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Neuroscience and Mental Health > 7. The somatosensory system > Flashcards

7. The somatosensory system Flashcards

1
Q

What is a modality?

A

A type of stimulus e.g. hot, cold, touch

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2
Q

What are the specialised receptors for the following:
• Touch
• Proprioception (joint position, muscle tension)
• Temperature
• Pain

A
  • Touch - mechanoreceptor
  • Proprioception - mechanoreceptor
  • Temperature - thermoreceptor
  • Pain - nociceptor
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3
Q

What are the 3 main categories of sensory fibres?

A
  • Mechanoreceptors of the skin (Aβ) - very fast (large, myelinated)
  • Pain, temperature (Aδ) - slighly fast (myelinated)
  • Pain, temperature, itch (C) - slow transducing (no myelination)
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4
Q

How are nerve endings different in thermoreceptors, nociceptors and mechanoreceptors?

A
  • Thermoreceptors/nociceptors - free nerve endings (C fibres)
  • Mechanoreceptors - encapsulated nerve endings (Aβ)
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5
Q

What is the absolute threshold?

A

Stimulus strength required to produce a positive response of detection 50% of the time

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6
Q

How does a stronger/longer stimulus affect the action potential and neurotransmitter release?

A
  • Larger generator potentials
  • Faster and more train of action potentials
  • More neurotransmitter released
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7
Q

Describe thermoreceptors

A

• Free nerve endings with high thermal sensitivity
• Change in temperature activates transient receptor potential (TRP) ion channels
• Have transmembrane portions:
- 4 heat-activated TRP channels (TRPV 1-4): ranging from noxious to tepid heat
- 2 cold-activated TRP channels: TRPM8 + TRPA1
• Combination of different receptor types on nerve endings

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8
Q

Describe the different mechanoreceptor endings

A
  • Meissner’s corpuscle - fine discriminative touch
  • Merkel cells - light touch and superficial pressure
  • Pacinian corpuscle - deep pressure, vibration and tickling
  • Ruffini endings - continuous pressure or touch + stretch
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9
Q

What are adaptations and name 2 types?

A
  • How the skin transmits signals, and how the brain interprets them
  • Tonic and phasic receptors
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10
Q

Describe tonic receptors

A
  • Detect continuous stimulus strength
  • Adapt slowly/do not adapt
  • Continue to transmit impulses as long as the stimulus is present
  • Keep brain constantly informed
  • e.g. Merkel cells slowly adapt - allows for fine touch to be perceived
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11
Q

Describe phasic receptors

A
  • Detect a change in stimulus strength
  • Transmit an impulse at the start and the end of a stimulus
  • Also called “movement receptors” or “rate receptors”
  • e.g. pacinian receptor
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12
Q

What is a receptive field?

A

• Region on the skin that causes activation of a single sensory neurone
• Different parts of the body have different sizes of receptive fields
• Smaller field:
- densely packed neurones
- precise perception
- more likely to recognise 2 points of touch

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13
Q

Describe Aδ nociceptors

A
  • Myelinated - quite fast
  • Type 1: Aδ-mechano-heat receptors (noxious mechanical and thermal stimuli)
  • Type 2: Aδ-mechanoreceptors (purely noxious mechanical stimuli)
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14
Q

Describe C-fibre nociceptors

A
  • Unmyelinated - slow
  • Mediate dull, persistent or second pain
  • Respond to thermal, mechanical and chemical stimuli (polymodal)
  • Chemical stimuli include inflammatory mediators
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15
Q

Where are the cell bodies of afferent neurones?

A
  • Dorsal root ganglia in the body

* Trigeminal ganglia in the face

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16
Q

Where do the 3 fibres enter the dorsal horn of the spinal cord?

A
  • Innocuous mechanical stimuli - Aβ (+Aα) - terminate in lamina III-VI (deep dorsal horn)
  • Pain and temperature - Aδ + C-fibres terminate in lamina I-II (superficial dorsal horn)
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17
Q

What is the main excitatory neurotransmitter released from the pre-synaptic neurone within the dorsal horn?

A
  • Glutamate

* Then transmits to the brain

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18
Q

What is the role of interneurones in the dorsal horn?

A
  • Conenct between different laminae and between adjacent peripheral inputs
  • Modulate pain and transmit mechanical stimulation through the dorsal horn
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19
Q

What is lateral inhibition?

A
  • Receptive fields can overlap with each other - difficult to distinguish between 2 stimulus locations
  • Lateral inhibition prevents this
  • Mediated by inhibitory interneurones within dorsal horn of spinal cord
  • Also facilitates enhanced sensory perception
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20
Q

What is gate control theory?

