Dan Part 2 Flashcards
Ptsd symptoms
Main stressor event- complex is trauma related to multiple event dove time. Intrusion symptoms (replaying it), changes to reactivity/hyperarousal. - changes in cog/mod- mirrors depression, avoidance behaviours. Stressor can be direct, witnessing, close relationship to person, indirect like medic
Amygdala
Emotion processing, stims hpa axis, reward, motivation and learning
Liberzon: ptsd veterans, normal veterans and controls did pet, played white noise or combat sounds. Ptsd showed greater stress and skin response to combat and greater response in L amygdala
Cingulate cortex
Anterior cc has attention, reward, decisions and emotion
Part of fronto striatal network and salience network- alerts attention to threats/ unexpected stim
Shin: 8 veterans w ptsd and 8 without counted no. combat words, - and neutral words
Showed less response to - words in rostral anterior cc, as it mediates response to - stim in a healthy brain
Thalamus
Brains relay station for sensory info
Important visual areas are pulvinar and lateral geniculate nucleus
Responds to bottom up and top down input
Hypothalamus forms key part of hpa axis
Dlpfc
Attention network in studies of cog control, greater bold when controlling cog response
Part of frontal striatal network
Orbitofrontal
Decision making and future planning, task switching and eval
Path between dlpfc and amygdala
Meta anal of brain areas
Etkin and wager: mri data from ptsd, as, phobia as ptsd was classed as anxiety disorder. All showed greater in amygdala and insula, ptsd less reactive in orbitofrontal, thalamus and cingulate
Hippo
Part of limbic system, memory processing, attenuated hpa axis. Logue meta anal found smaller hippo in ptsd across diff types of trauma. Gilberston: hippo vol in civilian twin predicts severity of ptsd in combat twin so smaller hippo risk factor - linked to neurotrophic hyp of depression so ptsd show depression symptoms
Hypothalamic pituitary adrenal axis- hpa
Neuro endocrine response, when stressor, neurones in hypothalamus release corticotropin releasing hormone, stim S adrenocorticotropic from pituitary, stim S glucocorticoids from adrenal glands. Which prepares for fight or flight. Hippo and pfc inhibit this process, amygdala stim S neurones in hypo, cortisol controls over hpa but regulating hippo so sustained cortisol damages hippo- hyp that ptsd due to overactive hpa
W for hpa
Studies not consistent in effect of hpa in ptsd, some say cortisol reduced due to - feedback, some suggest ptsd subtypes differ to hpa reactivity
Multiple ways to measure cortisol so may be less valid
Sleep disturbance and hyperarousal
Measure brain activity, shows REM and non split into n3 deep, n2 and n1. REM has theta/more waves, high AcH, low adren high cortisol, non has opposite. Sleep issues in ptsd: insomnia, nightmares, paralysis. Cortical hyperarousal includes intrusive thoughts while going to sleep, marked by beta waves. Ptsd have more cortical hyper- risk factor as patterns stable across person before ptsd but ptsd can cause so goes both ways
Theory behind sleep and ptsd
Sleep boosts emotional response to memories as replays to strengthen memories so deprivation/ replays emotional experiences. However, sleep can take away affective tone/ emotion , leaving memory so if sleep disturbed, this doesn’t happen
Treatments - cortisol, extinction and the brain regions
Cortisol treatment to help hpa doesn’t work as don’t know if risk or cause, hydrocortisone can be preventative after a trauma but not treatment. Extinction is presenting conditioned stim without unconditioned. Pitman: correlation between orbito and extinction, acc- linked to extinction, vmpfc signlas amyg to control fear response- high connectivity between vmpfc and acc leads to more extinction
Treatments: extinction and sleep , EMDR - eye movement desensitisation and reprogramming
Sleep helps consolidate memory of extinction , Denis: hyperarousal means worse extinction. Sleep also makes exposure therapy better. EMDR: by franccine Shapiro, ps follow rapid stim W eyes while recalling event- don’t know why it works, one idea ptsd is failed memory processing so emdr fakes REM. Rousseau: mri before and after found change in amyg, thalamus, caudate, dlpfc
Acquired vs traumatic
Acquired is Any damage not born with. Traumatic is caused by outside the body, non traumatic is from inside the body e.g stroke
Stroke
Ischemic is when attires become blocked, haemorrhaging I’d when blood vessel ruptures. Under diagnosis in kids, better now due to awareness and comorbid W heart issues, risk for kids are congenital heart disease, sickle cell, infection. Adults is diabetes, high blood pressure. In newborns see seizures, sleepiness. In kids see headaches, sleepiness, loss of balance, vomiting
Long term stroke impacts
Christeron and stromberg: kids who had strokes 10 years later, 4/51 died, majority had neur and school deficits, weakness in one side (hemiparesis) but no diffs in age of stroke schryver: 4 died, 9 dev seizures, 15 hemi, most needed extra school support but all considered themselves happy and not severely disabled. Anderson: compared stroke, normal and asthma kids W stroke had more social issues, lesion vol not correlated, younger age of stroke predicted better social and higher esteem
Foetal alc syndrome -FAS background
Not acquired as before birth, type of foetal alc spectrum disorder. Associated w poor growth, face features, organ issues, small brain, epilepsy or seizures, cc, learning diff, attention and behaviour. To get diagnosis need all 3 of face issues (smooth philturm, thin vermilion border, small palpebral fissures), growth deficits and CNS abnormalities (structural neuro or functional)
FASD diagnosis
For main don’t need confirmation of alc but confirmed absence would rule out. Face features only affect 25%. Partial FAS requires confirmed alc, cns abnormalities but may not have face or growth deficits. Neurobehavioural disorder associated w prenatal alc- don’t need confirmation of alc
FAS neuro bio cases
Alc passes via placenta, foetus can’t process so leads to diff cns dev including cell death, issues W neural migration (extreme is smooth brain) and disruption of gene expression (extreme foetus dies). Learning diffs, EF, more subtle diagnosed w adhd. Excessively friendly, preschoolers don’t discriminate between strangers and known, not linked to iq. When older at risk of abuse and exploitation
Traumatic brain injury
Closed when skull not damaged, penetrating when damaged. Damage primary (in the moment, rapid accel/decc ) or secondary (altered blood flow or inflammation- doctors try to prevent). Can be mild mod or severe mild e.g. concussion. Focal is one area, diffuse is across - can have combos
Tbi in kids
Many data use hospital records but majority are mild so will be missed, mckinlay found prevalence of 30%
For ages 0-14, most common cause is falls, 15025 contact sports and motor vehicle accidents, children under 5 and 15-19 at biggest risk for a tbi- incidence of tbi increased risk for future tbi
Cog effects of tbi- EF
Levin: wm impaired in children post severe tbi compared to mild. Schachar: impaired inhibition in some 2 years post tbi but only those who developed secondary adhd. Mangeot: tbi showed long term issues in executive function for severe and mod 5 years after- ef issues linked to psychosocial outcomes and also family functioning e.g. impacts of support or disruptions on fam life
Social effects of tbi
Childhood tbi linked to social impairment especially at young age of injury, frontal regions and cc, social disadvantage and family dysfunction. Hanten: virtual reality to test social problem solving, tbi showed sig social problem solving abilities, including describing issue, id solutions, appropriate response- issues apparent as cog load increased
