Sensory Physiology Flashcards by Liz Pennington

Describe type Aå fibers

subtypes

diameter

conduction

supplies

afferent

Iå and Ib

large

fast (80-120)

1’ muscle spindles, golgi tendon organs

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Describe type Aß fibers

subtypes

diameter

speed

supplies

afferent

smaller than Aå

less than Aå

2’ muscle spindles, skin mechanoreceptors

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Describe type Ad fibers

subtype

diameter

speed

supplies

afferent

III

smaller than Aß

slower than Aß

skin mechanoreceptors, thermoreceptors, nociceptors

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describe Type C fibers

subtype

diameter

speed

supplies

afferent

small

slowest

skin mechanoreceptors, thermoreceptors, nociceptors

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Describe type Aä (motor) fibers

supplies

efferent

extrafusal skeletal muscle fibers

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Describe Ay fibers

supplies

efferent

intrafusal muscle fibers

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Describe type B fibers

supplies

efferent

preganglionic autonomic fibers

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Describe type C fibers

supplies

efferent

postganglionic autonomic fibers

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What do Meissner’s corpuscles sense?

Where are they found?

fast or slow adapting?

flutter and tapping

glaborous skin

fast adapting (low threshold)

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What do Pacinian corpuscles sense?

Where are they found?

Fast or Slow adapting?

high frequency vibration

hairy and glaborous skin

fast adapting (low threshold)

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What does a Ruffini Corpuscle sense?

Where is it located?

Fast or slow adapting?

Mag/Dir. of stretch, touch, pressure, proprioception

hairy and glaborous skin

slow adapting (low threshold)

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What does a Merkel cell sense?

Where is it located?

Fast or slow adapting?

Pressure

glaborous skin

Slow adapting (low threshold)

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What does a hair-follicle receptor sense?

Where is it found?

Fast or Slow adapting?

direction and motion across skin

hair follcles

fast and slow adapting

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What do tactile free nerve endings sense?

Fast or Slow adapting?

pain and temperature

Slow adapting, high threshold

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Describe the significance of receptive fields and compare regions of highest and lowest tactile acuity across the body surface in relation to 2pt discrimination

allows for spatial resolution of detailed textures
acuity is highest in fingertips and lips (smallest receptive field
acuity is lowest on the calf, back and thigh (largest receptive field)
test is used as a diagnostic of peripheral sensory deficits

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Compare and Contrast the functions of SI, SII, and the parieto-temporal-occipital association area in sensory perception

somatic sensory area 1

primary sensory cortex in post-central gyrus

first stop for most cutaneous senses

somatotopic preservation

crude identification of sense

Compare and contrast the functions of SI, SII, and the parieto-temporal-occiptal association area in sensory perception

SII

compares sensations between objects and determines if something becomes a memory

technically, it’s an association area located in teh wall of the sylvian fissure (lateral sulcus)

receives input from SI

somatotopic distribution is less preserved

important for cognitive touch

Compare and contrast the functions of SI, SII, and the parieto-temporal-occipital assocation area in sensory perception

Parieto-Temporal-Occipital Association Area

high level interpretation of sensory input

input from multiple area

analyses space/coordination of self

ID’s objects

large amount of these assocation areas in humans

Describe the Law of Projection as it relates to phantom limb pain

“Regardless of the place along an afferent pathway that is stimulated, the sensation is perceived to come from the place that the innervation arises”

essentially, if there is a nerve “highway” from your thumb to your brain, anywhere along that highway that is stimulated is telling your brain that it’s coming from the thumb, even if the thumb has been amputated.

Is there a difference between Nociception and Pain?

Technically, yes.

Pain is an unpleasent sensory/emotional experience with actual or potential tissue damage

Nociception is the neural process of encoding nocious stimuli (can be related to HTN or withdrawal reflex) and pain is not necessarily implied

Define hypersensitivity

Define hyperaesthesia

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

Increased sensitivity to stimulation, excluding special senses

Define hyperalgesia

define allodynia

increased pain from a stimulus that normally provokes pain

pain due to a stimulus that does not normally provoke pain (shirt on sunburned back)

Compare and contrast Ad fibers and C fibers in regards to pain sensation

Ad fibers are fast, myelinated, and have small receptive fields, therefore providing precise, localized pain

C fibers are small, unmyelinated and slow and are activated by chemical/thermal stimuli. They comprise most of the fibers carrying nociception, and have a large receptive field, therefore providing a less precise pain localization

C uses substance P, glutamate/aspartate, CGRP, VIP and NO

What is the biphasic response to pain?

