B2 L3 - PTSD

normal to experience upsetting/confusing thoughts after a traumatic event

for most people these naturally improve over a few weeks

criteria for PTSD

lasts more than 1 month, causes functional impairment, and aren’t due to medication/substance use/other illness

symptoms of PTSD

stressor event (direct or indirect exposure), intrusion symptoms (‘flashbacks’, nightmares, emotional/physical reactivity after reminders), alterations in arousal/reactivity (aggression/irritability, risky behavior, hypervigilance, difficulty concentrating/sleeping), negatie alterations in cognition/mood (negative affect, thought about self and world, dec interest in activities), avoidance behaviors

complex PTSD

trauma related to multiple events over an extended period of time (e.g. abuse)

hypothalamic-pituitary-adrenal (HPA) axis

exposure to stress → hypothalamus releases corticotropin-releasing hormone (CRH) → stimulates anterior pituitary gland to produce and release ACTH → ACTH stimulates relase of cortisol from adrenal gland

glucocorticoids (cortisol)

modulate metabolism, immune response (suppresses it) and brain function, preparing ‘fight or flight’ response

brain pathways modulate HPA axis activity

hippocampus and PFC inhibit the HPA axis, amygdala stimulates neurons in the hypothalamus

final outputs of the HPA axis also act on the brain

glucocorticoids exert neg feedback control of the HPA axis by regulating hippocampal and hypothalamus neurons; sustained cortisol exposure neg impacts brain health (cell death in hippocampus)

unclear how HPA axis dysregulation relates to PTSD

no current corisol-based drug treatments recommended for PTSD

amygdala, hippocampus and PTC implicted in PTSD symptoms like

intrusions, avoidance, cognition/mood and arousal reactivity

Etkin & Wager, compared fMRI studies of PTSD, social anxiety, phobias and fear

patients with any of the three disorders showed grater activity than matched comparison subjects in the amygdala and insula → PTSD specifically showed hypoactivity in the PFC, thalamus and cingulate

hippocampus

part of the limbic system and involved in memory processing, PTSD is condition centered around an emotional memory → reduction in hippocampal volume is one of the most consistently reported differences in brain structure when looking at PTSD

Logue et al, hippocampal size and PTSD

smaller hippocampus = inc chance of having PTSD (regardless of military/non-military trauma)

Gilbertson et al, twin study examined if hippocampal volume was cause or result of trauma

showed hippocampal volume predicted severity of PTSD in the combat twin and non-combat exposed twin; smaller hippocampus = risk factor of PTSD not a result of trauma

neurotrophic hypothesis of depression

could the involvement of the hippocampus be due to depression rather than PTSD

memory replay in the hippocampus

during ‘online’ states such as learning or memory tasks the hippocampus involved in encoding or retrieving memories; during ‘offline’ states like rest or sleep the hippocampus spontaneously replays previously encoded info

Liu et al, replay with PTSD

spontaneous replay of traumatic memories could trigger memory intrusions and ‘flashbacks’ in PTSD

Catarino et al, used think-no-think apradigm to compare memory suppression in PTSD patients compared with trauma exposed controls

PTSD patients showed worse memory suppression, indicated by better memory for suppressed items; memory suppression ability correlated with thought control ability and PTSD symptoms

hippocampal-PFC connectivity in memory suppression

DLPFC (activates when we engage top-down regulatory control), hippocampus (activates when we retrieve a memory) → when we try to suppress a memory will activity go up or down in these brain regions?

Benoit et al, memory suppression in the DLPFC and hippocampus

successful memory suppression requires inc activation of DLPFC and dec activation of the hippocampus

Mary et al, memory suppression in survivors of the 2015 Paris terrorist attacks

during no-think trials, PTSD and non-exposed controls showed widespread suppression of hippocampus by prefrontal control regions; PTSD showed no top-down suppression of memory retrieval networks (DLPFC doesn’t suppress the memory) → memory suppression is a general risk factor that influences vulnerability or resilience to PTSD following trauma

measuring sleep

recorded on an EEG using polysomnography, records eye movements as well as brain/muscle activity

