interventions midterm Flashcards
what is pne utilized for
healthier responses to pain
nociceptive pain
short duration
well localized
neuropathic pain
pain travels
neuroplastic plain
persistant, chronic
spread in non dermatomal pattern
intensity out of proportion
pain neuroscience education
change belief that pain is marker of injury or disease
is there a pain signal or center in the brain?
no
pain is an experience
what is pain?
appraisal made by our protection system based on neural representation of threat/danger
our knowledge of pain is limited
its still in infancy
its complex - opioid epidemic didn’t solve it.
still learning about chronic pain
MOM (mature organism model of pain)
we evolved to tolerate pain
helps us to survive and pass on genes
stress response
pain helps us avoid bad things
What would happen if we didnt feel pain?
may not survive to adulthood
harm themself
dont realize they are hurt
what is the brain’s role in MOM?
continual sampling of the outside environment, own body, and relevant past experiences
experiences coded into memories
through what process does the brain scrutinize during MOM?
somatic: muscles
autonomic: subconscious control of body
neuroendocrine
immune
3 dimensions of pain in MOM
sensory: anatomical descriptions
cognitive: thoughts
affective: emotional reaction
how does MOM guide treatment?
therapeutic interventions (change tissue inputs)
therapeutic interactions (change environmental input - sleep better, stimulate parasympatetic)
therapeutic reframing (change brain’s self-sampling input via therapeutic neuroscience education)
input not mandatory
some neural processes can act in the absence of any inputs
stress and depression can cause physical pain
phantom pain in amputees
role of neural networks
suggests origins of patterns which underlie experiences lie in brain neural networks
the self
body perceived in unity
pain breaks the unity
genetic compenent
may explain why some are more at risk for chronic pain or maladaptive pain
neuroignature/neurotag
synaptic arrangement of multiple centers in the brain
modulated by protection being highest priority
fired together are wired together
thoughts affect ability
failed homeostasis equals
conditions producing chronic pain
cortical smudging
poor localization
blurring of pain map
need to retrain where the body is
biomedical approaches
medical/pharm treatments
anatomic education
emphasis on pain not function
facilitating avoidance
all have poor - modest results
biopsychosocial approach
emphasize PNE
develop therapeutic alliance with pt
focus less on diagnosis and more on changing maladaptive behaviors
central sensitization
become efficient at feeling pain
increase perception of pain in other regions
changes in properties in neurons
CNS is now on higher alert
allodynia
normally benign stimulus
cold, heat, light touch
hyperalgesia
increased perception of noxious stimulus
secondary hyperalgesia
spread beyond initial injury site
catastrophizing
worse case thinking
interpersonal coping style
affects family and caregivers
Let every photograph be taken from my bad side
So when the world sees my face
They’ll never ask why
I look the way I do
ruminating
overthinking and worrying about pain
pain related outcomes
increased behavioral pain expressions
more illness
higher pain severity
alterations in social support networks
partner either overprotective or over it
how can you treat catastrophizing?
graded exercise or exposure
hurt doesn’t equal harm
fear avoidance
avoid movement
over guarding
find what they can do
do not say “avoid what hurts”
role of stress on pain
HPA axis (hypothalamus-pituitary adrenal axis)
activated during periods of stress and homeostatic imbalance
amygdala activates HPA during stress
hypothalamus releases CRH
pituitary gland secretes ACTH
ACTH acts to release cortisol from adrenals
stress-pain likelyness
7-8x more likely to develop chronic pain
cortisol
helps respond to stress
good for ST, but not for LT
what is the LT stress effect?
if cortisol fails to function, we run out of fuel
lead to lack of other hormones