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U5 Neuroscience > Nociception > Flashcards

Nociception Flashcards

1
Q

What is nociception?

A

sensation in response to potentially harmful or tissue damaging stimuli

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2
Q

What is pain?

A

psychological perception of the sensation caused by noxious stimuli

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3
Q

What is CIPA and how does it present?

A

inability to feel any pain due to gene mutation for trophic factor that influences development of somatosensory system

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4
Q

Where are the cell bodies of primary sensory neurons for nociception?

A

DRG and trigeminal ganglia

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5
Q

Where do the peripheral nerve endings enter the spinal cord?

A

along the lateral margins of the dorsal columns

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6
Q

Do nociceptors have accessory structures at their peripheral endings?

A

No, exist as free nerve endings

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7
Q

What type of nociceptive afferent fibers are thermal or mechanical nociceptors?

A

small diameter, thinly myelinated A-delta fibers that conduct at 5-30 m/s

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8
Q

What kind of pain activation of thermal or mechanical nociceptors associated with?

A

sharp, pricking pain

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9
Q

What type of nociceptive afferent fibers are polymodal nociceptors?

A

small diameter, unmyelinated C fibers that conduct at 0.5-2 m/s

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10
Q

Which nociceptive fibers are fast activating? slow activating?

A

fast activating are thermal/mechanical nociceptors, slow activating are polymodal nociceptors

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11
Q

What are polymodal nociceptors activated by?

A

high intensity mechanical, chemical, and hot (>45 C) or cold stimuli

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12
Q

Are nociceptors their own distinct receptor type?

A

Yes, they are activated independently from the somatosensory system. Nociception is not just the somatosensory system being stimulated at a higher rate.

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13
Q

When do nociceptors begin to discharge?

A

when stimulus is intense enough to cause tissue damage

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14
Q

What is the response in firing rate to increasing noxious stimulus?

A

will continue to increase as noxious stimulus increases until receptor is killed or stimulus is removed

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15
Q

What kind of fiber mediates first pain? How would you describe the pain?

A

A-delta fiber, focused, sharp pain

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16
Q

What kind of fiber mediates second pain? How would you describe the pain?

A

C fiber, duller, longer lasting pain

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17
Q

What are the 3 stages of pain sensation?

A
  1. A-delta fibers stimulated by stimulus and tingling occurs
  2. stimulation intensifies further and feeling of sharp pain occurs
  3. stimulation intensifies even more, C fibers are activated, and duller, longer lasting pain occurs
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18
Q

What type of receptor is TrpV1? Where is it found?

A

vanilloid receptor, in A-delta and C fibers

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19
Q

What is TrpV1 activated by?

A

capsaicin, heat, acids, anandamide, endovallinoids (endogenous chemicals similar to capsaicin released with peripheral injury)

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20
Q

What sensation does TrpV1 convey?

A

conveys spicy feeling/burning sensations in skin and mouth

21
Q

What is hyperalgesia?

A

enhanced sensitivity and responsivity to stimulation of area in and around damaged tissue

22
Q

What is the flare region? Does it have a higher or lower threshold for mechanical pain than normal tissue?

A

hypersensitized tissue right around the damaged tissue/insult, lower threshold for mechanical pain

23
Q

What causes the sensitization of nociceptors leading to hyperplasia?

A

release of bradykinin, histamine, prostaglandins, and other chemokines upon tissue damage enhances responsiveness of nociceptive endings

24
Q

What does electrical activity in nociceptors stimulate the release of?

A

chemical substances like substance P that cause vasodilation, swelling and release of histamine frm mast cells

25
Q

How do aspirin and other NSAIDs work to inhibit pain?

A

inhibit cyclooxygenase, which is important in the biosynthesis of prostaglandins released in inflammation that sensitize nociceptors

26
Q

Can a patient still feel pain if there is no nociceptive stimuli? If so, give an example.

