pain Flashcards

1
Q

allodynia

A

sensitisation to normally innocuous stimulu

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2
Q

specificity theory

A

pain is a distinct sensation

detected and transited by specific recpetors and pathways to distinct pain areas of the brain

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3
Q

convergence theory

A

pain is an integrated plastic state represented by a pattern of convergent somatosensory activity within a distributed network (neuromatrix)

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4
Q

A delta fibres

A

lightly myelinated Fast (relative) about 20 m/s
mechano-sensitive
mechano-thermal sensitive

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5
Q

C fibres

A

unmyelinated SLOW about 2 m/s

polymodal: mechanical, thermal and chemical

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6
Q

types of free nerve endings

A

Although mechanoreceptors, thermoreceptors, and nociceptors are all examples of free endings, nociceptors are the most common type.

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7
Q

free nerve endings location and modality

A

location: widepsread in epithelia and connective tissues
modality: pain, heat, cold

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8
Q

thermoreceptor response to pain

A

is specific
i.e. can find afferents whose activity correlates with pain perception

it can be clearly shown with heat response that thermo-receptor activation has already started before pain is perceived by nociceptor

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9
Q

fast or ‘first’ pain

A

sharp and immediate

can be mimicked by direct stimulation of A delta fibre nociceptors

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10
Q

slow or ‘second’ pain

A

more delayed, diffuse and longer lasting

mimicked by stimulation of C fibre nociceptors

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11
Q

activation of which types of receptors never elicits pain sensation

A

stimulation of A alpha and A beta (proprioceptive and mechanoceptive) fibres

distinct set of A delta and C fibres specifically associated with pain detection

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12
Q

molecular pain receptors activated in nociceptive A delta and C fibres at 45 oC

A

the capsaicin receptors (TRPV1)

the vanilliod, capsaicin is also active component in chillies

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13
Q

TRP

A

Transient receptor potential proteins

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14
Q

nociceptors can detect release of chemicals

A

capsaicin is thought to mimic endogenous vanilloids released by stressed tissues so nociceptors may also work by detecting release of chemicals from stressed cells

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15
Q

sensory discrimation pathway of nocipetive info to the brain

A

signals location, intensity and type of stimulus

used the spinothamalmic tract

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16
Q

affective-motivational pathwah of nociceptive info to the brain

A

singals unpleasantness and enables autonomic activation, flight or fight response

17
Q

spinothalamic tract//anterolateral system

A

major skin to thalamus sensory pathway

transmits signals from receptors ending via dorsal root ganglion cells via spinal cord, medulla and midbrain to thalamus

18
Q

MRIs can show representation of pain

A

activation of C fibres or A beta fibres shows same area of somatosensory cortex activation for both non painful mechanical stimuli and painful ones

but pain also activates a distinct response that includes other regions

e.g. insula and cingulate cortex

19
Q

activation of insula and cingulate cortex

A

connected to the limbic system and regulate emotional responses
so part of the affective-motivational response to pain

20
Q

affective motivational pathways

A
  • shares some paths with spinthalamic pathway
  • little or no topographic mapping (neutrons from parabrachial nucleus can respond to painful stimuli from anywhere on the body’s surface)
  • number of points of input to the emotional (limbic) and homeostatic (hypothalamic) system
  • strong correlation of painful experience (unpleasantness) with activation in cingulate cortex
21
Q

affective motivational pathway points

A
information from upper body
via spinal cord
caudal medulla
middle medulla-- reticular formation-- hypothalamus and limbic system
mid pons
parabrachial nucleus 
projections to the amygdala and hypothalamus 
thalamus 
insula cingulate cortex
22
Q

phenomena that don’t fit with the theories of specificity

A

pain perceived not always proportional to intensity of stimulus

modulation of pain by other stimulus (acupuncture)

perception of pain in severed limbs (phantom)

referral of pain from viscera to skin (heart attack)

placebo effect

23
Q

hyperalgesia (sensitisation)

