11. Sensory Phys Flashcards
how are peripheral Ns classified
- based on contribution to a compound action potentials
- OR Fiber diameter, myelin thickness, & conduction velocity (classes I, II, III, and IV).
How are the two schemes of peripheral Ns related
- Conduction velocity = fiber’s contribution to compound AP
- Compound AP & conduction velocity = diagnostic test to evaluate peripheral N disease
what are the characteristics of A-alpha sensory fiber
1a & 1b
diameter = large
velocity: 80-120 m/s (FAST)
receptor: primary M. spindle & golgi tendon organ
what is the characteristic of A-beta sensory fibers
II
diameter - < A- alpha
velocity - < A-alpha
receptor: secondary M spindle & skin mechanoreceptors
what is the characteristic of A-delta sensory fibers
III
diameter < A-beta
velocity < A-beta
receptor: skin mechanoreceptors, thermal receptors & nociceptors
small receptive field: precise localization of pain
what is the characteristic of C sensory fibers
IV
Diameter: smallest
velocity: slowest (0.5-2 m/s) - unmyelinated
receptor: skin mechanoreceptor, thermal receptor & nociceptors
large receptive field: less precision for pain
what is the characteristic of A-alpha motor fibers
diameter : largest of motor fibers
velocity: fasted of motor fibers
receptor: Extrafusal sk. M fibers
what is the characteristic of A-beta motor fibers
diameter: < A-alpha
velocity: < A-alpha
receptor: Intrafusal M fibers
what is the characteristic of B motor fibers
diameter: < A-beta
velocity: < A-beta
receptor: Preganglionic autonomic fibers
what is the characteristic of C motor fibers
diameter: smallest of motor
velocity: slowest of motor
Receptor: Postsynaptic autonomic fibers
Meissner corpuscle
mechano: touch & vibration < 100 Hz (flutter//tap)
low threshold
rapid adaption
in glaborous skin
Pacinian corpuscle
mechano: rapid indentation of skin (high-freq vibration)
low threshold
rapid adaption
in hairy and glaborous skin
Ruffini corpuscle
mechano: magnitude/direction of stretch; touch/pressure/proprioception
low threshold
slow adaption
in hairy and glaborous skin
Merkel cells
mechano: pressure
low threshold
slow adaption
glaborous skin
Hair follicle receptor
mechano: motion across skin/direction
rapid/slow adaption
tactile free n endings
mechano- pain & temp
high threshold
slow adaption
what are receptive fields & their importance
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
what is 2 point discrimination
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
what are characteristics of two point discrimination
- 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
what does the somatosensory cortex (S1) do
the integration of the information for position sense as well as size, shape discrimination
- First stop for most cutaneous senses
- =crude sense
what does the somatosensory area II (S2) do?
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
what does the parieto-temporal-occipital association area (PTO) do?
responsible for high-level interpretation of sensory inputs.
- input from multiple sensory areas
- Analyzes spatial coordinates of self in environment
- Identification of objects
what is the law of projection
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.
what is phantom limb pain
e pain in a body part that is no longer present,
what is pain
An unpleasant sensory & emotional experience associated with actual/potential tissue damage, or described in terms of such damage
what is nociception
The neural process of encoding noxious stimuli (a stimulus that is damaging or threatens damage to normal tissues.)
what is hypersensitivity
Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs.
what is hyperaesthesia
Increased sensitivity to stimulation, excluding the special senses.
what is hyperalgesia
Increased pain from a stimulus that normally provokes pain
what is allodynia
Pain due to a stimulus that does not normally provoke pain.
Ex: lay of sheets after sunburn
what fibers are generally used for noxious mechanical stimuli
A-delta
what fibers generally respond to chem/thermal stimuli
C fibers
release substance P, Glu, Asp, CGRP, CIP & NO
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
mechanical nociceptors
respond to mechanical forces ranging from moderate pressure with a blunt object to overtly tissue-damaging stimuli
chemical nociceptors respond to
endogenous or exogenous chemical compounds, such as pro-inflammatory mediators, acids, or capsaicin, the pungent ingredient in chili peppers
thermal nociceptors respond to..
noxious heat and cold will directly activate thermal receptors
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.
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.
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
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.)
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)
Gate control theory of pain=
how is nociception reduced by descending paths
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
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
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
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
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)
what happens if you damage the insular cortex
asymbolia
-lesion in any area alters experiece of pain but doesnt get rid of it completely
