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M2 Neuron Brain Behavior > 8/29 Neurobiology of Pain - Suss > Flashcards

8/29 Neurobiology of Pain - Suss Flashcards

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1
Q

sensory neuron fibers

A-alpha

type I

A

13-20 um

myelinated

receptors:

  • muscle spindle : proprioception
  • Golgi tendon organ : proprioception
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2
Q

sensory neuron fibers

A-beta

type II

A

6-12 um

myelinated

receptors:

  • muscle spindle : proprioception
  • Meissner’s corpuscle : superficial touch
  • Merkel’s receptor : superficial touch
  • Pacinian corpuscle : deep touch, vibration
  • Ruffini ending : deep touch, vibration
  • hair receptor : touch, vibration
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3
Q

sensory neuron fibers

A-delta

type III

A

1-5 um

myelinated

receptors:

  • bare nerve ending : pain
  • bare nerve ending : temp (cool)
  • bare nerve ending : itch
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4
Q

sensory neuron fibers

C

type IV

A

0.2-1.5 um

UNmyelinated

receptors:

  • bare nerve ending : pain
  • bare nerve ending : temp (warm)
  • bare nerve ending : itch
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5
Q

nociception involved SPECIALIZED neurons and receptors

A

ex. temp sensation - thermoreceptors sense up to a certain point, nociceptors take over after that point

  • nonnociceptive thermoreceptors continue to respond at same rate even at higher temps
  • nociceptors respond at higher temps only
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6
Q

pain temporal elements

which fiber conducts?

A

first pain : A-delta fiber

second pain : C fiber

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7
Q

four components of pain

A

1. sensory discriminative component (who/what/when)

  • location, intensity, quality of stimulation
  • depends on pathways that target traditional somatosensory areas of cortex

2. affective motivational component

  • unpleasant quality of experience that activates autonomic nervous system
  • depends on addtl cortical and brainstem pathways

3. sensitization

  • hypersensitivity to protect injured area, promote healing, prevent infection

4. descending control/central modulation

  • reduce pain perception
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8
Q

anterolateral pathways that transmit nociceptive information

A

1. spinothalamic tract : discriminative aspects of pain, temperature

  • facts of what’s causing pain

2. spinoreticular tract : emotional and arousal aspects of pain

  • emotional aspects of pain (sweat, fear, desire for comfort)

3. spinomesencephalic tract : central modulation of pain

  • descending control of pain that helps reduce pain sensation
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9
Q

anterolateral pathways

A

starting in rostral medulla

  • STT continues up into thalamus
  • SRT sends axonal projection to reticular formation in pons
  • SMT sends projections to superior colliculus (bump in midbrain) and periaqueductal gray

also anterolateral projections to midline thalamic nuclei → cingulate cortex + insular cortex

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10
Q

thalamic relays of somatosensory system

A

VPL : medial lemniscus, spinothalamic tract

VPM : trigeminal lemniscus, trigeminothalamic tract

midline thalamic nuclei : spinoreticular & spinomesencephalic tracts

intralaminal nuclei : spinoreticular & spinomesencephalic tracts

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11
Q

chronic pain and gray matter

A

chronic pain can decrease gray matter

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12
Q

localization of lesions : paresthesia

lesion of parietal lobe or primary sensory cortex

A

contralateral numb tingling or pain

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13
Q

localization of lesions : paresthesia

lesion of thalamus

A

contralateral burning pain

[Dejerine-Roussy Thalamic/Central Syndrome]

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14
Q

localization of lesions : paresthesia

lesion of DCMLS

A
  • tingling, numb sensation
  • tight band-like sensation around trunk or limbs
  • feeling of having gauze on fingers
  • electric sensation down back/extremities upon neck flexion [Lhermitte’s sign]
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15
Q

localization of lesions : paresthesia

lesion of nerve roots

A

radicular pain with numbness and tingling in dermatomal distribution [radiculopathy]

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16
Q

localization of lesions : paresthesia

lesion of anterolateral STT pathways

A

sharp, burning, or searing pain

17
Q

causes of sensory neuropathies

diabetes

A
  • distal symmetrical polyneuropathy (glove and stocking)
    • compromised microvasculature to nerve roots
  • acute mononeuropathy
18
Q

causes of sensory neuropathies

mechanical

A

extrinsic compression, traction, laceration, or intrinsic entrapment

  • neurapraxia : mild insult [temp impairment of nerve conduction]
  • Wallerian degen : severe insult [degen distal to site of injury; regen may occur]
  • causalgia/complex regional pain syndrome : incomplete regen → burning sensation, edema
  • neuralgia : severe persistent pain in distributino of CN or spinal nerve
    • ex. trigeminal neuralgia
19
Q

causes of sensory neuropathies

diabetes

A
  • distal symmetrical polyneuropathy (glove and stocking)
    • compromised microvasculature to nerve roots
  • acute mononeuropathy
20
Q

causes of sensory neuropathies

Varicella/Herpes-zoster virus

A

increases excitability of sensory neurons in DRG → low threshold of firing and spontaneous activity

ex. shingles → severe pain in dermatomal distribution/rash
tx: antivirals

21
Q

Na channel mutations and pain sensation

which gene

how they found it

diff types of mutations in it

A

congenital insensitivity to pain in family in Pakistan → research has revealed the gene responsible

Na v1.7 encoded by SCN9A gene

  • recessive mutations → loss of function →
    • congenital insensitivity to pain (CIP)
  • dominant mutations → gain of function
    • inherited erythromelalgia (IEM) : extreme sensitivity to temp
    • paroxysmal extreme pain disorder (PEPD)
22
Q

sensitization

types

why?

