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LCRS Neuro > Somatosensory function > Flashcards

Somatosensory function Flashcards

1
Q

what are the 4 somatosensory modalities?

A

touch
proprioception
temperature
pain

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2
Q

what comes under touch?

A

light touch
pressure
vibration

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3
Q

what comes under proprioception?

A

joint position
muscle length
muscle tension

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4
Q

what are mechanoreceptors used for?

A

touch and proprioception

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5
Q

what receptors detect temperature?

A

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

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6
Q

what receptors detect damaging stimuli?

A

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)

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7
Q

3 main receptor types

A

mechanoreceptors
thermoreceptors
nociceptors

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8
Q

examples of mechanoreceptors

A

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)

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9
Q

describe a mechanreceptor detecting vibration

A

rapidly-acting
each fibre with a different threshold
generate cycles of APs
when thresholds overlap, the fibres may fire simultaneously

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10
Q

what Hz is the body most sensitive to?

A

250Hz
Pacinian peak at 250
Meissner peak at 20-50

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11
Q

what happens to vibratory threshold in neurodegeneration?

A

vibratory threshold increase

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12
Q

what leads to tickle detection?

A

relatively mild stimulation to areas of the body with naked unmyelinated afferent nerve fibres

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13
Q

what leads to itch detection?

A

o Caused by local mechanical stimulation or chemical agents (e.g. histamine).
o Relieved by scratching – stimulates large nerve fibres that overwhelm spinal transmission.

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14
Q

where in the body is temperature detection most sensitive?

A

face and chest

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15
Q

when do temperature gated channels open?

examples of TGCs

A

they open and close at different ranges of temperatures

TRPV channels are triggered by heat and capsaicin : TRPm8 and TRPv1

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16
Q

what does TRPM8 respond to?

A

cold e.g. menthol

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17
Q

what does TRPV1 respond to?

A

heat and capsaicin

includes V1-4

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18
Q

what do nociceptors respond to?

A

noxious or harmful stimuli

require high threshold for activation

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19
Q

how are nociceptors triggered?

A

direct activation of ion channel proteins, TRP, neurotrophin and GPLRs

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20
Q

what nociceptor detects a pH below 7

A

Acid Sensing Ion channels

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21
Q

what nociceptor senses intense pressure?

A

K+ channels

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22
Q

what are the commonest nociceptors

A

polymodal C fibres (cutaneous)- pressure, temperature, chemical

chemoreceptors (skeletal) - lactic acid

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23
Q

why are inflammations painful?

A

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

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24
Q

definition of stimulus threshold

A

weakest stimulus detectable

adequate stimulus required to elicit a specific response/reflex

minimum stimulus detected at least 50% of the time

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25
Q

how is stimulus intensity gauged?

2 ways involving APs and receptors

A

1) frequencies of APs generated

2) number of separate receptors activated (recruitment)

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26
Q

what is a receptive field?

A

area that a sensory nerve innervates

a small receptive field has high resolution and picks up stimuli more precisely

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27
Q

what allows the increased sensation of stimulus intensity?

A

the receptive fields overlap, so the recruitment of adjacent fields can increase stimulus intensity

28
Q

how is increased number of APs interpreted?

A

it is seen as increased intensity by the brain

29
Q

what enables pinpoint accuracy in location of the stimulus?

A

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
30
Q

what mediates lateral inhibition?

A

interneurones within the dorsal horn of the spinal cord

31
Q

what is two-point discrimination?

A

the ability to detect two stimuli as distinct from each other
there is two-point threshold

32
Q

what is the two-point threshold?

A

minimum distance required between 2 stimuli in order to perceive that they are two separate stimuli

33
Q

what does two-point discrimination depend on?

A

peripheral mechanoreceptors
spinal posterior column
cortical fuction
location e.g. back (65mm) vs fingers (2mm)

34
Q

what causes the difference in two-point discrimination in e.g. the back and the fingers?

A

density of innervation
area of receptive field
sensory homunculus

35
Q

what is neural adaption and how does neural adaption occur?

A
  • 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

36
Q

what affects the time taken for neural adaption?

A

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

37
Q

A fibre alpha

A

stimulus: proprioception, somatic motor
largest, myelinated
fastest

non-noxious

38
Q

A fibre beta

A

stimulus: touch, pressure
- large-medium, myelinated
- fast

non-noxious stimuli

39
Q

A fibre gamma

A

motor to muscle spindle
small
slow

40
Q

A fibre delta

A

stimulus: cold temperature, gross touch, sharp pain
- small myelinated
- slowest

noxious

41
Q

B fibre

A

postganglionic autonomics

42
Q

C fibre dorsal root

A

stimulus: burning pain, hot temperature and mechanoception
- non-myelinated
- slowest

noxious

43
Q

C fibre sympathetic

A

postganglionic sympathetic

44
Q

what nerve fibres are involved in pain (noxious)

A

A delta and C fibres

45
Q

what nerve fibres are involved in touch and pressure (non-noxious)

A

A beta

46
Q

which neurones are for perception and interpretation of pain?

A

cortical neurones

47
Q

which neurones are for modulation of nociceptive signals

A

thalamic neurones

ventrobasal complex and nucleus reticular

48
Q

which neurones process nociceptive signals

A

superficial dorsal horn neurones (sensory pathway)

49
Q

what is the pathway for touch and proprioception?

A

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
50
Q

what is the pathway for pain and temperature?

A

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
51
Q

Brown-Sequard syndrome

what are the effects of hemi-section of the spinal cord?

A

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
52
Q

how can cortical response mismatch the peripheral input?

i.e. the brain doesn’t do accordingly to the stimulus

A

Modulation:

  • spinal neurones respond to peripheral stimuli
  • but are modulated by :
    1) interneurones
    2) descending inhibitory controls
53
Q

what is glutamate and what receptors does it activate?

A

excitatory synaptic neurotransmitter

activates AMPA, NMDA, mGluR, Kainate

54
Q

activation of NMDAr

A

removing Mg2+ plug (no longer inactive)
causes large Ca2+ influx
intracellular action

55
Q

what is the effect of long term potentiation of NMDAr

A

hypersensitivity to pain

56
Q

effect of ketamine

A

NMDAr antagonist
painkiller
dissociative analgesia (pain that is there but you don’t notice)

57
Q

what is the gate control theory?

A

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

58
Q

what effect do the large fibres have in transmission of pain?

A
  • 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

59
Q

how can the dorsal root ganglia be targetted to treat neuronal dysfunction

A

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

60
Q

what happens in neuronal dysfunction?

A

sensitisation even to minor stimuli due to channelopathy or secondary messengers enabling depolarisation

61
Q

What rexed laminae are involved in noxious and non-noxious stimuli detection?

A

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

62
Q

descending modulation

A

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

63
Q

where is the primary somatosensory cortex located?

A

postcentral gyrus

64
Q

where is the secondary somatosensory cortex located

A

parietal operculum, posterior parietal cortex

65
Q

association cortex

A

complex mental functions
surrounds primary areas
most developed part of the brain

66
Q

what areas of the brain are active in pain?

A

o Cerebral cortices; SI, SII, Insular cortex, Anterior cingulate and prefrontal cortex.
o Brainstem.
o Amygdala.
o Cerebellum.

67
Q

what are the types of somatosensory fibres based on myelination?

A

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)

LCRS Neuro (19 decks)

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