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Neuro Exam 2 > 11. Sensory Phys > Flashcards

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
Q

what is pain

A

An unpleasant sensory & emotional experience associated with actual/potential tissue damage, or described in terms of such damage

26
Q

what is nociception

A

The neural process of encoding noxious stimuli (a stimulus that is damaging or threatens damage to normal tissues.)

27
Q

what is hypersensitivity

A

Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs.

28
Q

what is hyperaesthesia

A

Increased sensitivity to stimulation, excluding the special senses.

29
Q

what is hyperalgesia

A

Increased pain from a stimulus that normally provokes pain

30
Q

what is allodynia

A

Pain due to a stimulus that does not normally provoke pain.

Ex: lay of sheets after sunburn

31
Q

what fibers are generally used for noxious mechanical stimuli

A

A-delta

32
Q

what fibers generally respond to chem/thermal stimuli

A

C fibers

release substance P, Glu, Asp, CGRP, CIP & NO

33
Q

what is the biphasic response to pain

A

combination of sensations by Aδ and C-fibers

A-delta: phase 1; sharp/localized

C: phase 2; dull, throbbing and less localized

34
Q

mechanical nociceptors

A

respond to mechanical forces ranging from moderate pressure with a blunt object to overtly tissue-damaging stimuli

35
Q

chemical nociceptors respond to

A

endogenous or exogenous chemical compounds, such as pro-inflammatory mediators, acids, or capsaicin, the pungent ingredient in chili peppers

36
Q

thermal nociceptors respond to..

A

noxious heat and cold will directly activate thermal receptors

37
Q

transient receptor potential (TRP) family =

A

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
Q

TRPV1

A

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
Q

activation of TRPV1 leads to—-

A

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
Q

TRPA1

A

= 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
Q

TRPM8

A

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
Q

Gate control theory of pain=

A
43
Q

how is nociception reduced by descending paths

A
44
Q

what is central sensitization

A

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
Q

what is peripheral sensitization

A

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
Q

peptidergic nociceptors -

A
  • 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
Q

non-peptidergic nociceptors

A
  • 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
Q

where is nociception distributed to in the brain

A

S1 & S2

insular cortex (for interpretation)

amygdala (emotional)

hypothalmus/medulla (integrate phys changes that come with pain)

49
Q

what happens if you damage the insular cortex

A

asymbolia

-lesion in any area alters experiece of pain but doesnt get rid of it completely

Neuro Exam 2 (23 decks)

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