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Y2 - NMH > The Somatosensory System > Flashcards

The Somatosensory System Flashcards

1
Q

What are the somatosensory modalities detected by mechanoreceptors - and give examples within subcategories

A
  1. Touch - light touch, pressure, vibration
  2. Proprioception - joint position, muscle length, muscle tension
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2
Q

What is the somatosensory modality detected by thermoceptors?

A

Temperature

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3
Q

What is the somatosensory modality detected by nociceptors?

A

Pain

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4
Q

1) Which type of sensory receptors are separate entities and which are part of the sensory neurones?
a) mechanoreceptors
b) thermoreceptors
c) nociceptors
2) For the one(s) which is/are not separate entities, where are they in relation to sensory neurones?

A

1) a - Mechanoreceptors
2) Mechanoreceptors are the peripheral terminals of the peripheral axons of the primary sensory neurones

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5
Q

What is the general route of primary, secondary and tertiary sensory neurones that constitute the afferent sensory pathway?

A
  1. Primary sensory neurones have peripheral terminals and axons which lead into the cell body found at the dorsal root ganglion and then a centrally directed axon which leads into the spinal cord
  2. Secondary sensory neurones are found either in the spinal cord or in the brainstem and acts as a relay. Their ascending axons decussate, and they terminate either in the thalamus or the cerebellum (posture)
  3. Tertiary sensory neurones’ cell bodies are in the thalamus, from where they project to the brain (postcentral gryrus of parietal lobe for touch). Postural tertiary neurones are located in the cerebellum
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6
Q

What are the 2 types of modified axon terminals of sensory receptors - and which type of receptors have which?

A
  1. Free nerve endings - thermoreceptors and nociceptors
  2. Enclosed nerve endings - mechanoreceptors
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7
Q

How do we classify sensory neurones - what are the 3 classes (including subclasses where applicable) and what types of sensory information do they relay?

A
  1. Aß-fibres: innocuous mechanical stimulation
  2. Aδ-fibres:
  • Type 1: noxious mechanical
  • Type 2: noxious thermal stimulation
  1. C-fibres: noxious mechanical, thermal and chemical stimulation (polymodal)
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8
Q

1) What class of sensory neurones do thermoceptors transmit to and what is an adaptation of these fibres to their function in receiving thermal signals?
2) Outline further what these thermoreceptors actually are - how they function, and list how many cold and heat activated ones there are and what the names of these types of thermoreceptors are

A

1)

  • Aδ and C-fibres
  • Free nerve ending nerve terminals - i.e. unmyelinated at the nerve endings which increases thermal sensitivity

2)

  • Transient receptors potential (TRP) ion channels
  • 4 heat activated: TRPV1-4
  • 2 cold activated: TRPM8, TRPA1
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9
Q

Give 5 mechanoreceptors and what specifically do they detect?

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
  5. Peritracheal endings - nerve ending wrapped around hair
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10
Q

Define a stimulus threshold

A

‘The point of intensity at which the person can just detect the presence of a stimulus 50% of the time (absolute threshold)’

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11
Q

How does greater stimulus strength and duration correlate to greater stimulus intensity?

A

Increased stimulus strength and duration → increased frequency of action potentials transmitted along sensory fibres and increased NT release → greater intensity

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12
Q

1) Describe the 2 types of mechanoreceptor adaptation and what are each of their roles etc
2) Give an example of a type of mechanoreceptor that does both types of adaptation and then outline its use in each of these

A

1)

  1. Tonic receptors (slow-adapting): detect continuous stimulus strength, continuing to transmit impulses for as long as the stimulus is present in order to keep the brain constantly informed of the status of the body
  2. Phasic receptors (fast-adapting): detect a change in stimulus strength - transmitting an impulse at the start and end of the stimulus, but fading in the middle of the stimulus

1)

  • Merkel cells mechanoreceptors are tonic receptors which slowly adapt to allow superficial pressure and fine touch perception
  • Pacinian corpuscle mechanoreceptors are phasic receptors. Sudden pressure excites the receptor and then a signal is transmitted again when the pressure is released
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13
Q

1) Define what the receptive field on a region of skin is
2) How are these receptive fields formed?

A

1)

‘The region on the skin which causes activation of a single sensory neurone when activated’

2)

As the sensory neurone approaches the skin, its peripheral axon branches off and each of these branches have sensory receptors which when stimulated can activate the sensory neurone

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14
Q

What do small and large receptive fields facilitate functionally?

A
  • Small receptive fields allow the detection of fine detail
  • Large receptive fields allow the the cell to detect changes over a wider area (less precise perception)
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15
Q

How are the fingers adapted to allow detection of fine detail over a small area - precise perception?

