L11-L13 (Somatosensory) Flashcards
4 types of somatosensation
- touch: sensations caused by non-painful displacements in the skin
- kinesthesis (i.e. kinesthesia)
- temperature
- pain
kinesthesia is part of proprioception (includes internal sensations) and involves the perception of movement and location of limbs in space
Somatosensory receptors
i.e. touch receptors
neurons with peripheral and central axons
some have specialized endings in the skin
Mechanoreceptor
4 types in glaborous skin
sensory neuron that responds to mechanical stimulation
- glaborous skin has no hair follicles and is found in the palms, soles, lips, etc.
- 4 types: meissner corpuscle, merkel discs, ruffini endings, pacinian corpuscle
Receptive field of somatosensory receptors
particularly mechanoreceptors
body area that elicits a response from a sensory neuron
size depends on body part and mechnoreceptor type
Merkel discs (SA1)
receptor field size, adaption rate, maximum feature sensitivity, and primary perceptual functions
- small receptor field
- slow adaption rate
- most sensitive to small, slow sustained pressure at very low frequency (< 5 Hz)
- for coarse texture and pattern
e.g. reading braille with your fingertip
Meissner corpuscle (FA1)
receptor field size, adaption rate, maximum feature sensitivity, and primary perceptual functions
- small receptive field
- fast adaption rate
- most sensitive to small, fast temporal changes in skin deformation (i.e. skin slip) at 5-50 Hz
- for low-frequency vibration and grasp stability
Ruffini ending (SAII)
receptor field size, adaption rate, maximum feature sensitivity, and primary perceptual functions
- large receptive field
- slow adaptation rate
- most sensitive to large, slow sustained downward pressure (i.e. lateral skin stretch) at 5-50 Hz
- for finger position
Pacinian corpuscle (FAII)
receptor field size, adaption rate, maximum feature sensitivity, and primary perceptual functions
- large receptive field
- fast adaptation rate
- most sensitive to large, fast temporal changes in skin deformation at 50-700 Hz
- for high-frequency vibration and fine texture
Slow vs fast adapting mechanoreceptors
- slow adapting mechanoreceptors continue to fire throughout stimulation but stop once stimulus is removed
- fast adapting mechanoreceptors respond with a burst of firing as soon as displacement of skin starts
merkel and ruffini are slow while meissner and pacinian are fast
Hair follicle receptor
5th type of fast-adapting tactile mechanoreceptor in hairy skin
What are the receptors for muscle tension/joint position, pain, and temperature?
somatosensory receptors
- kinesthetic
- free nerve endings
- thermoreceptors
Kinesthetic receptors
mechanoreceptors that lie within muscles, tendons, and joints served by A-alpha and A-beta fibers
- muscle spindles convey rate at which muscle fibers are changing in length
- golgi tendon organs convey muscle tension and joint position
Physiological zero
normal skin temperature at 30-36°C with no sensation of warmth or cold
2 types of thermoreceptors
- warmth fibers increase firing rate to increases in skin temperature above 36°C
- cold fibers increase firing rate to decreases in skin temperature below 30°C
3 types of nociceptors and what stimulates them
- thermal nociceptors: extreme temperature
- mechano nociceptors: severe pressure or excessive stretching
- polymodal nociceptors: intense heat, chemicals released by injured tissues, and/or spicy food
Transduction
- occurs in peripheral axon of somatosensory receptors
- temperature or chemicals released by injured tissue open channels sensitive to mechanical force (e.g. Piezo 2)
- Na+ and Ca+ enter
- neuron depolarizes and action potential travels full length of axon to spinal cord (if threshold is reached)
mechanism not yet fully known
4 nerve fibers in the peripheral nervous system
that carry somatosensory information to spinal cord
- A-alpha fiber carries information from proprioceptors
- A-beta fiber from mechanoreceptors
- A-delta fiber from pain and temperature receptors
- C fiber from pain, temperature, and itch receptors
from fastest conduction speed and widest diameter to slowest and most narrow
A-delta fibers
associated receptors
thermoreceptors (cold fibers), thermal nociceptors (e.g. TRPM8 channels, extreme cold) or mechano nociceptors (severe pressure)
C fibers
thermoreceptors (warmth fibers) and polymodal nociceptors
- inflammatory cells release prostaglandin, bradykinin, or protons which activate prostaglandin, bradykinin, and acid-sensing ion channels, respectively
- intense heat, protons, and capsaicin (hot peppers) activate capsaicin receptors (TRPV1)
Double pain
initial sharp pain (A-delta fiber) followed by slower, throbbing pain (C fiber)
touch can stop pain temporarily
2 somatosensory pathways
and their functions
- dorsal column-medial lemniscal pathway: nerve fibers carrying neural signals for tactile perception and proprioception
- spinothalamic pathway: nerve fibers carrying neural signals for nociception and thermoreception
- cell bodies of A-beta, A-delta, and C fibers in the dorsal root ganglion of spinal cord
