Lec 16 Pain Flashcards

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1
Q

What does it mean that there are discriminative and affective components of pain?

A
  • discriminative = ability to perceive and localize

- affective = behaviors and emotions that affect mood and motivation

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2
Q

What is the discriminative pain pathway?

A
  • Ad + C fibers from body branch up and down a few segments [lisshauer’s tract] and synapse in dorsal horn [lamina I/V], cross immediately after synapsing, ascend in spinothalamic tract
  • Ad + C fibers from face come from CN V, go caudal through spinal trigeminal tract, synapse in spinal trigeminal nucleus, cross immediately after synapsing, ascend in trigeminothalamic tract
  • all fibers join together and synapse in VP thalamic nuclei then go to S1
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3
Q

What is the affective path of pain perception?

A
  • originates from ascending info from lamina I/V in dorsal horn or spinal nucleus of V
  • travels through spinothalamic/trigeminothalamic tracts
  • axon branches innervates a bunch of things along the way
periaqueductal grey [PAG]
rostroventral medulla [RVM] 
thalamic VM and MD nuclei
ventromedial hypothlamaus {VMH]
amygdala
globus pallidus
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4
Q

What is contained in the rostroventral medulla [RVM]?

A
  • parabrachial nucleus [pons]
  • reticular formation
  • raphe nuclei
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5
Q

Where do fibers that branch of off spinothalamic fibers into thalamic VM and MD nuclei project to? function?

A
  • project to insula and cingulate cortex

- encode emotional components of pain that affect mood and motivation

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6
Q

What is the role of periaqueductal gray [PAG] and RVM [rostroventral medulla] in control of pain?

A
  • receive collateral fibers off of spinothalamic tract that feedback into PAG and directly activate descending projections
  • integrate “top-down” info from cortex [S1, cingulate, insula] and limbic systems [amygdala and VMH] with ascending spinothalamic info
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7
Q

Where do PAG axons project? And what is the path by which they eventually effect spinal cord interneurons?

A

descend and synapse onto

  • norepinephrine neurons in locus ceruleus and
  • serotonin neurons in dorsal raphe
  • after synapse, send projections to spinal cord dorsal horn where release NE/5HT onto local inhibitory interneurons
  • local interneurons release enkephalin [endogeneous opioid] to inhibit lamina I and V spinothalamic neurons –> thus decrease throughput of nociceptive transmission
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8
Q

What is function of enkephalin?

A

acts both pre and post synaptically

pre: pain/temp A-delta and C fibers –> inhibits NE release
post: spinothalamic ascending neurons –> causes hyperpolarization, diminishing ESPs

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9
Q

What structures are responsible for emotional content of pain?

A

limbic

- amygdala + insula

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10
Q

what 3 structures are responsible for motivational content of pain?

A
  • globus pallidus
  • cingulate
  • S1
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11
Q

what structure is responsible for generating appropriate behaviors to threats?

A

ventromedial hypothalamus [VMH]

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12
Q

what happens in nociceptive pain syndrome?

A
  • first pain mediated by A-d, 2nd pain by C
  • gate theory: spinothalamic nerves receive convergent input from Ad/C and AB fibers, AB fibers can activate inhibitory interneuron which dampens throughput of pain info from Ad/C

= due to cross-talk

  • no nervous system lesion or inflamation
  • dampened feeling of pain from Ad/C due to inhibition by AB fibers that are close by
  • referred pain from visceral site of lesion to a far away cutaneous site
  • only pain in presence of stimulus [no pain with lack of stimulus or with light touch]
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13
Q

what happens in inflammatory pain syndrome?

A
  • pain hypersensitivity due to peripheral inflammation involving detection of active inflammation by nociceptors and a sensitization of nociceptive systme
  • spontaneosu and stimulus dependent pain
  • evoked by low and high intensity stimuli

= protective –> aids in healing in tissue trauama or joint inflammation

mech: neurochemical mediators secreted by immune cells cause pain fibers to discharge APs aberrantly –> peripheral and central amplification of pain

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14
Q

What is allodynia?

A

normally non-painful stimuli become painful

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15
Q

What is hyperalgesia?

A

exaggerated response to normally painful stimulus

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16
Q

What is disfunctional pain?

A

s

17
Q

What stimuli cause inflammatory pain?

A

tissue trauma, surgery, joint inflammation [rheum arthritis]

18
Q

What stimuli cause nociceptive pain?

A
  • abnormal mech forces, organ injury [angina, ischemic claudication]
19
Q

What is dysfunctional pain?

A

maladaptive pain – neither protects nor upports healing/repair

  • same components as inflammatory pain without evidence of inflammation or neuronal lesion
  • spontaneous and stimulus dependent
  • get sensory amplification
20
Q

What are examples of stimulus that can cause dysfunctional pain?

A

fibromyalgia [body wide pain in joints/muscle, central amplification]

primary erythermalgia [peripheral amplification of pain, red/war/burning in hands and feet

21
Q

What is neuropathic pain?

A
  • maladaptive plasticity caused by lesion or disease alters nociceptive processing so that pain is felt in absence of stimulus and responses to innocuous/noxious stimuli are enhanced
  • have hyperalgesia, allodynia, pain that outlasts stimulus
22
Q

What are mechs that might cause neuropathic pain?

A

CNS: stroke, spinal cord injury, multiple sclerosis

PNS: nerve trauama, metabolic [diabetes], herpes zoster, AIDS

23
Q

What is central sensitization? mech?

A
  • synaptic signaling strength of pain pathways greatly exaggerated by several maladaptive mech
  • causes pain to no longer be coupled so tightly to presence/intensity/duration of noxious peripheral stimuli
  • produces pain hypersensitivity of normal inputs
24
Q

What are 3 possible mechs leading to central sensitization

A
  1. increased membrane excitability in peripheral axons via upregulation of Na channels
  2. increased synaptic efficacy via upregulation of glutamate receptors at 2nd order neurons
  3. decreased inhibition in local interneuron networks, decreased inhibition by descending systems
25
Q

What is phantom limb pain?

A

pain in body part that has been amputated

2 mech:

  1. arises from central sensitization
  2. cortical reorginization of S1 – axons from neighboring cortex sprout into region of cortex that previously received input form amputated limb, causes axon firing unpredictably –> pain
26
Q

What are treatments for neuropathic pains?

A
  • give antidepressants [MAO reuptake inhibitors, improve MAO descending inhibition path]
  • give anticonvulsants [block ectopic discharge]
  • block neurotransmitter release [ Ca channel anticonvulsants]
  • opioids [enhance endogenous inhibitory analgesic system]

-

27
Q

what does inflammatory pain respond to?

A
  • often NSAIDs, other anti-inflammatory agents
28
Q

What are pitfalls of opioids?

A

addiction
tolerance
overuse
cognitive impairment