Phase 1: Ad fibers are activated with sharp, localized pain

Phase 2: C fibers are activated with dull, throbbing and diffuse pain

Where is TRPV1 found? What is it sensitive to? Describe its activation What type of pain is this receptor involved with?

C fibers (ligand gated channel) capsaicin, bradykinin, heat over 43'C Activation of TRPV1 leads to AP firing, release of CGRP, Substance P, and as it is sustained, releases more, causing vasodilation and migration of proinflammatory cells causing a feed back loop, potentiating TRPV1 and further nociceptive signaling Pain from migraines, dental, cancer, inflamation, neuropathic, visceral, osteoarthrtis

What activates TRPA1? What pain is it involved in? How is it involved in anesthetics?

many things, notably allyl isothicynate in mustard oil, wasabi and horseradish inflammatory pain like allergic dermatitis, chronic itch, painful bladder syndrome, IBS, migraine, pancreatitis many anesthetics have paradoxical pro-nociceptive effects by acting through TRPA1

How is TRPM8 activated? How is it used as an analgesic?

activated by innocuous cooling (15-26'C) and noxious cold (8-15'C) as well as "cooling agents" topical or otherwise such as menthol these "cooling agents" like menthol are commonly used as analgesias

What is the gate-control theory of pain modulation

"rubbing a spot that hurts makes it feel better" this is because the inhibitory interneuron is blocking the nociceptive signal from continuing to move forward; aka the gate is closed the gate opens during strong C fiber activation

Describe the physiology of the gate-control theory of pain

activte an Aß fiber by normal stimulus and that fiber goes to dorsal horn and synapses on an inhibitory internueron and releases EAA to activate it activated interneuron releases glycine and inhibits secondary snesory neuron of nociceptive pathway rubbbing the sore area activates teh Aß fiber to turn on this pathway and reduce pain

Describe descending inhibition

* periaquaductal gray is activated by opiates, EAA, and cannabinoids * descending projections then travel to locus cerulisu and raphe nucleus * serotinin and NE reelased into dorsal horn and acctivate inhibitoru interneurons * these local inhibitory interneurons release opiates (enkephalin) * these opiates activate Mu receptors on the presynaptic terminals of a C fiber * results in reduction of Substance P from C iber and reduces nociception

Describe Central Sensitization What is it? What does it cause?

generates post-injury pain hypersensitivity, usually caused by chronic exposure to peripheral inflammation type of activity dependent synaptic plasticity of the spinal cord * reduced threshold of dorsal horn neurons to nocious stimuli * alters receptors/ion channels, cahnges level of synpatic input produced by afferent fiber * receptive feild expands * persistent stimulation of EAA, ICCa+ nad other signaling cascades

Describe peripheral sensitization

neuroplastic changes in receptor, ion channel and NTM expression within the PNS can increase intensity and duration of pain at site of inflammation, PGE2 sensitizes nociceptors by activating receptors and reducing threshold and increasing responsiveness of the nociceptors this PGE2 may come from mast cells, neutrophils, macropahges, T cells after Peripheral nerve injury noninjured afferents can also become sensitized

What is expressed by Peptidergic Nociceptors? What are they responsive to? What upregulates them?

substance P, CGRP NGF chornic inflammation

Where are peptidergic nociceptors located?

visceral afferents (most of them are this type) cutaneous afferents (about half)

What is expressed by non-peptidergic nociceptors? What do they repsond to? Where are they found? involved in what condition?

NOT SP or CGRP GDNF very few visceral afferents, half of cutaneous afferents chronic pain, like diabetic neuropathy

Describe the cortical processing and wide spread distribution of nociceptive input in the cortex ## Footnote **SI and SII**

receive input from nocipceptors and play a role in localization of pain

Describe the cortical processing and wide-spread distribution of nociceptive input in the cortex ## Footnote **Insular Cortex**

Particularly important in interpretation of nociception process info about internal state contirbutes to autonomic response to pain integrates all signals related to pain damage causes asymbolia lesions in any single area alters experience of pain, but does not abolish it

Describe the cortical processing and wide-spread distribution of nociceptive input in the cortex ## Footnote **Amygdala**

important in emotional component of pain

How are the hypothalamnus and medulla involved in processing pain?

visceral input travels with autonomic nerves to the hypothalamus and medulla, integrating physiological changes associated with visceral pain