- many central axons (31 pairs of spinal nerves) combine into a single nerve trunk and synapse in the dorsal horn of the spinal cord
Dorsal column-medial lemniscal pathway
for skin below the head
- 1st synapse for some neurons in spinal cord
- 1st synapse for most neurons in the medulla (cuneate and gracile nuclei)
- 2nd synapse in the ventral poserior nucleus of the thalamus (contralateral)
- final synapse in S1 in the parietal lobe
Dorsal column-medial lemniscal pathway
for head only
- 1st synapse in the principal sensory nucleus of the trigeminal nerve in the pons
- 2nd synapse ventral posteromedial (VPM) nucleus of the thalamus
- final synapse in the parietal cortex
Spinothalamic pathway
for skin below head vs head only
- 1st synapse in substantia gelatinosa (layer II) in dorsal horn of the spinal cord
- 2nd synapse in the ventral posterior nucleus (VPL) of thalamus
- final synapse in the parietal cortex
in head only, 1st synapse is in the spinal trigeminal nucleus of the medulla
Cortical organization of somatosensory cortex
has 6 layers (1-6 from outermost to innermost) and includes Brodmann areas 3a, 3b, 1 and 2
divided into primary cortex or S1 (which comprise of areas 1, 2, and 3) and secondary cortex or S2 (throat, tongue, teeth, jaw, gums)
Where do neurons from the thalamus synapse in S1?
2 kinds of neurons!
- proprioception neurons synapse in layer 4 area 3a, which projects to area 2
- touch neurons synapse in layer 4 area 3b, which projects to area 1
each mechanoreceptor type connects to a different vertical column in area 3b
Somatotopic map
i.e. sensory homunculus
each point on the skin is represented by a corresponding area in the contralateral somatosensory cortex
- but the map is distorted (e.g. area for thumb is as big as that of the forearm)
- each area in the somatosensory cortex has a somatotopic map
How was the somatotopic map discovered?
by neurosurgeon Wilder Penfield
during electrical stimulation in the cortex of awake patients undergoing epileptic surgery
Cortical magnification
enlarged representation in the cortical somatotopic map relative to skin area (e.g. fingers)
Tactile sensitivity
body parts with highest and lowest sensitivity
- inverse of absolute threshold for deteting a touch
- low absolute threshold = high sensitivity
highest sensitivity on face and lowest on foot
Relationship between JND for touch and sensitivity
JND for touch is smaller (better discrimination) for areas of the skin with higher sensitivty (lower absolute threshold)
Weber fraction for touch is 0.02-0.2 (JND/magnitude of standard stimulus)
Acuity
i.e. 2-point threshold
minimum distance at which two stimuli are just perceptible as separate
- better acuity in skin regions with larger cortical representation or cortical magnification (e.g. low 2-point threshold on thumb)
- detection threshold can be high when 2-point threshold is low (e.g. feet)
Relationship between acuity and receptive field size
acuity is good (i.e. small 2-point threshold) on parts of the body with small receptive fields, which are more densely packed
- on parts of the body with small receptive fields, 2 points stimulate 2 different receptive fields and 2 points are perceived
- on parts of the body with large receptive fields, 2 points stimulate the same one and only one point is perceived
2 regions of the receptive field of somatosensory receptors
A is the excitatory center while B is the inhibitory surround of the receptive field
each somatosensory neuron in S1 responds to stimulation in only a specific small area of the body
Aristotle’s illusion
when your fingers are crossed and you touch both tips simultaneously with one pencil, you perceive two touches
2 separate receptive fields are stimulated
Nociceptive pain
results from the stimulation of free nerve endings (i.e. noxious stimuli) in skin, muscles, and joints
avoid potentially harmful stimuli and immobilize to promote healing
2 brain regions involved in nociceptive pain
and their functions
- limbic system (amygdala, insula, anterior cingulate): processing of emotion
- prefrontal cortex: chronic pain emotional response and modulating pain perception
pain perception is based on more than sensory factors
How is pain sensitivity modulated in the brain?
endogenous opiates (enkephalins and endorphins) released by descending input from the brain (e.g. periaqueductal gray in midbrain)
endogenous opiates are the body’s natural painkillers! they are released during stress to minimize pain and trigger adaptive responses (e.g. fight or flight)
Nociceptive pain pathway
- C fibre (from the skin) releases substance P neurotransmitter, which synapses onto the dendrites of spinal cord neuron
- pain signal travels from spinal cord up to the thalamus in the brain
- descending input from the brain releases endogenous opiates, which bind to receptors on the C fiber and block the release of substance P
this is why athletes don’t notice minor injuries for hours
- spinal cord neuron has substance P membrane receptors (NK-1)
- descending input from brain synapses in the substantia gelatinosa in the dorsal horn
Where do A-beta, A-delta, and C fibers synapse?
