28/ pain Flashcards
(18 cards)
1
Q
how is pain different from other senses
A
- both a discriminative sensation and a graded motivation (behavioral drive)
2
Q
specifity vs convergence
A
- specifity theory: pain is a distinct sensation, detected by pain receptors, transmitted to pain areas of brain
- convergence theory: pain is integrated and plastic, pattern of convergent somatosensory activity in a distributed network
- both are true
3
Q
types of nociceptors (myelination)
A
- lightly myelinated A delta fibres: fast. mechano sensitive, mechanothermal sensitive. sharp pain
- unmyelinated C fibres: slow. polymodal - mechanical, thermal, chemical. diffuse and longer lasting
- respond specifically to pain and are a subset of afferents w free nerve endings
4
Q
how is the fat nociceptors respond specifically to pain demonstrated w heat response
A
- magnitude of thermoreceptor saturated well before 45 degrees, when pain starts
5
Q
what does response to capsaicin suggest about function of A delta fibres, note about heat
A
- capsaicin receptor TRPV1 activated in nociceptive fibres A delta and C
- activated by capsaicin
- capsaicin thought to mimic endogenous vanilloids released by stressed tissue
- receptors also known to detect heat as well as pain
6
Q
central pain pathways - 2 components
A
- sensory discriminative: signals location, intensity and type of stimulus. easiest to define, involves spinothalamic tract/anterolateral system
- affective motivational: signals unpleasantness, enables autonomic activation - fight or flight
7
Q
what does measurement of activity in the somatosensory cortex indicate
A
- this region does respond to pain and response correlates to intensity of pain
- this is spatially mapped
8
Q
complex cortical representation of pain
A
- painful stimuli activate same area of somatosensory cortex as non painful stimuli to the same area
- however pain activates a distinct response including other regions - eg insula and cingulate cortex
- these areas are linked to limbic system which is involved in emotional response - affective motivational repsonse
9
Q
affective motivational pathways
A
- share some paths w the anterolateral system
- little or no topographic mapping
- number of inputs to emotional (limbic) system and homeostatic (hypothalamic) system
- NOT intensity of pain - this is via discriminative pathway
- unpleasantness
10
Q
what challenges specifity theory
A
- pain not always proportional to stimulus intensity
- modulation by other stimuli like acupuncture
- pain in phantom limbs
- referral of pain from viscera to skin
- placebo effect
11
Q
hyperalgesia, what is it, mechanism
A
- hyperalgesia: increased response to pain on area of damaged skin
- tissue damage releases soup of inflammatory substances which affect nerve function
- lowered nociceptor threshold
- prostaglandins lower threshold for ap generation
- analgesic painkillers aspirin and ibuprofen inhibit COX enzyme which produced prostaglandins
12
Q
allodynia what is it, mechanism
A
- allodynia: painful response to
normally unpainful stimulus - relay neurons become sensitive to nearby non-nociceptive inputs like pressure - perceived as painful
13
Q
hyperpathia
A
- variant of hyperalgesia and allodynia
- when fibre damage centrally or peripherally resulting in raising of detection threshold
- when threshold is exceeded, explosive pain
14
Q
what is neuropathic pain
A
- central sensitisation, central pathways themselves are damaged
- can be experienced after limb amputation
15
Q
phantom limb pain, what does it indicate, can children born w/o limbs experience this
A
- central representation of the body is not passive - persists in absence of peripheral input
- yes - central maps partly pre formed
- pain is partly what we expect it to be
16
Q
referred pain
A
- pain in viscera (organs) perceived as coming from specific locations in the skin, eg left arm pain = heart attack
- reflect convergence of visceral afferents onto same pathways as cutaneous afferents in cns
- useful in clinical diagnosis
17
Q
physiological basis of pain modulation - stimulating areas, mechanism, opioids
A
- stimulating certain regions of midbrain produced pain relief
- stimulation of periaqueductal grey matter activates brainstem nuclei that modulate the activity of dorsal horn neurons
- in dorsal horn descending inputs activate enkephalin releasing interneurons which presynaptically inhibit nociceptive fibres
- enkephalins part of endogenous opioid peptides
18
Q
theory for why rubbing painful area relieved the pain
A
- local inhibition by mechanoreceptive A beta fibres of nociceptive C fibres input to spinal cord
- gate/ sensory interaction theory of pain
- pain perception result of CONVERGANT sensory info - challanges specifity
