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
Two neuropeptides expressed by peptidergic free nerve endings
Substance P, CGRP
26
Where are peptidergic free nerve endings found vs non-peptidergic?
Peptidergic: most visceral afferents + 1/2 of cutaneous afferents Non-peptidergic: few visceral + 1/2 of cutaneous afferents
27
Peptidergic free nerve endings are involved in what?
Chronic inflammation, visceral pain
28
What are non-peptidergic free nerve endings involved in?
Somatic chronic pain states (ex: diabetic neuropathy)
29
Neuropeptides released by C fibers and A(delta) fibers
A(delta): EAA | C fibers: EAA, SP/CGRP
30
Two ways nociception is modulated
1. Local system: gate control theory | 2. Descending inhibition: dampens on way up to cortex
31
Most powerful form of inhibitory control of all primary afferent fibers
Pre-synaptic inhibition
32
What happens in presynaptic inhibition?
1. GABAergic associated influx of Cl into axon 2. Hyperpolarization 3. Less Ca enters cytosol 4 .less NT release
33
Six steps of descending inhibition
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
Central vs peripheral sensitization
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
Central inflammation
Pro-inflammatory signals from glial cells that contribute to central sensitization
36
What causes peripheral sensitization
Inflammatory soup due to injured tissues - sensitized nociceptors
37
What factors of sensitization play a role in chronic pain
Both peripheral and central sensitization
38
Insular cortex functions
1. Interpreting nociception 2. Processing info about internal state of body 3. Autonomic response to pain 4. Integrates all signals related to pain
39
What does damage of insular cortex cause?
Asymbolia
40
Asymbolia
Altered experience of pain
41
What is the amygdala important for with pain?
Emotional component of pain