A

increased response to a painful stimulus
e.g.hypersensitivity of damaged skin to a normally tolerable painful stimulus (e.g. light skin prick)

a result of lowered nociceptor thresholds which heightens pain response

24
Q

allodynia (sensitisation)

A

painful response to a normally innocuous stimulus

e.g. painful sensitivity of sunburnt skin to gentle mechanical stimulus (e.g. light brushing) or mild temp

25
Q

inflammatory response peripheral effects of tissue damage

A

tissue damage releases inflammatory substances which affect nerve function, recruit mast cells and neutrophils and increase local blood flow

e.g. bradykinin directly affects the function of nociceptive molecular receptors such as TRPV1

26
Q

pain relief

A

aspirin and ibuprofen act on cyclooxygenase (COX) an enzyme for prostaglandin biosynthesis

27
Q

dorsal horn

A

The posterior grey column (posterior cornu, dorsal horn, spinal dorsal horn posterior horn) of the spinal cord is one of the three grey columns of the spinal cord. It receives several types of sensory information from the body, including fine touch, proprioception, and vibration.

28
Q

release of prostaglandins from nociceptive dorsal horn neurons results in what

A

a lowering of the thresholds for action potential generation for neurones relaying nococpetive info – giving rise to hyperalgesia

another consequence is that these neutrons become sensitive to non nociceptive inputs- allodynia (non painful perceived as painful)
because release of prostaglandins in dorsal horn affect thermal and mechanic receptors (the non pain fibres)

29
Q

hyperpathia

A

a variant of hyperalgesia and allodynia (different underlying causes)

when there is axonal loss (centrally or peripherally) results in raising of the detection threshold (i.e. need greater stimulation to detect stimulus)
but when the detection is felt the pain is explosive!!

30
Q

central sensitisation in diseases

A

can occur when the central pathways themselves are damaged e.g. in diabetes, shingles, MS and after a stroke

the virus of shingles sits latent in nerves

31
Q

what is suggested by the phenomenon of phatom limb pain

A

indicates central representation of the body is not passive
it persists in the absence of peripheral input

children born without limbs still get phantoms suggesting the brain’s map of the body may be pre- formed

phatom limb pain is hard to control suggesting that the pain is also centrally represented

NOT fitting with specificity theory

32
Q

referred pain

A

pain due to damage in the viscera (gut) is often perceived as coming from specific locations in the skin according to what organ is affected e.g. heart attack- pain in left shoulder and arm

(not easily explained by specificity theory)

33
Q

why do we get referred pain

A

thought to reflect convergence of visceral afferent onto the asme pathways as cutaneous afferents in CNS

useful in aiding clinical diagnosis of organ dysfunction!

34
Q

central modulation of pain

A

mind of matter - when walking through fire

Henry Beecher - soldifers in WW2 with severe wounds often felt no or little pain

mere suggestion that pain will be controlled by pain relief creates ‘placebo effect’

35
Q

physiological basis of pain modulation

A

experiemnts stimlating regions of the midbrain produced pain relief

e.g. the periaquecductal grey activates brainstem nuclei that modulate activity of dorsal horn neutrons

in the dorsal horn, descending inputs activate enkephalin-relseaing interneurons which presynaptically inhibit nociceptive fibres

36
Q

enkephalins

A

members of a family of endogenous opioid peptides that also include endorphins and dynorphins

interneurons that release encephalon presynaptically inhibit nociceptive fibres

37
Q

local modulation of pain

A

rubbing an injury often reeves pain

thought to be due due local inhibit by mechanoreceptors (Adelta fibres) of conceptive (C fibres) inputs in the spinal cord

Melzack and Wall (1965)– proposed ‘gate’ or ‘sensory interaction’ theory of pain

suggested pain perception to be the result of integration of convergent sensory info

again challenges the assumptions of a straight through pain input of specificity theory

38
Q

we know that pain is not due to ramping up of normal thermo-receors in part because…?

A

thermoreceptor firing is saturated by the time pain is perceived in response to heat