23: Sensory Phys And Pain Flashcards

1
Q

What determines how much a fiber contributes to a compound AP?

A

Conduction velocity

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2
Q

Two types of skin (thick and thin)

A

Thick: glabrous
Thin: hairy

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3
Q

Receptor adaptation

A

When a stimulus persists unchanged for a period of time, the neural response diminishes and sensation is lost

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4
Q

Slowly vs rapidly adapting receptors

A

Slow: respond to prolonged and constant stimulus - you feel it the whole time
Rapid: respond only at the beginning or end of a stimulus

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5
Q

Receptive field

A

Area of innervation where individual mechanoreceptors fibers convey info from a limited area of skin

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6
Q

What does 2-point discrimination test?

A

Tactile acuity

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7
Q

Where is tactile acuity highest?

A

Fingertips, lips (small receptive fields)

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8
Q

What principle describes why phantom limb pain exists?

A

Law of Projection

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9
Q

Law of Projections

A

No matter where along the afferent pathway a stimulation is applied, the perceived sensation arises from the origin of sensation

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10
Q

Pain vs nociception

A

Pain: unpleasant sensory and emotional experience associated with actual or potential tissue damage
Nociception: neural process encoding noxious stimuli, without pain necessarily being implied

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11
Q

Consequences of nociception

A

Can be autonomic (ex: elevate BP) or behavioral (ex: motor withdrawal reflex)

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12
Q

Hypersensitivity

A

Increased responsiveness of nociceptive neurons to their normal input

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13
Q

Hyperaesthesia

A

Increased sensitivity to stimulation, excluding special senses

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14
Q

Hyperalgesia

A

Increased pain from a stimulus that normally provokes pain

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15
Q

Allodynia

A

Pain due to stimulus that does not normally provoke pain (ex: laying on sheets while sunburnt)

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16
Q

Myelination of C fibers vs A(delta) fibers

A

C fibers: unmyelinated

A(delta): myelinated

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17
Q

Three types of pain characterization/nociceptor modalities

A
  1. Mechanical
  2. Chemical
  3. Thermal
18
Q

Two reasons we have referred pain

A
  1. Brain requires experience to localize pain - visceral pain is not typically experienced early in development to train the brain to localize it
  2. Afferents converge in dorsal horn
19
Q

What does TRP stand for?

A

Transient receptor potential

20
Q

What type of receptors are TRPs?

A

Ligand gated non-selective cation channels (for Ca, Na, K)

21
Q

What happens when a TRP V1 is activated?

A

AP occurs + neuropeptides are released -> further signaling occurs -> vasodilation and immune cell recruitment -> inflammation

22
Q

Two fiber types in nociceptors

A

C fibers and A(delta) fibers

23
Q

What type of receptor is a nociceptor

A

Free nerve endings

24
Q

Two types of free nerve endings

A

Peptidergic: expresses neuropeptides

Non-peptidergic: does not express neuropeptides

25
Q

Two neuropeptides expressed by peptidergic free nerve endings

A

Substance P, CGRP

26
Q

Where are peptidergic free nerve endings found vs non-peptidergic?

A

Peptidergic: most visceral afferents + 1/2 of cutaneous afferents
Non-peptidergic: few visceral + 1/2 of cutaneous afferents

27
Q

Peptidergic free nerve endings are involved in what?

A

Chronic inflammation, visceral pain

28
Q

What are non-peptidergic free nerve endings involved in?

A

Somatic chronic pain states (ex: diabetic neuropathy)

29
Q

Neuropeptides released by C fibers and A(delta) fibers

A

A(delta): EAA

C fibers: EAA, SP/CGRP

30
Q

Two ways nociception is modulated

A
  1. Local system: gate control theory

2. Descending inhibition: dampens on way up to cortex

31
Q

Most powerful form of inhibitory control of all primary afferent fibers

A

Pre-synaptic inhibition

32
Q

What happens in presynaptic inhibition?

A
  1. GABAergic associated influx of Cl into axon
  2. Hyperpolarization
  3. Less Ca enters cytosol
    4 .less NT release
33
Q

Six steps of descending inhibition

A
  1. PAG activated by opiates, EAA, and cannabinoids
  2. Descending projections -> locus ceruleus + raphe nucleus
  3. Serotonin and NE released into dorsal horn -> activate inhibitory interneurons
  4. Local inhibitory interneurons release opiates
  5. Opiates activate mu receptors on pre-synaptic terminals of C-fiber
  6. Reduction of SP from C-fiber, reduces nociception
34
Q

Central vs peripheral sensitization

A

Central: post-injury hypersensitivity due to neuronal plasticity in the CNS
Peripheral: neuroplastic chnages in function, chemical profile, or structure of the PNS involving the receptors, ion-channels, and nt expression levels

35
Q

Central inflammation

A

Pro-inflammatory signals from glial cells that contribute to central sensitization

36
Q

What causes peripheral sensitization

A

Inflammatory soup due to injured tissues - sensitized nociceptors

37
Q

What factors of sensitization play a role in chronic pain

A

Both peripheral and central sensitization

38
Q

Insular cortex functions

A
  1. Interpreting nociception
  2. Processing info about internal state of body
  3. Autonomic response to pain
  4. Integrates all signals related to pain
39
Q

What does damage of insular cortex cause?

A

Asymbolia

40
Q

Asymbolia

A

Altered experience of pain

41
Q

What is the amygdala important for with pain?

A

Emotional component of pain