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PHTH 7303 Neuro > Exam 3 Week 13 ppt 6 Pain peripheral and central component > Flashcards

Exam 3 Week 13 ppt 6 Pain peripheral and central component Flashcards

1
Q

Nociceptors are

A

unencapsulated endings that are categorized by the environmental stimulus

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2
Q

Nociceptors responds to

A

mechanical, thermal, chemical or all of these (polymodal)

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3
Q

Mechanical nociceptors- respond to

A

respond to intense mechanical stimuli

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4
Q

Mechanical nociceptors- fibers

A

have small myelinated (Ad) afferent axons

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5
Q

Thermal nociceptors- respond to

A

Respond to intense cold (below 5°C) or intense heat (above 45 C)

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6
Q

Thermal nociceptors- fibers

A

have myelinated (Ad) or unmyelinated (C ) afferent axons

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7
Q

Chemical nociceptors- respond to (3)

A

Respond to ions (K+ and H+), local inflammation mediators (histamine) and other chemicals (capsaicin)

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8
Q

Polymodal nociceptors- respond to

A

Respond to mechanical, thermal or chemical stimuli

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9
Q

Polymodal nociceptors- fibers

A

Small unmyelinated (C) afferent axons

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10
Q

two calibers of nociceptive afferent fibers there lead to a theory called

A

phenomenon of Double pain

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11
Q

phenomenon of Double pain (created by)

A

~First described by Lewis and Pochin (1937) where all the illustrations were labeled with their initials because they studied it by dropping hot metal on each other

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12
Q

phenomenon of Double pain (details)

A

~Sharp, stabbing pain followed by burning and aching sensation
—-Fast (1st) pain – Ad fiber 1° afferent – small myelinated
—-Slow (2nd) pain – C fiber 1° afferent - small unmyelinated
~More of theoretical than practical value

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13
Q

phenomenon of Double pain (details on fast pain)

A

~sharp stabbing pain or Fast (1st) pain arises from Ad fiber 1° afferent, small myelinated fibers

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14
Q

phenomenon of Double pain (details on slow pain)

A

~achy burning pain or Slow (2nd) pain arises from the C fiber 1° afferent, the unmyelinated fibers

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15
Q

3 different abnormal responses to stimulation of nociceptors

A

~peripheral sensitization
~hyperalgesia
~allodynia

(I’m pretty sure that hyeralgesia and allodynia are types of peripheral sensitization)

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16
Q

Peripheral sensitization (general/ what is it)

A

~enhance responsiveness of nociceptors
~Increased sensitivity of nociceptors and primary afferents to noxious stimuli or a responsiveness of these receptors to non-noxious stimuli such as touch

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17
Q

Hyperalgesia

A

Exaggerated sensitivity to noxious stimuli

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18
Q

Allodynia

A

Normally innocuous stimuli evokes the perception of pain

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19
Q

Peripheral sensitization can be produced by

A

~Local release of sensitization agents from mast cells

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20
Q

examples of sensitization agents form mast cells (in peripheral sensitization)

A

~Prostaglandins
~Bradykinin
~Histamine
~Serotonin (5-HT)

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21
Q

in peripheral sensitization, local release of sensitizing agents may produce

A

Axon reflexes where Antidromic impulses from 1° afferent will cause the release of substance P at distal ending producing inflammation

[An antidromic impulse in an axon refers to conduction opposite of the normal (orthodromic) direction[citation needed]. That is, it refers to conduction along the axon away from the axon terminal(s) and towards the soma.
(wikipedia)]

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22
Q

Variety of nerve problems result in

A

pain

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23
Q

most severe form of nerve pain is

A

ectopic pain

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24
Q

Ectopic pain is

A

~activity along nociceptive afferents from site of damage not nerve terminal.
~results from a denuded axon
~can lead to an accumulation of Na+ channels in denuded area
~gives rise to an excitable area of axon

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25
Q

ectopic pain (signs)

A

~positive Tinel’s sign over an unusual area of nerve

~only light tapping over an area of inflammation can produce severe pain

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26
Q

CRPS stands for

A

Complex Regional Pain Syndrome

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27
Q

Complex Regional Pain Syndrome is

A

~severe chronic musculoskeletal pain syndrome

~commonly seen in the extremities where non-nociceptive stimulation causes pain

28
Q

Complex Regional Pain Syndrome: 2 forms

A

Type 1

Type 2

29
Q

Complex Regional Pain Syndrome- type 1

A

~not associated with demonstrable nerve lesions

~formerly called reflex sympathetic dystrophy (RSD)

30
Q

Complex Regional Pain Syndrome- type 2

A

associated with nerve lesions formerly called causalgia

31
Q

Complex Regional Pain Syndrome- likely the results of

A

peripheral sensitization

32
Q

Myofascial Trigger Points

A

~Localized point pain generally in fascial covering of muscle or within muscle
~have been related to localized peripheral sensitization and axon reflexes

33
Q

Where do 1° nociceptive afferents synapse?

