Pain Flashcards
pain in neonates
1. function of pain
2. preterm infants and demographics
3. McGraw 1941
4. fMRI
- necessary perception to identify danger or harm to body
- experience repeated and prolonged procedures, racial disparities in preterm births increase infant mortality, highest in black and indigenous people, lowest in asian and white
- observed pin pricks ing children from 0 to 4 years old, results neonates may exhibit no over response concluding newborns have diminished capacity for physical sensation, leading to idea that infants don’t feel the same level of pain as children or adults thus were not offered pain relief
- neural activity overlap b/w adult and infant pain suggest that infant pain experience is similar to adult
challenges in recognizing pain in others
1. pain perception
2. measuring pain
3. verbal reports of pain
- not physical sensation, unpleasant sensory and emotionally, may be associated with tissue damage and subjective based on person, even with same painful stimulus, females have higher pain sensitivity (feel greater pain); negative emotions can increase pain
- Visual Analog Scale is a subjective measure of pain from (none) 1-10 (unbearable) with faces expressing level of pain; pain scales are subject to measurement error since pain is subjective experience, the level of pain could change depending on other experiences individual has
- learn that increase verbal report of pain leads to greater medical attention or lead to catastrophizing; caregivers must trust that patient is accurately conveying pain; those who cannot express pain verbally suffer such as neonates
non-verbal responses to pain
1. facial expression
2. crying
3. stress response
- forehead brow bulge, eyes squeezed shut, cheeks raised, mouth open and squarish, nose broad and bulging, brows low and drawn
- high pitched and rhythmic crying indicative of pain
- circumcison with sham and without anesthetic increases crying and cortisol since pain is a stress experience; with anestetic have lower level of crying and cortisol; exposure of pain as stressor in early life increases risk of anxiety in adulthood
mechanoreceptors and nociceptors
1. hair receptor follicle
2. meissner corpuscle
3. Pacinian corpuscle
4. Merkel disk
5. Ruffini corpuscle
6. free nerve endings
all mechanoreceptors have low stimulus thresholds and alpha-beta fibres
1. detect light brush of hair in dermis, has a-delta that triggers sharp pain when hair is pulled, rapid adaptation (quickly desensitized)
2. just below epidermis (skin), detect dynamic deformation, RA
3. deep in dermis, big SA, detect vibration, RA
4. attached to epidermis, depth it is deformed into dermis produces indentation depth, moderate adapation
5. Ruffini corpuscle in dermis detect stretch, MA
4. nociceptor, has C-fibres or alpha-delta fibres sensitive to injurious forces, slow adaptation, high stimulus threshold (req strong stimulus to activate), to continue to signal danger until dangerous stimulus removed
sensory fibre types
- alpha-beta; carry touch info, myelinated, diameter 6-12 micrometre, 35-90 m/s
- alpha-delta; carry mechanical and thermal pain info, myelinated (fast for sharp pain), diameter 1-5 micrometre, 1-40 m/s
- C; carry mechanical, thermal, and chemical pain info, non-myelinated (dull lingering ache), diameter 0.2-1.5 micrometre, 0.5-2 m/s
how is peripheral pain transmitted to brain?
1. spinal cord
2. touch info
3. pain info
- info from specific part of body is sent to specific part of sp cd where dorsal root communicates info from periphery to spinal cord
- lemniscal tract a beta fibres (1st order neuron) carrying info about touch passes through the dorsal root of spinal cord, synaspe with 2nd order neuron at medulla oblongata where it cross to contralateral side, synase with 3rd order neuron at thalamus, info sent to top layer of somatosensory cortex to be processed
- spinothalamic tract a delta and C fibres (1st order neuron) carrying info about pain synapse with 2nd order neuron at dorsal horn of spinal cord and info crosses to contralateral side, through medulla oblongata, synapse with 3rd order neuron at thalamus, info sent to bottom layer of somatosensory cortex to be processed
how is pain perceived by brain?