A
  • You can modulate a pain response in the dorsal horn by activating an Aβ-fibre
  • Aβ-fibre - involved with innocuous mechanical stimulation
  • If you hurt yourself, you ‘rub it better’ - assimilates Aβ-fibres - inhibits stimulated pain fibres
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21
Q

What are 3 of the central sensory structures in the brain?

A
  • SI: Primary somatosensory cortex (in postcentral gyrus)
  • SII: Secondary somatosensory cortex (in parietal operculum)
  • Posterior parietal cortex - spatial awareness
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22
Q

How do sensory inputs get into the brain? (2 pathways)

A
  • Dorsal column system (touch and proprioception)

* Spinothalamic pathway (pain, temperature and crude touch)

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23
Q

Describe how Aβ-fibres enter the dorsal column system?

A
  • Enter via the dorsal horn and enter ascending dorsal column pathways
  • Information from lower limbs (below T6) travel ipsilaterally along the gracile tract
  • Information from the upper limbs travel ipsilaterally along the cuneate tract
24
Q

Describe how Aβ-fibres travel through the dorsal column system once entered each tract, with reference to each order

A

1st order neurones
• Fibres in the Gracile/Cuneate Tract first synapse in the Gracile/Cuneate Nucleus (in the medulla)

2nd order neurones
• Decussate (cross sides) in the caudal medulla
• Forms the contralateral medial lemniscus tract
• Terminate in the thalamus (ventral posterolateral nuclei) - topographic: lower extremities more lateral

3rd order neurones
• Project from the VPL to the somatosensory cortex
• Size of somatotopic areas is proportional to density of sensory receptors in that body region (somatosensory homunculus)
• Pain and temperature localisation not as precise

25
Q

What are the 2 different pathways within the spinothalamic tract?

A
  • Lateral - pain and temperature

* Anterior - crude touch

26
Q

Describe how neurones travel through the spinothalamic tract

A

1st order neurones
• Terminate upon entering the spinal cord - i.e. dorsal horn

2nd order neurones
• Decussate immediately in the spinal cord
• Form the spinothalamic tract
•Terminate in the thalamus (ventral posterolateral nucleus) - topographic

27
Q

What are the key differences between the dorsal column and spinothalamic tract?

A

Dorsal column tracts
• Transmits light touch, vibration and 2-point discrimination
• Cross in brainstem

Spinothalamic tracts
• Transmits pain, temperature and coarse touch
• Cross in spinal cord

28
Q

How does pain reach the limbic system, giving it its emotional aspect?

A
  • Emotional component of pain transmitted from the spinal cord to the parabrachial area - then to the limbic system
  • Spino-reticular system
  • Sensory component bypasses the parabrachial area and goes to the cortex
29
Q

What is the cerebral signature for pain in an fMRI?

A
  • Loss of activity in the cortex - SI, SII, Insula, cortex, anterior cingulate cortex, prefrontal cortex
  • Amygdala, cerebellum and brainstem have more activity
30
Q

What is quantitive sensory testing (QST)?

A
  • Use of tools to look into different modalities e.g. temperature thresholds, vibration sensitivity
  • Allows us to look at whether or not the sensory system is sensitised/any pathology
31
Q

What can a blocked anterior spinal artery lead to?

A
  • Ischaemic damage to anterior part of the spinal cord - lesion of spinothalamic tract
  • Pain and temperature loss below level of the lesion
  • Retained light touch and vibration due to intact dorsal columns
32
Q

How are electrical perceptual thresholds different to QSTs?

A
  • Like QST, but use a semi-automated method - electrical current passed through the skin
  • Ask patient whether or not they can feel it - can then map the whole body
  • Spinal cord injury - lose sensation - threshold goes up
33
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

34
Q

What are 6 types (causes) of pain?

A
  • Nociceptive - tissue damage, typically acute pain
  • Muscle - lactic acidosis, ischaemia e.g. stretching
  • Somatic - well-localised e.g. inflammation
  • Visceral - deep, poorly localised
  • Referred - from an internal structure
  • Neuropathic - dysfunction of the nervous system
35
Q

What is neuropathic pain?

A
  • Pain caused by a lesion or disease of the somatosensory nervous system
  • Typically sharp, burning “electric shocks”
  • Poor response to usual analgesic drugs e.g. opiates
36
Q

Give examples of neuropathic pain

A
  • Radicular pain (sciatica)
  • Diabetic neuropathy
  • Post-surgical pain
  • Chemotherapy induced neuropathy
37
Q

What is allodynia?

