The Somatosensory System Flashcards

1
Q

List the major somatosensory modalities

A

Touch
Temperature
Nociception
Proprioception

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2
Q

Which receptors have free nerve endings and which have enclosed nerve endings?

A

FREE: thermoreceptors and nociceptors

ENCLOSED: mechanoreceptors

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3
Q

Classify the different sensory neurone axon types

A

(in order of decreasing diameter and myelination, and hence transmission speed)

Aβ-fibres: innocuous mechanical stimulation (so mechanoreceptors)

Aδ-fibres: noxious mechanical and thermal stimulation (nociceptors and thermoreceptors)

C-fibers: noxious mechanical, thermal and chemical stimulation (nociceptors and thermoreceptors)

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4
Q

What are sensory receptors?

A

Sensory receptors are transducers that convert energy from the environment into neuronal action potentials

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5
Q

What types of ion channels expressed by thermoreceptors mediate the ability to detect thermal changes?

A
  • Transient receptor potential (TRP) ion channels
  • 4 heat activated ones = TRPV1-4
  • 2 cold activated = TRPM8
    and TRPA1

Temperatures above neutral = C-fibres
Temperatures below neutral = Aδ-fibres

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6
Q

What are the four different types of mechanoreceptors, and what roles do they each have?

A
  1. Meissner’s corpuscle:
    - Fine discriminative touch, low frequency vibration
  2. Merkel cells:
    - Light touch and superficial pressure
  3. Pacinian corpuscle:
    - Detects deep pressure, high frequency vibration and tickling
  4. Ruffini endings:
    - Continuous pressure or touch and stretch
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7
Q

State what is meant by Stimulus Threshold

A

The point of intensity at which the person can just detect the presence of a stimulus 50% of the time - known as the absolute threshold

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8
Q

How do you interpret stimulus intensity?

A

Increased stimulus strength and duration = increased neurotransmitter release = greater intensity

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9
Q

What are tonic receptors? Give an example.

A
  • Do not adapt/very slowly adapting
  • Detect continuous stimulus strength and continue to transmit impulses to the brain as long the stimulus is present
  • Keeps the brain constantly informed of the status of the body

e.g. Merkel cells

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10
Q

What are phasic receptors? Give an example.

A
  • Fast adapting
  • Detect a change in stimulus strength
  • Transmit an impulse at the start and the end of the stimulus

e.g. Pacinian receptor

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11
Q

What is a receptive field?

A

The receptive field is the region on the skin which causes activation of a single sensory neurone

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12
Q

Describe how the receptive fields in the lips, mouth and fingers vary from the receptive fields of the upper arm and back.

A

Lips, mouth and fingers:

  • Densely packed mechanoreceptors
  • Small receptive fields allow for the detection of fine detail over a small area - precise perception

Upper arm and back:
- Large receptive fields allow the cell to detect changes over a wider area - less precise perception

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13
Q

Define two point discrimination. What is it related to?

A

Minimum distance at which two points are perceived as separate.
Related to the size of the receptive field

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14
Q

Define somatosensory dermatome

A

A dermatome is an area of skin that is supplied by sensory neurones from a single dorsal root of a spinal nerve (forms a part of a spinal nerve)

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15
Q

Aβ-fibres, Aδ-fibres and C-fibres synapse with others neurones in which areas of the dorsal horn?

A

Aδ-fibres and C-fibres: superficial layers of dorsal horn (lamina I and II)

Aβ-fibres: deeper layers of dorsal horn (lamina III, IV, V)

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16
Q

Define Lateral Inhibition

A

Lateral inhibition is the capacity of an excited neuron to reduce the activity of its neighbors by disabling the spread of action potentials from excited neurons to neighboring neurons in the lateral direction => enhanced sensory perception
Means that receptive fields don’t overlap
(Mediated by inhibitory interneurons within dorsal horn of spinal cord)

17
Q

Recall the pathway of the 1st order sensory neurones (dorsal column pathway)

A

Aβ fibers enter via the dorsal horn and enter the ascending dorsal column pathways;
- Information conveyed from lower limbs and body (below T6) travel ipsilaterally along the gracile tract. Neurones synapse in the Gracile Nucleus (medulla)

  • Information conveyed from upper limbs and body (above T6) travel ipsilaterally along the cuneate tract. Neurones synapse in the Cuneate Nucleus (medulla)
18
Q

Where do the 2nd order sensory neurones decussate, name the tract that they form and where do they terminate?