1. neuro matrix of pain
2. sensory homunculus
- many areas of the brain are involved in pain, amygdala in fear and stress response to pain, prefrontal cortex and insula in emotion, anterier cingulate cortex in expectation of pain, the periaqueductal gray as internal morphine centre to modulate pain, primary somatosensory cortex (SI) responsible for intensity and localization of pain to a body part
- visual rep of sensitivity (nociceptor density) of different body parts to pain, bigger = more dense
gate control theory of pain perception
- concurrent mechanical input from a-beta fibre passing through dorsal root activates interneuron in the dorsal horn to release GABA to inhibit 2nd order neuron of the pain pathway to close the gate of pain, can’t send signal of pain to spinothalamic tract
- mech input must be at site of pain since info from different parts of the body are sent to specific regions of spinal cord, corresponding to specific interneurons
counter-irritation in modulating pain
- periaqueductal grey in midbrain receives input from brain and body to stim raphe nucleus to send signal to interneurons containing endogenous opioids (enkephalins) in the dorsal horn of the spinal cord, enkephalins released bind to opioid receptors to increase activation threshold to inhibit 2nd order neuron of pain pathway
- a more painful acute stimulus than chronic pain stimulus triggers high activation of periaqueductal grey to signal increased endogenous opioid release to whole body, temporarily completely inhibit chronic mod pain signal (C-fibres) while intense pain is dulled
- opioids reduce activation of neuro matrix of pain
cognition/emotional response to pain
1. expectation
2. anxiety about pain
3. attention to pain
- positive expectancy of opioids (placebo) decreases pain intensity rating while negative expectancy of opioids (nocebo) results in pain intensity rating on par with no opioid administration
- condition to assoc square with high heat stimulus and triangle with low heat, during test even though square had chance to be followed by low heat, expectation of pain evoked higher anxiety due to higher ACC expectation and greater insula emotional aversion (biological basis of nocebo); anxiety amplified pain
- greater intensity and aversion when attending to pain; connectivity between PFC and PAG increase when not attending to pain, PFC send greater signal to PAG for greater analgesic effect to distract from pain
vision
1. importance
2. rubber hand illusion
3. VR on pain perception
- vision is dominant sense, visual info takes priority thus can use visual input to manipulate other senses
- when tactile and visual info to actual and rubber hand are presented synchronously, somatosensory cortex temporaily adopt rubber hand into sensory homunculus (ownership); rubber hand threatened during ownership activates somatosensory cortex is same way that threat to actual hand will while threat will not activate somatosensory cortex when there is no ownership
- use bogus visual feedback to alter perception of movement-evoked neck pain; understated (laggy image) had longer ROM before onset of pain since motion was faster than image, visual info tricks brain into thinking head rotated less than it had, no change in accurate image, overstated (faster image) had lower ROM onset pain
phantom limb pain
1. overview
2. mirror therapy
3. Graded motor imagery
- pain in limb that has been amputated; S1 (somatosensory cortex) neurons that rep amputed limb get adopted by neighbouring regions, when activating neighbouring regions encroaching neurons activate region of amputed limb in S1 , making brain think there is input from limb, can be interpreted as phantom limb pain
- visual input of movement of good limb in mirror representing amputated limb gen inhibitory effect which quiets hyperactivity in S1 from neighbouring areas visually signaling to the brain that there is an activity in amputated limb
- using visual input to activate S1 and speed up rehab; post injury/condition, cortex rep of limb shrinks due to lack of input, gen complex regional pain syndrome; use images to id left/right limb, visualize movement of injured limb to prime brain for motion, mirror therapy with good limb at the same time as motion with dmg limb
social pain
1. empathy
2. social pain and hurt feelings
3. intention
- understand and share feelings of others, female participant experienced pain or watch romantic partner experience pain, no activation of somatosensory cortex for pain to others, similar activity in emotional neuro matrix of pain in insula and ACC for self and partner, positive correlation between activation of the insula and lvl of empathy
- pain experienced from social rejection hurts as much as physical pain, when recounting physical pain and emotional pain, emotional pain hurts more, easier to recall and activate emotional neuro matrix of pain, why traumatic events stick
- shocked unintentionally decreased pain as endorphins released to numb pain, shocked knowing pain was intentional/ premeditated hurts more than unintentional pain because emotional pain amps physical pain
treating social distress with painkillers and other methods
- tylenol (acetaminophen) reduces hurt feelings, when hurt feelings induced through cyberball social rejection simulation, feel expectation that ball should be thrown to you and emotion from rejection measured by fMRI brain activity shows tylenol reduced activity in ACC and insula
- after experience of cyberball comforting touch from friend reduced unpleasantness from social rejection, no change from reframing mindset text from friend
- laughter increases endogenous opioid release in ACC
- larger social network (close connections engaged weekly/monthly) associated with higher pain tolerance
chronic pain
1. overview
2. nociceptive pain
3. neuropathic pain
4. nociplastic pain
- pain persisting/recurs for longer than 3 months even after source has healed, possibly due to maladaptation, 20% people worldwide have chronic pain
- tissue damage or inflammation affecting nociceptor or non-nociceptor neuron in peripheral or CNS, protective adaptive pain but can be pathological, high or low threshold
- damage to c-fibre/a delta fibres/pinched affecting nociceptor and non-nociceptor in P/CNS, long lasting pathological unless dmg repaired, low threshold
- CNS sensitization to pain affecting non-nociceptors in CNS, pathological, low threshold