A

Pain due to a stimulus that does not normally provoke pain

38
Q

What is hyperalgesia?

A

Increased pain from a stimulus that normally provokes pain

39
Q

What is sensitisation?

A

• Increased responsiveness of nociceptive neurones to their normal input

40
Q

What is hypoalgesia?

A

Diminished pain in response to a normally painful stimulus

41
Q

What is paraesthesia?

A

Abnormal sensation, whether spontaneous or evoked

42
Q

If you repeat a stimulus a number of times, it becomes more painful, what are the underlying mechanisms for this called?

A
  • Central sensitisation

* Happens in the dorsal horn

43
Q

What can persistant activation of the NMDA receptor lead to?

A

• Development of chronic pain e.g. arthritis
• NMDA receptors are involved with inducing plasticities in the CNS
- they allow big post-synaptic depolarisation
- Ca2+ mediated synaptic plasticity in dorsal horn neurones
- increased sensitivity
• Inhibitory interneurons can become less influential in chronic conditions
• Persistant activation causes stimuli to become more painful

44
Q

Describe the neuropathic phenotype profile?

A
  • Sigmoidal graph - stimulus intensity vs pain intensity
  • Following injury - graph shifts left - higher pain with lower stimulus
  • Allodynia - area where there is pain following injury where the pain intensity was previously 0
  • Hyperalgesia - higher pain at low stimulus intensity
45
Q

What are the 2 main types of neurotransmitters in the brainstem (that inhibit spinal cord excitability)?

A
  • Serotonin (from serotonergic nuclei, medulla)

* NA (from noradrenergic neruones, pons)

46
Q

What are the 2 types of descending control of nociception?

A
  • The PAM-RVM axis

* The locus cereleus (LC)

47
Q

What is the role of the PAM-RVM axis

A

• Contains serotonergic neurones, which project into the dorsal horn releasing serotonin
• Can either inhibit or facilitate pain depending on which receptors are activated:
- 5-HT1a: predominantly inhibitory
- 5HT3: predominantly facilitatory on NT release

48
Q

What is the role of the locus cereleus?

A
  • Main noradrenergic nuclei involved with descending control of nociception in the dorsal horn
  • Predominantly inhibitory
  • Dampens response by binding to pre-synaptic α2 receptors on primary afferents and projection neurones
49
Q

Describe how endogenous opioids work?

A

• The PAG and RVM contain high concentrations of μ opioid receptors
• Endogenous opioids (enkephalin, dynorphin) enhance descending inhibition from the PAG-RVM axis
• Reduce pain transmission in the dorsal horn
- inhibit glutamate release
- inhibit activation of spinothalamic neurones

50
Q

What effect does placebo have on pain?

A
  • Placebo induced analgesia is another form of endogenous analgesia
  • RAG and RVM show activity
  • Assume the spinal cord is involved - either inhibited or facilitated
51
Q

How can descending control systems be targeted for pain relief (medication)?

A

• Opioids - work in the PAG and RVM
• Antidepressants treat neuropathic pain (TCA, SNRI, SSRI)
- SSRIs are not very effective - low analgesic efficacy
- amitriptyline (TCA) is widely prescribed for neuropathic pain due to its noradrenergic component

52
Q

How do SNRIs provide pain relief?

A
  • Damaged primary afferent neurone => increased excitability => central sensitisation in spinal cord
  • Antidepressant binds to pre or post-synaptic terminal in the dorsal horn
  • NA increases in synaptic cleft - binds to α2 receptors - inhibitory
  • Sensory input to the brain is reduced - less pain
53
Q

What is conditioned pain modulation

A

• Experimental measure of the endogenous pain inhibitory pathway in humans
- level of descending control
• Good descending control - better efficacy of duloxetine (SNRI)

54
Q

What is tDCS?

A
  • Transcranial direct current stimulation
  • Non-invasive brain stimulation
  • Changes in cortical excitability in M1 have been show to reduce chronic pain in fibromyalgia and migraine patients
  • Mechanism not understood
55
Q

How is QST being changed for the future of pain control?

A

• QST has been expanded - 13 different tests to tease out patient’s phenotype
• 3 different neuropathic phenotypes:
- sensory loss, thermal hyperalgesia and mechanical hyperalgesia
• e.g. opioids feasible for patients with thermal hyperalgesia

Neuroscience and Mental Health (17 decks)

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