A
  • Decussate in the caudal medulla.
  • Form the contralateral medial lemniscus tract
  • Terminate in the ventral posterior lateral nucleus of the thalamus
19
Q

Where do the 3rd order sensory neurones project to?

A

Project to the somatosensory cortex
Somatotopy = correspondence of an area of the body to a specific point on the central nervous system; Size of somatotopic areas is proportional to density of sensory receptors in that body region

20
Q

Pain and temperature, and crude touch sensory information (2nd order neurones) ascend within which tracts?

A

Pain and temperature - lateral spinothalamic tract

Crude touch - anterior spinothalamic tract (mediated by Aδ-fibres)

Remember: 1st order terminate upon entering the spinal cord; 2nd order neurones decussate immediately and terminate in VPL nucleus of thalamus)

21
Q

What method is used to test the integrity of ascending pathways?

A

Quantitative sensory testing (for pain and temp, discriminative touch etc.)

22
Q

Which nociceptor fibres mediate which types of pain?

A

Aδ fibers mediate sharp, intense or first pain;
Type 1: noxious mechanical
Type 2: noxious heat

C-fibres mediate dull, aching or second pain
- Noxious thermal, mechanical and chemical stimuli

23
Q

State the major excitatory neurotransmitter released from sensory afferents in response to noxious stimuli (essential for pain signalling)?

A

Glutamate

24
Q

What two components make up the pain pathway? State the relevant tracts

A

Sensory component: Lateral spinothalamic tract

Emotional component: Spinoreticular tract

25
Q

Explain the significance of the pain matrix

A

Functional MRI (fMRI) has shown there is a ‘cerebral signature for pain’

Involves many areas of the cortex (SI, SIII, Insula cortex, Anterior cingulate cortex, Prefrontal cortex) and other brain areas (Amygdala, Cerebellum, Brainstem)

26
Q

Briefly describe the Gate Control Theory

A

Gate Control Theory of Pain describes how non-painful sensations can override and reduce painful sensations,
i.e. Inhibition of primary afferent inputs (stimulated by noxious stimulus) by touch/Aβ-fibres, before they are transmitted to the brain through ascending pathways (via inhibitory interneurones)

27
Q

What is the descending pain modulatory system?

A
  • Descending influences on spinal nociceptive processing involves the Periaqueductal Grey (PAG) and the rostral ventromedial medulla (RVM)
  • These are linked to a number of higher level brain areas including; cingulofrontal regions, the amygdalae and the hypothalamus (helps explain the role that emotions and cognition have in processing nociceptive information)
  • (In dorsal horn) Inhibition of substance P from noxious mechanical stimulation is via release of noradrenalin, and thermal nociceptive stimuli via the release of serotonin.

Essentially, “strong emotions” block pain.

Placebo activates descending inhibition in humans

28
Q

Define Allodynia

A

Pain due to a stimulus that does not normally provoke pain

29
Q

Define Hyperalgesia

A

Increased pain from a stimulus that normally provokes pain

  • Primary (at the site of stimulus)
  • Secondary (adjacent site to stimulus)
30
Q

Distinguish between central and peripheral sensitisation

A

CENTRAL = “Increased responsiveness of nociceptive neurones in the central nervous system to their
normal or sub-threshold afferent input.”; due to neural plasticity => recruitment of additional, sub-threshold synaptic inputs to nociception

PERIPHERAL = “Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to
the stimulation of their receptive fields.”; initiated by inflammatory mediators in damaged tissue