Pain Transmission Flashcards

1
Q

pain

A

unpleasant sensory and emotional experience associated w/ actual or potential tissue damage or described in terms of such damage

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2
Q

hyperalgesia

A

magnification of pain perception to normally minimally painful stimuli

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3
Q

allodynia

A

perception of pain to normally non painful stimuli

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4
Q

hyperesthesia

A

magnified sensation of any type

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5
Q

dysesthesia

A

distorted, magnified and unpleasant sensation to normal stimulation

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6
Q

neuropathic pain

A

generated by or magnified by disorders of neural tissue

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7
Q

nocioceptive pain

A

mostly acute

high threshold mechanoreceptors- usually free nerve endings

also react to chemicals- tissue metabolites, transmitters, tissue cell products, inflammatory mediatiors

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8
Q

pain afferent fibers

A

either Adelta or C fibers

slow conducting
slow adapting

transmitters- substance P, neurokinin A

release transmitters on both ends of axon- neurogenic inflammation

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9
Q

why isnt pain input focused in the spinal cord

A

distribute over 4-8 segments

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10
Q

central terminals

A

initial termination is in dorsal horn - substantia gelatinosa

c fibers terminate in layer 1 or layer 5

cells from layer 1 transmit stinging pain, sharp. dont encode intensity

cells from layers 4,5 respond to intensity, but not location

these go up spinothalamic tract

A-beta fibers (normal touch) terminate in 3 and 4

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11
Q

neospinalthalamic tract

A

spinothalamic tract

decussate in ventral commissure in cervical cord

reach ventral posterolateral nucleus of thalamus (VPL)

most direct pathway

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12
Q

paleospinothalamic pathway

A

most of projections are from WDR neurons

terminates in nonspecific thalamic nuclei that project broadly over cortex

can affect many areas of the cortex including those involved w/ mood, attnetion, etc

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13
Q

spino-reticulo-thalamic pathway

A

collateral branches terminate in the brainstem resulting in changes in autonomic activity

ie- sweating, paleness, tachycardia, etc

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14
Q

referred pain

A

caused by convergence of pain inputs on highly convergent cells

common in head b/c of convergence of trigeminal nerve

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15
Q

how does pain produce muscle spasms?

A

reflexes mediated by interneurons produce withdrawals reflexes d/t pain

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16
Q

causes of chronic pain

A

chronic inflammation

damaged peripheral nerves causing increased Na channel expression

potentiation of synapses

17
Q

long term potentiation

A

caused by increased intracellular Ca d/t activation of NMDA receptors

at higher levels of stimulation, brain neurotrophic growth factor is also released, which act on tyrosine kinase and enhance synaptic conductivity

18
Q

how can you modify acute pain

A

anti inflammation

inhibit pain nerve fiber

activate large diameter sensory axons

activate receptor that block transmission

19
Q

why does rubbing help prevent pain

A

activates A-beta sensory fibers that synapse on inhibitory interneurons that block pain signals

20
Q

how can you modify chronic pain

A

control inflammation

inhibit pain nerve fiber

activate large diameter sensory axons

activate systems that block transmission

21
Q

descending pain control system

A

act thru descending serotonin and norepi pathways

activated by periacqueductal gray

22
Q

modifying neuropathic pain

A

activation of serotonin systems- antidepressants

activation of norepi systems- SNRI

altering voltage gated calcium channels- anti convulsants

23
Q

thalamic pain syndrome

A

injury to thalamus deactivates inhibitory neurons and allow sensation of more pain

24
Q

suffering

A

affective components of pain mediated by frontal lobe and anterior cingulate gyrus

25
Q

cingulate cortex

A

most active on the border of pain- deciding how to react