A 
in the dorsal horn of the spinal cord, specifically in:
~Posteriomarginal nucleus
~Substantia gelatinosa
~Base of dorsal horn (lamina V)
~Some in ventral horn
34
Q

What type of axon fibers go to all areas

A

Neurons in all areas receive input from C fibers

35
Q

What type of axon fibers go to postero-marginal nucleus

A

receive Ad afferents

36
Q

What type of axon fibers go to lamina V

A

~receive Ad afferents

~receive both nociceptive and low-threshold touch (Ab) input are referred to as wide, dynamic-range neurons (WDRNs)

37
Q

major 1° afferent excitatory transmitters on to central nervous system neurons are

(2-4)

A

~glutamate (glut)
~substance P (SP)
~calcitonin gene related peptide (CFRP) and adenosine triphosphate (ATP) have been discovered to modulate 1° afferent input

38
Q

Primary afferent released Glutamate (glut) binds to

A

AMPA/KA receptors

39
Q

Primary afferent released Glutamate (glut) produce

A

fast EPSPs seen in post-synaptic neurons

40
Q

Primary afferent released Substance P (SP) produces and activates

A

produces slow EPSPs and actives 2nd messenger systems in the post-synaptic cells

41
Q

CFRP and ATP also appears to activate

A

2nd messenger intracellular systems

42
Q

GABA produces

A

both pre-synaptic and post-synaptic inhibition at these primary afferent terminals

43
Q

Serotonin (5-HT) and enkephalins (ENK) produce

A

post-synaptic inhibition

44
Q

A number of agents locally released by glial cells can

A

~increase presynaptic neurotransmitter release

~increase post-synaptic excitability

45
Q

allodynia may develop in an area where (and causes)

A

~there is no apparent peripheral inflammation

~painless stimuli are now experienced as painful

46
Q

allodynia is the result of

A

altered processing by of non-nociceptive input to wide, dynamic-range neurons (WDRN)

47
Q

central sensitization- suggested mechanism involves

A

~inputs to these wide, dynamic-range neurons
~input to WDR neurons through AMPA receptors from Ab afferents is minimal
~NMDA receptors for glutamate are blocked by the action of Mg++ ion

48
Q

central sensitization- activity of nociceptors is

A

~elevated and/or prolonged the Mg++ ion blockage is removed

49
Q

central sensitization- the activation of both AMPA and NMDA receptors causes

A

the non-nociceptive Ab fibers to activate pain pathways

50
Q

central sensitization- Ordinarily painless stimuli are experienced as ——– (why?)

A

**PAINFUL
~a negative from of synaptic plasticity that has resulted in the altered processing of non-nociceptive input to wide, dynamic-range neurons (WDRN)
~the result of pain now arising from non-nociceptive stimuli

51
Q

the nociceptive signals are relayed ____ by the ____ system

A

rostrally by the spinothalamic system – specifically by the lateral spinal thalamic tracts

52
Q

the nociceptive signal- many divide this pain pathway up into two subdivisions

A

the neospinothalamic component and the paleospinothalamic component

53
Q

the nociceptive signal- neospinothalamic component is composed of

A

neurons innervated by Ad afferent fibers.

54
Q

the nociceptive signal- neospinothalamic component signals travel to

A

VPL of the thalamus via anterolateral pathway (spinothalamic) and to 1° somatosensory cortex

55
Q

the nociceptive signal- neospinothalamic component mediates

A

~fast pain

~sharp, well-localized, rapidly perceived pain

56
Q

the nociceptive signal- paleospinothalamic component is sometimes referred to as

A

Paramedial ascending system- PAS

57
Q

the nociceptive signal- paleospinothalamic component involves neurons actived by

A

the unmyelinated C primary afferent fibers

58
Q

the nociceptive signal- paleospinothalamic component rise through the

A

~ascending pathways initially rise in the lateral spinothalamic pathway

59
Q

the nociceptive signal- paleospinothalamic component projects to

A

~brainstem
~hypothalamus
~midline thalamus
~cingulate cortex

60
Q

the nociceptive signal- paleospinothalamic component mediates

A

~affective slow pain

~poorly localized, emotional content of pain

61
Q

What does Antidromic mean?

A

An antidromic impulse in an axon refers to conduction opposite of the normal (orthodromic) direction[citation needed]. That is, it refers to conduction along the axon away from the axon terminal(s) and towards the soma.
(wikipedia)

62
Q

what does denude mean

A

strip (something) of its covering, possessions, or assets; make bare.

(so a denuded axon is probably an axon stripped of its myelin or something like that).

63
Q

what is reflex sympathetic dystrophy?

A

RSD is the former name for CRPS type 1 (lacks nerve lesions)

64
Q

what is causalgia?

A

the former name for CRPS type 2 (nerve lesions present)

65
Q

CFRP

A

calcitonin gene related peptide (CFRP)

one of the neurotransmitters that modulate 1* afferent input to the CNS

PHTH 7303 Neuro (89 decks)

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