REM sleep

vivid dreaming, most of it occurs towards the end of the night, generates theta waves and erratic eye movement patterns

non-REM sleep

subdivided into N1, N2, N3 (reflects growing level of sleep depth); most time spent in N2; generates slow oscillations and sleep spindles (spindles involved in memory function during sleep)

common sleep disturbances in PTSD

insomnia, longer sleep latency (takes longer to fall asleep), more awakenings during the night, shorter total sleep time, frequent nightmares, disruptive nocturnal behavior (night terrors, sleep paralysis, dream enactment)

cortical hyperarousal in PTSD

increased 24-hr cognitive, emotional, physiological and cortical hyperarousal; during sleep, cortical hyperarousal indexed as inc power in high frequencies (beta and gamma bands)

Denis et al, cortical arousal in sleep

inc levels of cortical hyperarousal during sleep in PTSD patients; hyperarousal during sleep interacts with other domains of hyperarousal experienced during the day

sleep enhances emotional memory and reduces emotional reactivity

consolidates memories by strengthening memory traces during NREM sleep, sleep preferentially consolidates emotionally charged experiences

Denis et al, sleep and memory

sleep amplifies memory for negative scene components at the expense of accompanying background info

van der Helm, following sleep participants rated emotional images as less emotionally intense

assoc with reduced amygdala activity after sleep and correlated with amount of time spent in REM sleep; NREM sleep strenghtens memory representations and REM sleep reduces affective tone

Ben Simon et al, examiend participant’s anxiety levels before and after a night of sleep deprivation

sig elevated anxiety levels after sleep deprivation, sleep deprived participants showed greater amygdala activity and reduced PFC activity when viewing negative images

Harrington et al, participants performed think/no-think task after sleep or sleep deprivation

more intrusions of suppressed memoires after sleep deprivation, this coincided with reduced DLPFC activity and increased hippocampus activity during suppression trials, sleep deprivation disrupts memory controls

Kleim et al, used an experimental analogue trauma film to study traumatic memory intrusions over the following week, participants in the wake group watched the film in the morning, participants in the sleep group watched the film in the evening and then slept at home

unwanted intrusions recorded over following week, sleep participants reported fewer intrusions and lower associated distress than wake participants

extinction

the reduction of the conditioned response by repeated presentation of the conditioned stimulus in the absense of the unconditioned stimulus; extinction retention is essential for long-term attenuation of fear responses

Milad et al, PTSD patients and trauma exposed controls underwent a fear conditoning and extinction paradigm

no group differences in fear acquisition or extinction learning (PTSD patients can extinguish fear), but 24 hrs later PTSD patients were unable to retain memory for fear extinction (treated as un-extinguished stimulus) → assoc with reduced vmPFC and hippocampal activity during extinction recall (a failure to retain extinction memories could underpin PTSD development and maintenance)

good quality sleep solidifies extinction memories

hyperarousal in the brain means worse ability to retain extinction, more of slow oscillations and sleep spindles (neuro-signature of good quality sleep) then extinction recall is better

sleep enhances e xposure therapy

therapist creates a safe environment to expose patientts to the things they fear, one of the main psychological therapies for PTSD (and phobias, panic disorder, social anxiety disorder, etc.) → fosters new extinction learning in a safe environment

Kleim et al

sleeping after an exposure session enhances therapeutic effectiveness

eye movement desensitization and reprogramming (EMDR)

patient follows with their eyes a rapidly moving stimulus (often the clinician’s finger) while holding different aspects of a traumatic event in mind

Wilson et al, systematic review of RCTs

suggest that EMDR is effective

why does EMDR work?

related to memory processes(?) → PTSD arises when the brain fails to appropriately consolidate traumatic memories and REM sleep important for emotional memory re-processing

Rousseau et al, EMDR changes activity in the PFC, amygdala, thalamus and caudate nucleus

inc activity in the vmPFC, amygdala, hippocampus, anterior cingulate; dec activity in inf parietal, dlPFC, posterior cingulate

targeted memory reactivation (TMR)

experimental technique to bias memory reactivation during sleep, sound cues assoc with learning are played back to the participant while they are sleeping

Van der Heijden et al, played EMDR clicks during period of slow wave sleep

TMR participants showed sig improvement in PTSD avoidance symptoms

top-down memory suppression in resilient individuals

non-exposed and PTSD- suppress intrusive memories through top-down regulation from the right DLPFC, which suppresses the hippocampus and precuneus

executive memory control in PTSD+

reduction in connectivity between control and memory systems nearly absent, generalized disruption of the prefrontal regulation signal → intrusive PTSD symptoms stem from maladaptive failure of brain’s control system to regulate memory activation

memory suppression

central mechanism of positive psychological adaptation following trauma