Sensory Physiology Flashcards
A-alpha afferent sensory fiber
Largest, fastest fiber 80-120m/s
Ia and Ib types
Primary muscle spindles, Golgi tendon organ
A-beta afferent sensory fiber
Secondary muscle spindles, skin mechanoreceptors
Type II
A-delta afferent sensory fiber
Skin mechanoreceptors, thermal receptors, nociceptors
Type III
C afferent sensory fiber
Smallest, slowest fiber 0.5-2m/s
Type IV
Skin mechanoreceptors, thermal receptors, nociceptors
A-alpha efferent motor fiber
Largest, fastest fiber
Motor for extrafusal skeletal muscle fibers
A-gamma efferent motor fiber
Motor for intrafusal muscle fibers
B efferent motor fiber
Preganglionic autonomic motor fibers
C efferent motor fiber
Smallest, slowest fiber
Preganglionic autonomic motor fibers
Meissner corpuscle
Low threshold, rapidly adapting
Found in glaborous skin
Touch and vibration (under 100Hz), flutter and tapping
Found in glaborous skin
Pacinian corpuscle
Low threshold, rapidly adapting
Rapid indentation of skin such as during high frequency vibration (over 100Hz)
Found in both hairy and glaborous skin
Ruffini corpuscle
Low threshold, slowly adapting
Magnitude and direction of stretch. Touch and pressure proprioception
Found in both hairy and glaborous skin
Merkel cell
Low threshold, slowly adapting
Pressure
Found in glaborous skin
Hair-follicle receptor
Rapidly and slowly adapting
Motion across the skin and directionality of that motion
Tactile free-nerve ending
High threshold, slowly adapting
Pain and temperature
Somatosensory area I - SI primary sensory cortex
Involved in integration of the information for position sense as well as size, shape discrimination
First stop for most cutaneous senses
Somatosensory area II- S2
Responsible for comparisons between objects, different tactile sensation and determining whether something becomes a memory
Located in wall of sylvian fissure
Receives input from S1
Parieto-temporal-occipital association area PTO
Responsible for high-level interpretation of sensory inputs
Analyzes spatial coordinates of self in environment
Identification of object
Law of projection
Regardless of the place along an afferent pathway that is stimulated, the sensation is perceived to come from the place that the innervation arises. Explains phantom limb pain.
Hyperaesthesia
Increased sensitivity to stimulation, excluding the special senses
Hyperalgesia
Increased pain from a stimulus that normally provokes pain
Allodynia
Pain due to a stimulus that does not normally provoke pain. Classic example is the lay of sheets on skin that has been sunburned
A-delta vs C-fiber nociceptors
A-delta fibers are myelinated and faster than C-fibers, and carry info mainly from nociceptive-mechanical or mechanothermal specific nociceptors. They provide precise localization of pain.
C-fibers are slower and are activated by a variety of high-intensity mechanical, chemical and thermal stimulation from polymodal nociceptors. They comprise 70% of all fibers carrying noxious input. Less precise pain localization.
Biphasic response to pain
First stimuli and carried by A-delta fibers and gives a sharp, localized pain. Second phase activates C-fibers and creates a dull, throbbing and less localized pain.
TRPV1
Ligand gated non-selective cation channel
Expressed by many C-fibers
Sensitive to capsaicin
Activated by endogenous/exogenous compounds, especially bradykinin and heat greater than 43 Celsius
Leads to release of CGRP and substance-P
Sustained activation leads to buildup of those neuropeptides and causes vasodilation and pro-inflammatory mediator release causing a positive feedback loop
Migraine, dental pain, cancer, inflammation, neuropathic pain, visceral pain, osteoarthritis
TRPA1
Most common recognized activator is active ingredient in mustard oil, wasabi and horseradish
Paradoxical pro-nociceptive effect from anesthetics
Involved in inflammatory pain states-Allergic contact dermatitis, chronic itch, painful bladder syndrome, IBS, pancreatitis
TRPM8
Activated by innocuous cooling and noxious cold temperatures, as well as cooling agents like menthol
Gate-control theory of pain
No pain is sensed because the inhibitory interneuron is blocking the nociceptive signal from continuing to move forward - gate is closed
Gate opens during strong C-fiber activation
Rubbing area of pain causes activation of A-beta fiber which activates an inhibitory interneuron and helps block stimuli from C-fiber
Descending inhibition
Periaqueductal gray neurons activated by opiates, EAA and cannabinoids
Descending projections travel to locus coeruleus (NE) and raphe nucleus (serotonin)
Serotonin and NE released into dorsal horn activate inhibitory interneurons
Inhibitory interneurons release opiates (enkephalin) which activate mu receptors on C-fiber
Results in reduction of SP release from C-fiber and reduced nociception
Central sensitization
Activity dependent synaptic plasticity in spinal cord that generates post-injury pain hypersensitivity
Reduced threshold of dorsal horn neurons to noxious stimuli
Commonly caused by chronic exposure to peripheral inflammation
Peripheral sensitization
Neuroplastic changes related to function, chemical profile or structure of the peripheral nervous system that encompasses changes in receptor, ion channel and NT expression
At sites of inflammation, prostaglandin E (mast cells, neutrophils, macrophages) sensitizes peripheral nociceptors by reducing the firing threshold and increasing responsiveness
Peptidergic nociceptors
Expresses neuropeptides like SP or CGRP
Responsive to NGF nerve growth factor
Most visceral afferents are peptidergic- contribute to chronic visceral pain syndromes
Half of cutaneous afferents are peptidergic
Chronic inflammation upregulates neuropeptides
Non-peptidergic nociceptors
Do not express CGRP or SP
Responsive to GDNF glial derived neurotropic factor
Few visceral afferents are non-peptidergic, half of cutaneous afferents are
Involved in somatic chronic pain states such as diabetic neuropathy
Nociceptive input distribution in cortex
S1 and S2 receive input and play role in localization
Insular cortex responsible for interpretation of pain, processes info about internal state of body, contributes to autonomic responses to pain, integrates pain signals- damage causes asymbolia (pain without unpleasantness)
Amygdala important for emotional component
Visceral input travels to hypothalamus and medulla, integrating physiological changes associated with visceral pain
