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C&M Neuroanatomy > Week 10 Clinical Lecture: Pain and Somatosensory Disorders > Flashcards

Week 10 Clinical Lecture: Pain and Somatosensory Disorders Flashcards

1
Q

What receptors are frree nerve endings that terminate in the dermis and epidermia?

A

nociopceptive nerve endings (pain)

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2
Q

What are the general principles when classifying sensory afferents that innervate somatosensory receptors?

A
  1. large diameter = rapidly conducting afferents associated with mechanoreceptors
  2. small diameter = slow conducting afferents associated with nocioceptors and thermoreceptors
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3
Q

What is the relationship between conduction velocity and axon diameter?

A
  • positive correlation

- the larger nerves conduct faster and the smaller diameter nerves conduct slower

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4
Q

What are the 4 types of somatosensory fibres?

A
  1. Aa (a alpha)
  2. Ab (a beta)
  3. Ad (a delta)
  4. C
    in order of decreasing diameter (and therefore speed)
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5
Q

Aa fibres are responsible for transmitting information from which receptors?

A

proprioceptors of skeletal muscle

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6
Q

AB fibres are responsible for transmitting information from which receptors?

A

mechanoreceptors

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7
Q

Ad and C fibres are responsible for transmitting information from which receptors?

A

pain and temperature

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8
Q

Which fibres convey ‘1st pain’

A
  • fast Ad fibres
  • sharp or prickling pain
  • occurs rapidly
  • short duraration
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9
Q

Which fibres convey ‘2nd pain’

A
  • slow C-fibres
  • dull ache, burning
  • slow onset
  • persistant
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10
Q

What is the primary event in somatosensation?

A

Generation of an action potential in an afferent fibre ending

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11
Q

Certain regulators of neuronal excitability are specific for nociceptive neurons. What are they?

A
  1. Voltage-gated sodium channels:
    - Nav1.7
    - Nav1.8
    - Nav1.9
  2. Sensory TRP channels:
    - TRPV1
    - TRPM8
    - TRPA1
  3. Purinergic ligand-gated channels:
    - P2X2
    - P2X3
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12
Q

What is CIP? What is the genetic basis of CIP?

A
  • congenital insensitivity to pain
  • rare disease characterised by inability to feel pain
  • caused by loss of function mutations in the Na 1.7 gene
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13
Q

What happens to peripheral nerve endings during inflammatory pain?

A

they become over sensitive –> peripheral sensitisation

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14
Q

There are 4 types of inflammatory mediators. What does each one do?

A
  1. act to directly activate ligand-gated ion channels
    - ATP
    - H+
  2. Act via activation of G-protein coupled receptors
    - prostaglandins
    - substance P
    - bradykinin
    - proteases
    - histamine
  3. Act via activation of receptor tyrosine kinases
  4. ‘Gasotransmitters’
    - CO
    - NO
    - H2S
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15
Q

Explain the signalling cascade of inflammatory nociception

A
  1. Activation/sensitisation of sensory channels
  2. Modulation of ion channels through intracellular signalling cascade
  3. Modulation of gene expression
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16
Q

Different types of peripheral somatosensory neurons terminate at different lamina. Where do each of the following terminate:

  1. Ab myelinated fibres
  2. Peptidergic C fibres
  3. Ad myelinated fibres
  4. Nonpeptidergic C fibres
A
  1. lamina V and PKCy+
  2. Lamina I and Outer lamina II
  3. Lamina I and V
  4. Inner lamina II
17
Q

Explain the spinal pain pathway

A
  1. First-order neurons – These are pseudounipolar neurons which have cells bodies within the dorsal root ganglion. They have one axon which splits into two branches, a peripheral branch (which extends towards the peripheries) and a central branch (which extends centrally into the spinal cord/brainstem)
  2. Second-order neurons – The cell bodies of these neurons are found in the Rexed laminae of the spinal cord, or in the nuclei of the cranial nerves within the brain stem. These neurons ascend cranially in the spinothalamic tract to the ventral posterolateral (VPL) nucleus of the thalamus
  3. Third-order neurons – The cell bodies of third-order neurons lie within the VPL of the thalamus. They project via the posterior limb of the internal capsule to terminate in the ipsilateral postcentral gyrus.
18
Q

Do the majority of the pain signals travel ipsilaterally or contralaterally in the spinothalamic tract?

A

contralaterally

19
Q

How do most non painful somatosensory signals travel in the DCML pathway?

A

ipsilaterally

20
Q

Explain dissociated sensory loss

A
  • a unilateral spinal lesion will produce sensory loss of touch, pressure, vibration and proprioception below the lesion on the SAME side (as DCLM is ipsilateral)
  • diminished sensation of pain below the lesion will be observed on the opposite side (as spinothalamic tract travels contralaterally)
21
Q

Explain the trigeminal pathway for pain and temperature

A

There is a seperate system for the facial area:

  1. 1st order afferents from face project to pars interpolaris and pars caudalis of medulla/upper cervical cord
  2. 2nd order neurones ascend contralaterally to thalamus (via trigemino-thalamic tract)
  3. 3rd order neurones project to cortex
22
Q

What are inhibitory interneurones?

A

gate keepers that monitor how much peripheral information enters the brain

23
Q

What is the gate control theory of pain?

A
  1. inhibitory interneurones receieve input from either descending inhibitory pathways or mechanoreceptors
  2. this input either activates the inhibitory interneuron or shuts down the projection neuron
  3. the nocioceptive input will therefore not be transmitted and will stop pain entering the brain
24
Q

What is central sensitization?

A
  • refers to the process through which a state of hyperexcitability is established in the CNS, leading to enhanced processing of nocioceptive (pain) messages
  • contributes to sustained pain states
25
Q

What is sensitisation?

A
  • a form of plasticity where 2nd order projection neurones become more responsive to peripheral input
  • this produces exaggerated pain
26
Q

Explain the 3 steps of sensitisation

A
  1. 1st degree of mechanisms that leads to sensitisation of 2nd order neurones is NMDA-mediated signalling
  2. 2nd group are due to disinhibition –> inhibitory neurons control how much nociocetive input is propagated to the brain. this inhibition is lost
  3. microglia activation in the spinal cord –> they release cytokines that trigger faster activation of 2nd order neurons
27
Q

What is FHM?

A
  • Familial hemiplegic migraine

- autosomal dominant subtype of severe migraine accompanied by visual disturbances known as aura

28
Q

What is the aura in FMH caused by?

A

the aura is caused by cortical spreading depression (CSD) –> a slowly advancing wave of tissue depolarisation in the cortex

C&M Neuroanatomy (44 decks)

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