pain Flashcards
people with an absence of pain
some people are congenitally insensitive to pain
loss of pain sensation (nerve damage) can be caused by diabetes mellitus and leprosy
absence of pain means you are unaware of minor injuries – bad!!
pain as an enigma
differs from classical senses as it is discriminative and a graded motivation (behavioural drive)
mystifying symptoms e.g. allodynia, placebo
pain of intolerable levels can disappear in some intense situations
theories of pain: specificity vs convergence
specificity = pain is a distinct sensation, detected and transmitted by specific receptors and pathways to distinct pain areas in brain
convergence = pain is integrated and plastic, pattern of convergent somatosensory activity within distributed network - neuromatrix
specificity theory - sensory receptor classifications (2 categories)
classified by: activating stimulus, fibre-type, conduction velocity
lightly myelinated A(delta) fibres - fast ~20m/s
- mechano-sensitive
- mechano-thermal-sensitive
unmyelinated C fibres - slow ~2m/s
- polymodal = mechanical, thermal, chemical
specificity theory - nociceptors proof with heat
respond specifically to pain
subset of afferents with free nerve endings
demonstrated with heat where thermoreceptor activation is already saturated before pain is perceived - therefore must be separate receptors for pain
fast vs slow pain
fast = sharp and short = mimicked by stimulation of A(delta) fibre nociceptors
slow/second pain = delayed, long lasting = mimicked by stimulation of C fibre nociceptors
stimulation of Aa or Ab proprioceptive and mechanoceptive fibres never elicits pain – therefore must be distinct receptors for pain
molecular pain receptors e.g. heat and spice
receptors with nociceptive nerve endings - activated by heat and spicy food
capsaicin receptor (TRPV1 - transient receptor potential protein) activated by nociceptive A(delta) and C fibres at 45 degrees and by capsaicin (in chilis)
other TRPs activated in A(delta) fibres alone at 52 degrees (direct response to heat)
capsaicin mimics endogenous vanilloids (heat chemicals) released by stressed tissues - therefore nociceptors could also work by detecting these
2 central pain pathways
sensory discriminative:
- signals: location, intensity, type of stimulus
- easiest to define - spinothalamic tract (anterolateral system)
affective-motivational:
- signals: unpleasantness
- enables autonomic activation - fight or flight
pain in somatosensory cortex
region responds to painful stimuli
response correlates to intensity of pain
spatially mapped
cortical representations of pain shown by MRI
comparison of cortical activation by painful (C fibre) or painless (Ab fibre) mechanical stimuli on skin
painful stimuli activates same region of somatosensory cortex as non-painful
therefore pain activates a distinct response that includes other regions:
- insula and cingulate gyrus activated:
- connected to limbic system (emotional response)
- part of affective-motivational response to pain
affective-motivational pathway
shares some paths with anterolateral system
little or no topographic mapping
parabrachial nucleus = responds to pain from anywhere on surface of body
input to limbic (emotions) and hypothalamic (homeostasis) systems
strong correlation of painful experiences with cingulate cortex (not pain intensity - that is on the discriminative pathway instead)
specificity vs convergence: evidence supporting (3) and unexplained by specificity (5)
supporting:
- presence of cellular and molecular receptors which respond to pain specifically - Ao and C fibres, TRPV1
- specific pathways that convey pain
- regions of CNS specifically and distinctly activated in response to pain
unexplained:
- pain perception is not always proportional to intensity of stimulus
- modulation by other stimuli (e.g. acupuncture)
- perception of pain in severed limbs (phantom limbs)
- referral of pain from viscera to skin
- placebo effect
sensitisation - hyperalgesia
increased response to painful stimulus
normally tolerable painful stimulus e.g. light skin prick
result of lowered nociceptor thresholds so pain response is heightened
e.g. prostaglandin lowers threshold for action potential generation
sensitisation - allodynia
painful response to normally innocuous stimulus
relay neurons become sensitive to nearby non-nociceptive inputs
e.g. painful sensitivity of sunburnt skin to gentle stimulus e.g. light brushing
central sensitisation
activity dependent local release of substances from nociceptive dorsal horn neurons
e.g. hyperalgesia (periphery, makes painful stimuli more painful, lowers action potential thresholds); allodynia (innocuous stimuli perceived as painful)
can also occur when central pathways are damaged e.g. diabetes, shingles, MS, stroke
