11. Sensory Phys Flashcards

1
Q

how are peripheral Ns classified

A
  1. based on contribution to a compound action potentials
  2. OR Fiber diameter, myelin thickness, & conduction velocity (classes I, II, III, and IV).
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2
Q

How are the two schemes of peripheral Ns related

A
  • Conduction velocity = fiber’s contribution to compound AP
  • Compound AP & conduction velocity = diagnostic test to evaluate peripheral N disease
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3
Q

what are the characteristics of A-alpha sensory fiber

A

1a & 1b

diameter = large

velocity: 80-120 m/s (FAST)
receptor: primary M. spindle & golgi tendon organ

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4
Q

what is the characteristic of A-beta sensory fibers

A

II

diameter - < A- alpha

velocity - < A-alpha

receptor: secondary M spindle & skin mechanoreceptors

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5
Q

what is the characteristic of A-delta sensory fibers

A

III

diameter < A-beta

velocity < A-beta

receptor: skin mechanoreceptors, thermal receptors & nociceptors

small receptive field: precise localization of pain

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6
Q

what is the characteristic of C sensory fibers

A

IV

Diameter: smallest

velocity: slowest (0.5-2 m/s) - unmyelinated
receptor: skin mechanoreceptor, thermal receptor & nociceptors

large receptive field: less precision for pain

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7
Q

what is the characteristic of A-alpha motor fibers

A

diameter : largest of motor fibers

velocity: fasted of motor fibers
receptor: Extrafusal sk. M fibers

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8
Q

what is the characteristic of A-beta motor fibers

A

diameter: < A-alpha
velocity: < A-alpha
receptor: Intrafusal M fibers

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9
Q

what is the characteristic of B motor fibers

A

diameter: < A-beta
velocity: < A-beta
receptor: Preganglionic autonomic fibers

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10
Q

what is the characteristic of C motor fibers

A

diameter: smallest of motor
velocity: slowest of motor

Receptor: Postsynaptic autonomic fibers

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11
Q

Meissner corpuscle

A

mechano: touch & vibration < 100 Hz (flutter//tap)

low threshold

rapid adaption

in glaborous skin

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12
Q

Pacinian corpuscle

A

mechano: rapid indentation of skin (high-freq vibration)

low threshold

rapid adaption

in hairy and glaborous skin

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13
Q

Ruffini corpuscle

A

mechano: magnitude/direction of stretch; touch/pressure/proprioception

low threshold

slow adaption

in hairy and glaborous skin

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14
Q

Merkel cells

A

mechano: pressure

low threshold

slow adaption

glaborous skin

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15
Q

Hair follicle receptor

A

mechano: motion across skin/direction

rapid/slow adaption

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16
Q

tactile free n endings

A

mechano- pain & temp

high threshold

slow adaption

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17
Q

what are receptive fields & their importance

A

Areas of innervation – each mechanoreceptor fibers convey information from a limited area of skin

vary in size

higher density: small receptive field, fine discrimination

lower density: large receptive field

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18
Q

what is 2 point discrimination

A

ability to identify site of stimulation and distinguish btn stimuli that are close

= min distance btn the two stimuli

variation different regions of the skin –> diff explained by observation that the mechanoreceptors are much more numerous with smaller receptive fields

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19
Q

what are characteristics of two point discrimination

A
  • Allows for spatial resolution of detailed textures
  • Tactile acuity is highest in fingertips and lips (smallest receptive fields).
  • Tactile acuity is lowest on the calf, back and thigh (largest receptive field).
  • Test is used a diagnostic tool of peripheral sensory deficiencies
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20
Q

what does the somatosensory cortex (S1) do

A

the integration of the information for position sense as well as size, shape discrimination

  • First stop for most cutaneous senses
  • =crude sense
21
Q

what does the somatosensory area II (S2) do?

A

responsible for comparisons between objects, different tactile sensations & determining whether something becomes a memory

in the wall of the lateral sulcus

receive input form S1

imp in cognitive touch/interpretation

22
Q

what does the parieto-temporal-occipital association area (PTO) do?

A

responsible for high-level interpretation of sensory inputs.

  • input from multiple sensory areas
  • Analyzes spatial coordinates of self in environment
  • Identification of objects
23
Q

what is the law of projection

A

states that regardless of the place along an afferent pathway that is stimulated, the sensation is perceived to come from the place that the innervation arises.

