Pain - Tom Salomon Flashcards

1
Q

What is pain

A

unpleasant sensory and emotional experience due to actual or potential tissue damage or described in terms of such pain

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2
Q

why is pain good

A

guides behaviour by signalling harm to our bodies - learn how to avoid injury

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3
Q

What are melzachs 3 forms of pain

A

short term - ie reflexive withdrawal from a stimulus
long term - ie promotion of recuperative behaviours
expression - social signalling to others of potential harm and to elicit caregiving behaviours

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4
Q

what is a bottom up theory of pain

A

pain determines by the properties of the stimulus and teh receptor that encodes it

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5
Q

what is specificity theory

A

stimulus activates fibres that sends message to the brain - specific fibres, pathways and brain regions associated with specific pain

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6
Q

types of specific receptors

A

parcinian corpuscles
meisseners corpuscles
merkels discs
ruffinis corpuscles

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7
Q

what are nociceptors

A

pain receptors with free nerve endings that response to nocious stimuli that could lead to tissue damage

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8
Q

types of nociceptors

A

a delta

c fibre

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9
Q

define a delta nociceptors

A

low threshold, thick and myelinated for fast conduction of info for initial fast sharp localised pain

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10
Q

define c fibre nociceptors

A

high threshold thing unmyelinated receptors for slow conductance of diffuse pain ie burning

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11
Q

describe the spinothalamic tract (highter order path)

A

A delta/c fibre decussate at dorsal horn of spinal cord

Ascend to contra lateral thalamus

Ascend to somatosensory cortex and periacqueductal gray PAG

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12
Q

describe spinoreticular tract (higher order path)

A

A delta and c fibre decussate at dorsal horn

ascend to reticular formation at brain stem

Ascend to intralaminar nuclei of thalamus and hypothalamus

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13
Q

problems with bottom up theories

A

peripheral input not account for variety of pain experienced
i.e. why ovverride when distracted, how alter via placebo and percieved control influence

Invariable link between pain and injury - pain but no injury ie phantom limb or injury without pain ie episodic/congenital analgesia

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14
Q

define episodic analgesia

A

absence of pain in response to pain stimuli

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15
Q

define congenital analgesia

A

no sensation of physical pain from stimuli from birth

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16
Q

define melzack and wall gate control theory

A

Inhibitory pain modulation at the spinal cord level - explain why when we bang our head, it feels better when we rub it.
activating A fibres with tactile, non-noxious stimuli, inhibitory interneurones “gate” in the dorsal horn are activated leading to inhibition of pain signals transmitted via C fibres

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17
Q

describe periacquductal gray

A

PAG in midbrain and rostral ventromedial medulla (RVM) - involved in descending inhibitory modulation. centres contain high concentrations of opioid receptors and endogenous opioids - analgesic(pain relief). Descending pathways project to the dorsal horn and inhibit pain transmission & modulate emotion ie defence and fear responses

18
Q

describe rostral ventromedial medulla

A

strong connection to PAG
projects heavily to dorsal horn

forms part of a descending pathway that modulates nociceptive neurotransmission at the dorsal horn

3 categories of neurons:
On-cells, off-cells, and neutral cells. Off-cells decrease in firing rate right before a nociceptive reflex - inhibitory
On-cells activity immediately preceding nociceptive input - excitatory.
Neutral cells no response to nociceptive input.

Increase/decrease in perception of pain

19
Q

what is the pain matrix (apkarian et al 2005)

A

meta analysis of brain regions active across modalities during experience of pain
indicated cortical and subcortical substrates underlying pain perception and network of somatosensory, limbic and associated structures recieving nociceptive input

20
Q

Areas directly involved in the pain matrix

A

Primary & secondary somatosensory cortex

Insula

Anterior cingulate cortex

Prefrontal cortex

Thalamus

21
Q

what is secondary hyperalgesia

A

increased sensitivity to pain due to nococeptive damage outside of the main injury site - heightened pain response to stimuli as a measure of central sensitisation and role in descending modulatory system ie activity of RVM

22
Q

testing secondary hyperalgesia

A

expose pps to thermal stimuli and measure SH before and after
one group given pain relevant CBT and the other psychotherapeutic intervention
intensity remains tehsame but resuction in way pain is viewed in CBTgrou
+ sig reduction in SH sensitivity - mind over matter

23
Q

how does the brain modulate pain

A

reduced pain assoc with reduced response in accumbens and insula

regulation of pain activates preganule acc, vmPFC, vl/dlPFC (emotional regulation involvement)

24
Q

salomons et al 2004 perceieved control and pain

A

response to pain depend on peripheral nociceptive input as well as cog and affective context - degree pain is percieved as controllable
manipulate belief - tell reduce stimulus to non painful duration if respond in correct direction and response less than threshold response

25
Q

findings of salomons et al 2004

A

regions involved in pain sensitive to cog context - reduced sensitisation when thought to be in control of stimulus intensity

vmPFC active only when pain uncontrollable - not primary but thought to modulate

overlap between acc and insula

dl/vl 65% variation in pain rate - high involvement in pain modulation

26
Q

Melzach and cadet dimensions of pain

A

Sensory discriminative
Motivational affective
Cognitive evaluative

26
Q

Melzach and cadet sensory discriminative define

A

info of intensity, location or quality ie throbbing

27
Q

Melzach and casey motivational affective define

A

emotional component that determines avoidance of a stimulus ie sickening

28
Q

Melzach and casey cognitive evaluative define

A

evauation of the meaning/context ie mild or excrutiating pain

29
Q

Spinothallamic tract linked to

A

Pain localisation

30
Q

What is the spinoreticular pathway linked to

A

Emotional/feeling aspect of pain

31
Q

Areas thought to be involved in pain and pain modulation

A

Hippocampus

Brain stem

Amygdala

PAG/RVM

Basal ganglia

Posterior partial cortex

32
Q

Types of cortical responses in pain modulation

A

Altered pain matrix responses

Activation of pain modulation regions

33
Q

What areas in pain matrix alter response to modulation

A

ACC
insula

(Reduction in activity)

34
Q

What areas in brain activate in pain modulation

A

Vl/dl/vmPFC

pregenual ACC

35
Q

Pain matrix activation in pain modulation - evidence

A

ACC activate when subjects distracted by task

Salomons
Perceived control reduces

36
Q

Descending Cortical modulation areas activity

A

Perceived control - Activation of vlPFC vmPFC and PAG

Placebo analgesia (perceive analgesic effect because believe they will) - vmPFC dlPFC and PAG

Attention to pain - vmPFC and PAG

37
Q

Diabetic encephalitis patient emotional response to pain

A

lesions to ACC amygdala and insula (involved in experience and modulation of pain)

Capable of experiencing pain despite no regions

Can modulate pain based on meaning to him

38
Q

Social pain problem

A

Media makes quick inferences about studies into pain and make incorrect judgements about how to treat etc

Reverse inferences

39
Q

Define reverse inference

A

Logical error by affirming the consequent - perceive that activation leads to pain when not necessarily true

40
Q

Mouraux reverse inference

A

Does pain matrix activation mean feel pain

NO

Same areas also activate for non painful sensory stimuli ie tactile auditory or visual