Somatosensory function Flashcards
what are the 4 somatosensory modalities?
touch
proprioception
temperature
pain
what comes under touch?
light touch
pressure
vibration
what comes under proprioception?
joint position
muscle length
muscle tension
what are mechanoreceptors used for?
touch and proprioception
what receptors detect temperature?
thermoreceptor
- slow adapting
- transient receptor potential channels (e.g TRPVs)
- TRPVs are also activated by spicy food e.g. capsaicin
- heat detection: deep in the dermis
- cold detection: superficial dermis (e.g TRPV8)
at extreme cold temperatures, thermoceptors are inactive and nociceptors become active
what receptors detect damaging stimuli?
nociceptor
- trigger pain as a protective mechanism
- respond to extremem temperatures
- respond to excess pressure and deformation
- respond to a mix of both
pain sensitive people have a reduced pain tolerance (not pain threshold)
3 main receptor types
mechanoreceptors
thermoreceptors
nociceptors
examples of mechanoreceptors
plexuses
peritrichial endings
end bulbs
1) Proprioceptors:
- muscle spindles
- Golgi tendon organ
- joint receptors
2) Mechanosensors: touch (pressure and skin deformation)
- Merkel endings (epidermis; slow adapting)
- Pacinian corpuscles (dermis and subcutaneous; fast adapting)
- Meissner’s corpuscles (finger tips; fast adapting)
- Ruffini endings (joints; slow adapting)
describe a mechanreceptor detecting vibration
rapidly-acting
each fibre with a different threshold
generate cycles of APs
when thresholds overlap, the fibres may fire simultaneously
what Hz is the body most sensitive to?
250Hz
Pacinian peak at 250
Meissner peak at 20-50
what happens to vibratory threshold in neurodegeneration?
vibratory threshold increase
what leads to tickle detection?
relatively mild stimulation to areas of the body with naked unmyelinated afferent nerve fibres
what leads to itch detection?
o Caused by local mechanical stimulation or chemical agents (e.g. histamine).
o Relieved by scratching – stimulates large nerve fibres that overwhelm spinal transmission.
where in the body is temperature detection most sensitive?
face and chest
when do temperature gated channels open?
examples of TGCs
they open and close at different ranges of temperatures
TRPV channels are triggered by heat and capsaicin : TRPm8 and TRPv1
what does TRPM8 respond to?
cold e.g. menthol
what does TRPV1 respond to?
heat and capsaicin
includes V1-4
what do nociceptors respond to?
noxious or harmful stimuli
require high threshold for activation
how are nociceptors triggered?
direct activation of ion channel proteins, TRP, neurotrophin and GPLRs
what nociceptor detects a pH below 7
Acid Sensing Ion channels
what nociceptor senses intense pressure?
K+ channels
what are the commonest nociceptors
polymodal C fibres (cutaneous)- pressure, temperature, chemical
chemoreceptors (skeletal) - lactic acid
why are inflammations painful?
there is no single pain neurotransmitter so substances modulate nociception
e.g. prostaglandin, substance P, histamine, serotonin, bradykinin etc
there are associated with inflammation hence painful inflammation
definition of stimulus threshold
weakest stimulus detectable
adequate stimulus required to elicit a specific response/reflex
minimum stimulus detected at least 50% of the time
how is stimulus intensity gauged?
2 ways involving APs and receptors
1) frequencies of APs generated
2) number of separate receptors activated (recruitment)
what is a receptive field?
area that a sensory nerve innervates
a small receptive field has high resolution and picks up stimuli more precisely
what allows the increased sensation of stimulus intensity?
the receptive fields overlap, so the recruitment of adjacent fields can increase stimulus intensity
how is increased number of APs interpreted?
it is seen as increased intensity by the brain
what enables pinpoint accuracy in location of the stimulus?
lateral inhibition: activation of one neural unit inhibits the activation of other neural units
- strong stimuli in a receptive field could mildly stimulate nearby neurones
- the receptor receiving the strongest stimuli sends inhibitor signals via interneurones to adjacent 1st order neurones to suppress the activity
- this enables point discrimination as boundaries are being defined
what mediates lateral inhibition?
interneurones within the dorsal horn of the spinal cord
what is two-point discrimination?
the ability to detect two stimuli as distinct from each other
there is two-point threshold
what is the two-point threshold?
minimum distance required between 2 stimuli in order to perceive that they are two separate stimuli
what does two-point discrimination depend on?
peripheral mechanoreceptors
spinal posterior column
cortical fuction
location e.g. back (65mm) vs fingers (2mm)
what causes the difference in two-point discrimination in e.g. the back and the fingers?
density of innervation
area of receptive field
sensory homunculus
what is neural adaption and how does neural adaption occur?