A

Yes, pain due to injury of peripheral nerve such as nerve root avulsion

27
Q

Where do axons of nociceptive nerve cells enter the spinal cord?

A

dorsal roots in the dorsolateral tract

28
Q

When do nociceptive axons decussate? What tract do they join?

A

within one or two segments of entering the spinal cord, join the anterolateral spinothalamic tract

29
Q

What lamina of the superficial dorsal horn do the A-delta fibers terminate in? C fibers?

A

A-delta fibers in lamina I and V, C fibers in II

30
Q

Where are wide dynamic range neurons? What do they receive input from?

A

in lamina IV and V, receive input from A-alpha and A-beta somatosensory mechanoreceptors and A-delta nociceptive receptors

31
Q

Why is visceral pain referred?

A

due to the convergence of visceral and cutaneous nociceptors on the same dorsal horn projection neurons (wide dynamic range neurons)

32
Q

What is phantom limb syndrome?

A

sensory info about phantom body parts exists in absence of peripheral input due to unused cortex gathering info from nearby areas, can be accompanied by pain

33
Q

What path does nociceptive input from the upper body except the face and lower body travel in?

A

anterolateral spinothalamic tract

34
Q

What path does nociceptive input from the face travel in?

A

trigeminothalamic tract

35
Q

What is the target of the ascending nociception pathways?

A

ventral posterior nucleus of the thalamus

36
Q

In what part of the VPN does nociceptive info from the face go?

A

ventral posterior medial nucleus (VPM)

37
Q

In what part of the VPN does nociceptive info from the body go?

A

ventral posterior lateral nucleus (VPL)

38
Q

Where does the nociceptive info travel to from the VPN?

A

somatosensory cortex

39
Q

Is nociceptive information organized in somatotopic maps like epicritic information is in the somatosensory cortex?

A

No, damage to large areas of somatosensory cortex does not result in impaired responses to noxious stimuli or loss of pain

40
Q

What is dissociated sensory loss?

A

contralateral diminished sensation of pain below a unilateral spinal lesion and ipsilateral mechanosensory loss below the lesion

41
Q

Why does dissociated sensory loss occur?

A

protopathic information crosses in the spinal cord almost immediately upon entry and travels up the contralateral side to the VPN, epicritic information travels ipsilaterally up the spinal cord to the VPN so a lesion on one side would block the epicritic info from the same side and protopathic info from the opposite side

42
Q

Why does it not matter that protopathic information is not segregated into maps like epicritic information is?

A

don’t need to know exactly where pain is on body, just need to respond to it quickly
fine discrimination of pain signals comes from somatosensory tactile information

43
Q

What is descending pain modulation?

A

info comes down from the brain onto the output neurons of the dorsal horn and dampens the stimulus of pain

44
Q

What is are the locations in the pathway for descending pain modulation?

A

electrical stimulation of brainstem –> PAG –> nucleus raphe magnus (in the medulla) –> inhibitory synpases on laminae I, II, and V of dorsal horn (where the nociceptive afferent neurons terminate)

45
Q

What is the name of the pathway for descending pain modulation?

A

dorsolateral funiculus

46
Q

What is ENK? What does it act upon to dampen afferent pain stimuli?

A

enkephalin, an endogenous opioid, dampens afferent pain stimuli by inhibiting projection neurons of the dorsal horn carrying protopathic information

47
Q

How do opiates affect presynaptic nociceptive sensory neurons? postsynaptic dorsal horn projection neurons?

A
  • inhibit release of glutamate and neurotransmitters from presynaptic sensory neurons
  • hyperpolarize postsynaptic neurons to suppress their activity
48
Q

What is the first place in the nociception transmission path that opiates work?

A

level of the primary afferent synapse in the central system (in the dorsal horn) by a combination of pre and post synpaptic effects
-doesn’t work on peripheral free endings receiving the stimuli

U5 Neuroscience (35 decks)

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