synapse in the substantia gelatinosa in layer II of the dorsal horn in the spinal cord
Gate control theory
- Slow nociceptor signals (C and A-delta fibers) open the pain gate
- Spinal cord neurons transmit the pain signal to the brain along the spinothalamic pathway when pain gate is open
- Descending inputs (central control) from the brain and fast mechanoreceptor signals (A-beta fibers) activate inhibitory neurons in dorsal horn and close the pain gate
substantia gelatinosa in the dorsal horn gates the flow of pain to the brain
4 treatments for nociceptive pain
- transcutaneous electrical nerve stimulation (TENS): commercial method based on gate control theory
- anesthetics: produce total loss of sensation by interrupting signals travelling to the brain
- analgesics: produce loss of pain sensations only
- acupuncture
mechanism of acupuncture not understood but may release endogenous opiates
How does TENS relieve nociceptive pain?
electrical current is passed through the skin near the site of pain, which activates A-beta fibers to close the pain gate and stimulates the release of endogenous opiates
2 main types of anesthetics
for nociceptive pain relief
- local anesthetics that act at the site of injection that block sodium channels and provide temporary relief
- general anesthetics that act on the brain and lead to unconsciousness
Non-opiate analgesics
- useful for mild or moderate pain
- non-steroidal anti-inflammatory drugs (e.g. aspirin, ibuprofen) block prostaglandin production
- acetaminophen (tylenol) and COX-2 inhibitors (Celebrex) block prostaglandin with fewer gastrointestinal side effects
Opiate analgesics
- most potent painkillers
- morphine, codeine, and heroin block nociceptor release of neurotransmitter and inhibit spinal cord neurons
2 kinds of persistent pain
their mechanisms and causes
- inflammatory pain: nociceptors become increasingly sensitive with continuing stimulation (sensitization)
- neuropathic pain: not related to nociceptor stimulation and potentially harmful stimuli
- inflammatory pain is caused by damage/inflammation of tissues or by tumor cells but usually goes away when tissue heals
- neuropathic pain is caused by damage/dysfunction of peripheral (e.g. sciatica) or central nervous (e.g. multiple sclerosis) system
2 ways in which nociceptors are sensitized in inflammatory pain
- nociceptors become overly reactive to noxious stimuli, causing hyperalgesia
- nociceptors have lower thresholds for stimulation, causing allodynia
- hyperalgesia: painful stimuli become more painful
- allodynia: gentle touch stimuli become painful
2 kinds of sensitization in neuropathic pain
- peripheral: change in nociceptors
- central: increased number of pain receptors, rewiring of connections or loss of inhibitory cells in the spinal cord
hyperalgesia and allodynia exacerbated when pain is not treated
4 kinds of treatments for persistent pain
- anticonvulsants (gabapentin, pregabalin)
- capsaicin
- marijuana
- NMDA-receptor blockers (e.g. methadone)
Anticonvulsants
treatment for persistent pain
inhibit specific type of calcium channel to prevent the release of nociceptor neurotransmitters
Capsaicin
- stimulates nociceptors and may kill them or deplete their neurotransmitter supply
- may cause pain initially but then relieves pain
Marijuana
cannabinoids (e.g. THC, CBD) block neurotransmitter release from nociceptors and reduce inflammation
NMDA-receptor blockers
prevent glutamate from binding with NMDA receptors on spinal cord neurons
- prevents pain signal from traveling up to the thalamus
- NMDA receptors are involved in central sensitization
Phantom limb
and 2 treatments
type of neuropathic pain wherein sensations perceived to come from an amputated limb
- could be due to central sensitization that occurs during surgery
- can be treated with mirror box and electrical stimulation implant
How does general and local anesthesia produce phantom limb?
- only general anesthesia: nociceptors still activated and central sensitization can occur
- general and local anesthesia: local anesthetics block nociceptors and reduce central sensitization (but phantom limb can still occur)
What causes phantom limb pain in the amputated hand?
following amputation, a glitch in the remapping of the somatosensory cortex causes touching of face and upper arm to produce pain that seems to come from the amputated hand
face (below hand) and upper arm (above hand) regions take over hand region in somatotopic map
Mirror box
treatment for phantom limb pain
- place injured limb in a box and uninjured limb in front of a mirror
- move both limbs symmetrically while looking in the mirror
- feels like amputated hand is moving, which relieves pain
Electrical stimulation implant
treatment for phantom limb pain
electral stimulator is implanted in ther dorsal column of the spinal cord to close the pain gate
prevents pain signal from traveling up to the brain