- a strong stimulus increases the firing of 1st order neurones
- when a stimulus of constant strength is maintained for a period of time, the frequency of APs diminished as the
e. g. after sitting on the chair, you don’t feel the chair anymore after the initial sensation of the chair
- this uses fast adapting (phasic) and slow adapting (tonic) receptors
what affects the time taken for neural adaption?
due to the type of neurones and receptors:
1) phasic- rapidly adapting
- initially very active when the stimuli first starts, but stops firing eventually
2) tonic- slowly adapting
- keep firing without loss of sensitivity
A fibre alpha
stimulus: proprioception, somatic motor
largest, myelinated
fastest
non-noxious
A fibre beta
stimulus: touch, pressure
- large-medium, myelinated
- fast
non-noxious stimuli
A fibre gamma
motor to muscle spindle
small
slow
A fibre delta
stimulus: cold temperature, gross touch, sharp pain
- small myelinated
- slowest
noxious
B fibre
postganglionic autonomics
C fibre dorsal root
stimulus: burning pain, hot temperature and mechanoception
- non-myelinated
- slowest
noxious
C fibre sympathetic
postganglionic sympathetic
what nerve fibres are involved in pain (noxious)
A delta and C fibres
what nerve fibres are involved in touch and pressure (non-noxious)
A beta
which neurones are for perception and interpretation of pain?
cortical neurones
which neurones are for modulation of nociceptive signals
thalamic neurones
ventrobasal complex and nucleus reticular
which neurones process nociceptive signals
superficial dorsal horn neurones (sensory pathway)
what is the pathway for touch and proprioception?
via dorsal column (medial leminiscal pathwayP
- uses A-alpha and A-beta fibres (large myelinated)
- up the cuneate fasciculus (arms and chest); located laterally
- up the gracilis fasisculus (trunk and legs); located medially
- decussation occurs in the caudal medulla (where 2nd order neurone begins)
- synapses at ventroposterior nucelus (VPN) in the thalamus where the 3rd order neurone starts
- lateral inhibition occurs in the dorsal column nuclei
what is the pathway for pain and temperature?
via spinothalamic tract
- sharp pain and cold via small myelinated A-delta fibres
- burning pain and heat via non-myelinated C fibres
- decussation occurs at the same level in spinal cord (about 2 vertebral levels up) where the 2nd order neurone starts
- run up the lateral and anterior funiculi
Brown-Sequard syndrome
what are the effects of hemi-section of the spinal cord?
caused by damage to one half of the spinal cord, i.e. hemisection of the spinal cord i.e below medulla:
- ipsilateral paralysis (corticospinal) and loss of touch+ proprioception (dorsal column)
- contralateral loss of pain and temperature (spinothalamic) sensation on the opposite
how can cortical response mismatch the peripheral input?
i.e. the brain doesn’t do accordingly to the stimulus
Modulation:
- spinal neurones respond to peripheral stimuli
- but are modulated by :
1) interneurones
2) descending inhibitory controls
what is glutamate and what receptors does it activate?
excitatory synaptic neurotransmitter
activates AMPA, NMDA, mGluR, Kainate
activation of NMDAr
removing Mg2+ plug (no longer inactive)
causes large Ca2+ influx
intracellular action
what is the effect of long term potentiation of NMDAr
hypersensitivity to pain
effect of ketamine
NMDAr antagonist
painkiller
dissociative analgesia (pain that is there but you don’t notice)
what is the gate control theory?
non-painful/non-noxious stimuli can inhibit the transmission of pain from peripheries to the brain
e.g. rubbing elbow after hitting it
small A delta and C fibres transmit noxious stimuli
large A beta fibres transmit non-noxious stimuli
stimulating the large fibres you can reduce neuropathic pain
what effect do the large fibres have in transmission of pain?
- prevent/reduce transmission of the smaller fibres within the dorsal horn of the spinal cord that are used to stimulate painful stimuli
- instead, the larger fibres are being used (e.g. A-beta) so transmission in noxious fibres is reduced
this “closes” the gate
inhibitory interneurones have been activated
how can the dorsal root ganglia be targetted to treat neuronal dysfunction
X-ray guided techniques to reduce the sensitivity of the DRG
electrical stimulation leads to reduced frequency and amplitude of APs which can compensate for neuronal dysfunction
what happens in neuronal dysfunction?
sensitisation even to minor stimuli due to channelopathy or secondary messengers enabling depolarisation
What rexed laminae are involved in noxious and non-noxious stimuli detection?
1) These respond to non-noxious stimuli:
o Rexed Lamina LIII-LVI = Large myelinated (A-beta, A-alpha)
- respond to mechanical stimuli.
2) These respond to noxious stimuli:
o Rexed Lamina LI-LII = Small myelinated (A-delta)
- respond to Cold and fast pain nociception.
o Rexed Lamina LI-LII = Small unmyelinated (C fibres).
- respond to pain and temperature.
3) Rexed Lamina LII = Substantia Gelatinosa
- involved in pain perception
noxious use small fibres (C and A-delta)
non-noxious use large fibres (A-beta, A-alpha)
all connected by interneurones
descending modulation
pain pathway neurones are active even without the noxious stimulus
descending pathways have inhibitory or excitatory influences on spinal nociceptive transmission mediated by 5HT3, NA, GABAa and glycine receptors
where is the primary somatosensory cortex located?
postcentral gyrus
where is the secondary somatosensory cortex located
parietal operculum, posterior parietal cortex
association cortex
complex mental functions
surrounds primary areas
most developed part of the brain
what areas of the brain are active in pain?
o Cerebral cortices; SI, SII, Insular cortex, Anterior cingulate and prefrontal cortex.
o Brainstem.
o Amygdala.
o Cerebellum.
what are the types of somatosensory fibres based on myelination?
1) non myelinated: Type C; slow (hot temperature, burning pain)
2) small myelinated: Type A-delta; faster (cold temperature, gross touch, sharp pain)
3) large myelinated: Type A-alpha and Type A-beta; fastest (fine touch, proprioception, vibration)