A

repeated application of noxious stimulus leads neighboring neurons that were NOT responsive to become responsive!

  • hyperalgesia : phenomenon of stimuli that are normally perceived as slightly painful → significantly more painful
  • allodynia : induction of pain by what is normally an innocuous stimulus

why?

protects injured area, promotes healing, prevents infection

results from changes in sensitivity of peripheral nociceptive receptors and/or central targets

23
Q

peripheral sensitization

A

sensitization of first order (DRG) neuron

result of interaction of nociceptors with substances in “inflammatory soup” → decrease threshold of activation for nociceptors

examples:

Substance P → vasodilation of blood vessels (edema), degranulation of mast cells → histamine released (lowers threshold of DRG neuron activation)

prostaglandins : increase response of nociceptive fibers

  • application: NSAIDs (ex. aspirin, ibuprofen) fx by inhibiting COX to prevent synthesis of prostaglandins!
24
Q

central sensitization

A

sensitization of CNS neuron (second order neuron)

immediate, activity-dep increase in excitability of neurons in dorsal horn of spinal cord following high levels of activity in nociceptive afferents to increase pain sensitivity

mechanisms:

  1. transcription independent (windup)
    * lasts only during stimulation (acute)
  2. transcription dependent (allodynia)
  • can outlast stimulus for hours (chronic)
  • can be mediated by COX
  • devpt of or increase in spontaneous activity
  • reduction in threshold for activation by peripheral stimuli
  • expansion of receptive field size (conversion of cociceptive-specific neurons → wide dynamic neurons that can response to both innocuous and noxious stimuli)
25
Q

capsaicin as analgesic

A

moderate heat and capsaicin activate

  • vanilloid receptor (VR1) in C fibers
  • transient receptor potential (TRPV1) in C fibers

repeated application of capsaicin…

  • causes desensitization of C fibers → blocks peripheral sensitization!
    • how? continuous activation causing them to run out of nt!
  • depletes Substance P → blocks peripheral sensitization!
26
Q

descending control of pain perception

A

1. stress-induced analgesia

  • battlefield/athletic injuries often don’t present until AFTER stressful situation
    • fight or flight response is overriding pain perception

2. placebo effect : physiological response following admin of a pharmocologically inert “remedy”

  • effects can be blocked by naloxone (inhibitor of opiate receptors)
  • may explain hypnosis, meditation, acupuncture, mother’s kiss
27
Q

overlap in brain activation:

pain & meditation

A
  • anterior cingulate cortex
  • insula

both areas are triggered by both pain and meditation

28
Q

how do endogenous opioids work to reduce pain perception?

A

enkephalins, endorphins, dynorphins affect descending control of nociceptive info

descending inputs through downward projections (ex. Raphe nuclei) synapse on enkephalin-containing local circuit neuron (interneuron) → INHIBITS the signal of the C fiber (nociceptor) onto the dorsal horn projection neuron

29
Q

gate theory of pain

what is it?

example of the stubbed toe

  • players at work, what they do

application of theory

A

local modulation of nociceptive information

  • pain results from the balance of activity in nociceptive and non-nociceptive afferents

implication : when you stub your toe…

  • PAIN RELAY: activation of C fibers → hit secondary dorsal horn neuron with pain signal + inhibit inhibitory interneuron (so as to open the gates to pain reception)
  • RUBBING YOUR TOE: activation of mechanoreceptors (A-beta fibers) → activate inhibitory interneurons to MODULATE the transmission of pain (close the gates a little)!

application : TENS (transcutaneous electrical nerve stimulation) activates A-beta fibers → reduces pain

30
Q

dorsal column pathway for visceral pain

A

pain signal on primary neuron hits DRG cells and synapses close to midline

secondary neuron ascends in dorsal column pathway

  • DOES NOT decussate right away!
  • instead, moves ipsilaterally up to medulla before second synapse

tertiary neuron decussates in medulla → heads up to ventral posterior thalamus to third synapse

quarternary neuron sends signal out to insula

31
Q

surgical interventions for intractable pain

A
  1. midline myelotomy for visceral pain
    * selective cutting out of transmission areas
  2. cordotomy for cutaneous pain
    * cut lateral funiculus from dentate ligament to line of ventral rootlets several segments rostral to highest dermatomal level of pain
32
Q

referred pain

A

visceral pain that is conveyed centrally by neurons that carry cutaneous pain

when multiple primary order neurons converge on same secondary order neuron, you cannot distinguish which “primary site” the pain originated at

→→→ referred pain!

ex. esophagus and heart have overlap → GERD can present as pain on L ant chest wall, so you get mixup between MI and GERD

M2 Neuron Brain Behavior (53 decks)

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