognitive factors that impair treatment.
Brain Derived Neurotrophic Factor (BDNF)
Relates to the Neurotrophic theory of Depression.
Maintains and supports growth of neurons / synapses.
Expressed in many brain areas but especially related to memory formation in the
hippocampus
.
The Neurotrophic Hypothesis of Depression
Human post-mortem data shows decreased BDNF in the hippocampus.
In depression, via the Hypothalamic Pituitary Gland Axis, controlled from the brain, runs all the way down the spinal cord to the liver, liver reduces cortisol going into the blood through the adrenal gland axis, cortisol comes back up through the blood into the brain, heightened activity in the amygdala all the time in depression, so cortisol is constantly being dumped into the blood which all travels up into the brain, and cortisol ‘uses up’ the BDNF in the brain.
Because in depression, your emotional brain network is on all the time, there’s more cortisol in the blood,
decreasing the BDNF in the hippocampus.
Hence,
memory encoding is impaired,
less able to form new memories, and the size of the hippocampus starts to shrink because the synapses between the neurons are not being maintained in the same way, so those synapses weaken and die, causing the connections to fall away, neurons start to die, and
overall hippocampal volume decreases.
Demonstrates
neuroplasticity
at a very specific, anatomical level.
Not clear if this is a
cause or a result
of depression (and some studies show the reverse) .
Reduced Hippocampal Volume in MDD
Videbech & Ravnkilde. (2004)
Performed a meta-analysis of studies.
VBM evidence
Almost all of the studies showed a reduction in hippocampal volume for Depressed patients, compared to healthy controls.
Hippocampus and PTSD
Gilbertson et al. (2002)
MZ twin study examined if hippocampal volume was the cause or result of trauma.
Combat Veterans.
Results showed hippocampal volume predicted severity of PTSD in the combat exposed twin and the non-combat exposed twin.
Smaller hippocampus increases likelihood of mental illness.
Speaks against using the Neurotrophic model as an explanation for PTSD (role for experience?)
Meta-analysis of 1868 patients (794 PTSD patients)
Concluded:
Smaller hippocampus = increased chance of PTSD.
CBT
Problems are broken down into 5 main interconnected areas:
Situations
Thoughts
Emotions
Physical feelings
Actions
CBT is different from other psychotherapies...
Pragmatic
- identifies specific problems and tries to solve them.
Highly structured
- discuss specific problems and set goals
Focused on current problems
- doesn't attempt to relive past issues.
Collaborative
- therapist isn't in charge, they work with you to find solutions to your current problems.
Extinction
The means by which a fear response can be inhibited
Heavily studied in animal literature (e.g. Pavlov)
Offers a behavioural and neural explanation of why CBT works.
Extinction is a form of learning, it is not “unlearning”
Extinction = learning new skills
Pavlovian Fear Conditioning = Extinction
Pairing of the conditioned stimulus (CS) and unconditioned stimulus (US) leads to the conditioned response (CR)
Extinction is the reduction of the CR by repeated presentation of the CS in the absence of the US
A model of Extinction
Myers & Davis (2002)
(A)
Extinction ≠ (not the same as) Forgetting
because the fear response is reduced or removed
(B)
Spontaneous Recovery
- At relatively extended intervals following extinction, the extinguished CR reappears. The magnitude of this “spontaneous recovery” increases over time
(C)
Renewal
- Extinction is context specific. Following acquisition in context A and extinction in context B, a retention test in context B reveals extinction-appropriate behaviour.
(D)
Reinstatement
- An extinguished CR reappears (is “reinstated”) when unsignaled presentations of the US are interposed between the completion of extinction training and a subsequent retention test, but only if the USs are presented within the context of the retention test.
Results...
(A) If untreated anxiety will re-occur in situations / interactions unrelated to the original trauma.
(B) If the original trauma is severe it will require treatment over the lifespan.
(C) If patients can change their “environment” the treatment will be more effective (environment is defined very broadly in this context).
(D) Re-exposure to the stressful environment may reinstate the anxiety.
Extinction in the Brain
Pitman et al. (2012)
Greater vmPFC (also called OFC) activity equals greater extinction learning
Dorsal Anterior Cingulate Cortex (dACC) activity is negatively correlated with extinction
vmPFC signals amygdala to reduce and control fear response
High connectivity between vmPFC and dACC leads to stronger extinction