24
Q

what is phantom limb pain

A

e pain in a body part that is no longer present,

25
what is pain
An unpleasant sensory & emotional experience associated with actual/potential tissue damage, or described in terms of such damage
26
what is nociception
The neural process of encoding noxious stimuli (a stimulus that is damaging or threatens damage to normal tissues.)
27
what is hypersensitivity
Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs.
28
what is hyperaesthesia
Increased sensitivity to stimulation, excluding the special senses.
29
what is hyperalgesia
Increased pain from a stimulus that normally provokes pain
30
what is allodynia
Pain due to a stimulus that does not normally provoke pain. Ex: lay of sheets after sunburn
31
what fibers are generally used for noxious mechanical stimuli
A-delta
32
what fibers generally respond to chem/thermal stimuli
C fibers release substance P, Glu, Asp, CGRP, CIP & NO
33
what is the biphasic response to pain
combination of sensations by Aδ and C-fibers A-delta: phase 1; sharp/localized C: phase 2; dull, throbbing and less localized
34
mechanical nociceptors
respond to mechanical forces ranging from moderate pressure with a blunt object to overtly tissue-damaging stimuli
35
chemical nociceptors respond to
endogenous or exogenous chemical compounds, such as pro-inflammatory mediators, acids, or capsaicin, the pungent ingredient in chili peppers
36
thermal nociceptors respond to..
noxious heat and cold will directly activate thermal receptors
37
transient receptor potential (TRP) family =
receptor ion channels= major class of sensory detection and transducers in nociceptive neurons sense broad range of changes: pH, inflammatory mediators, heat, cold, and exogenous chemicals.
38
TRPV1
a ligand-gated nonselective cation channel Many C-fibers express this = sensitive to vanilloid compounds, _(capsaicin_)- exogenous compound = also activated by endogenous substances, esp the inflammatory mediator, _bradykinin_, and by _heat greater than 43°C._ _-_migraine, dental pain, cancer pain, inflammatory pain, neuropathic pain, visceral pain, and osteoarthritis.
39
activation of TRPV1 leads to----
sensory N fiber AP -also release of neuropeptides, CGRP & neurokinins/substance P (SP). Sustained activation --\> increased CGRP and SP release --\> vasodilation & activation of immune/other cell in skin --\> pro-inflammatory mediator release ==\> positive signaling feedback loop --\> potentiation of TRPV1 channel activation and signaling
40
TRPA1
= modulators, regulators of function, and agonists --\> recognize active ingredient (allyl isothiocyanate) in mustard oil, wasabi, and horseradish. --\> Anesthetics --\> paradoxical pro-nociceptive effects by acting thru TRPA1. =inflammatory pain (allergic contact dermatitis, chronic itch, painful bladder syndrome, migraine, irritable bowel syndrome, and pancreatitis.)
41
TRPM8
activated by innocuous cooling (26–15 °C) and noxious cold (15–8°C) temp and a “cooling agents,” (topical and otherwise) like menthol (analgesic properties)
42
Gate control theory of pain=
43
how is nociception reduced by descending paths
44
what is central sensitization
Activity-dependent synaptic plasticity in spinal cord --\> generates post-injury pain hypersensitivity with cellular and molecular mechanisms * Reduced threshold of dorsal horn neurons to noxious stimulation. * Caused by chronic exposure to peripheral inflammation. * Alter transcription and translation of channels --\> changes level of syn input by the afferent fiber. * Receptive fields - expands. = persistent stimulation of EAA receptors, intracellular Ca2+ signaling, and activation of various intracellular signaling cascades
45
what is peripheral sensitization
Neuroplastic changes related to function, chemical profile, or structure of PNS that encompasses changes in receptor, ion-channel, and neurotransmitter expression levels. * Neuroimmune activation --\> increase intensity & duration of pain. * Site of inflam--\> Prostaglandin E2 (PGE2) sensitize peripheral nociceptors by activation of receptors on the peripheral terminals of nociceptor by r_educing the firing threshold and increasing responsiveness_, (key) * inflam mediators: PGE2 from nearby mast cells, neutrophils, macrophages, & T-lymphocytes after injury
46
peptidergic nociceptors -
* Express Substance P & CGRP * Responsive to NGF (nerve growth factor) * Viseral afferents --\> chronic visceral pain syndromes * Half of *cutaneous* afferents * Chronic inflammation upregulates neuropeptides
47
non-peptidergic nociceptors
* Do NOT express CGRP or Substance P * Responsive to GDNF (glial-derived neurotrophic factor) * Very few visceral afferents * Half of cutaneous afferents * = somatic chronic pain like diabetic neuropathy
48
where is nociception distributed to in the brain
S1 & S2 insular cortex (for interpretation) amygdala (emotional) hypothalmus/medulla (integrate phys changes that come with pain)
49
what happens if you damage the insular cortex
asymbolia -lesion in any area alters experiece of pain but doesnt get rid of it completely