A
  • Densely packed mechanoreceptors
  • Small receptive fields
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16
Q

What is 2-point discrimination, how is it carried out, and what is it related to?

A
  • Minimum distance at which 2 points are perceived as separate
  • Carried out using calipers which are gradually contracted until the 2 points are percieved as 1 - the distance is then measured
  • Related to the size of the receptive field
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17
Q

What are somatosensory dermatomes?

A
  • Each spinal nerves have specific dermatomes on the skin (regions they innervate)
  • Spinal nerves involved in somatosensory function innervate skin dermatomes
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18
Q

Where are the cell bodies of primary sensory neurones located for those related to…

1) The body
2) The face

A

1) Dorsal root ganglion
2) Trigeminal ganglia

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19
Q

What are the 2 types of dorsal horn neurons?

A
  1. Projection neurons - axonal projections to the brain
  2. Interneurons - axons remain in the spinal cord
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20
Q

1) Describe the function of lateral inhibition?
2) What mediates lateral inhibition?

A

1)

  • Prevents the overlap of receptive fields
  • Facilitates pinpoint accuracy in localisation of the stimulus and therefore enhanced sensory perception (discrimination)

2)

  • Inhibitory interneurons within dorsal horn of spinal cord
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21
Q

Describe the route of the dorsal column system - Aß fibres - including the different tracts

A
  1. Aß fibres enter via the dorsal horn and enter the ascending dorsal column pathways via primary sensory neurones
  2. Information conveyed from lower limbs and body (below T6) travel ipsilaterally along the Gracile tract, while information from the upper limbs and body (above T6) travel ipsilaterally along the Cuneate tract
  3. Primary order neurones terminate in the medulla - have their first synapse in the Gracile nucleus which is more medial in the spinal cord, while fibres in the Cuneate tract have their first synapse in the Cuneate nucleus which is more lateral in the spinal cord
  4. Second order neurones decussate in the caudal medulla and form the contralateral medial lemniscus tract
  5. These second order neurones terminate in the ventral posterior lateral nucleus of the thalamus (VPL) if from the body or in the ventral posteriomedial (VPM) nucleus of the thalamus if from the head and neck
  6. Third order neurones from the VPL or VPM nuclei of the thalamus project to the somatosensory cortex where the sensory information is processed
22
Q

In the somatosensory homunculus, the size of somatotopic areas is proportional to what?

A

The density of the sensory receptors in that body region

23
Q

Outline the ascending pathway for the spinothalamic (anterolateral pathways), first mentioning what type of sensory information it relays

A
  • Pain and temperature
  • Crude touch (not fine touch)
  1. Pain and temperature sensation ascends within the lateral spinothalamic tract while crude touch ascends within the anterior spinothalamic tract. Primary sensory neurones enter the spinal cord, directed along these tracts in the spinal cord
  2. Primary order neurones terminate upon entering the spinal cord
  3. Second order neurones decussate immediately in the spinal cord and form the spinothalamic tract (lateral and anterior)
  4. Second order neurones terminate in the ventro-posterior-lateral (VPL) nucleus of the thalamus
  5. Third order neurones from the VPL nucleus of the thalamus project to the somatosensory cortex
24
Q

What are the differences between the sensation and functionalities of the spinothalamic and dorsal columns?

A
  • Spinothalamic - Pain + Temperature (Aδ and C fibres) and Coarse touch
  • Dorsal column - Light touch, vibration and 2-point discrimination (Aß fibres)
25
Q

How can quantitative somatosensory testing (QST) be used to test the integrity of ascending pathways?

A
  • Thermal threshold test used to see if temperature sensation is preserved - tests integrity of spinothalamic tract
  • Test response to pain to see if pain sensation is preserved - tests integrity of spinothalamic tract
  • 2 point-discrimination tests used to test dorsal column integrity - posterior column patency
26
Q

What does blocked anterior spinal artery cause?

A
  • Causes ischaemic damage to the anterior part of the spinal cord
  • Spinothalamic tract damage - loss of pain and temperature below the level of the lesion
  • Whereas retained light touch and vibration sensation due to intact dorsal columns
27
Q

What will be the symptoms of spinothalamic tract damage / lesion and where?

A
  • Causes temperature sensation loss and pain below the level of the lesion
28
Q

1) What are the 2 types of nociceptive fibres (including subtypes where necessary), are these myelinated or unmyelinated, and what type of information do they relay?
2) What is another type of sensory fibre which is not a nociceptor and describe the same details as the others

A

1)

  1. Aδ fibres - Myelinated (so fast) - sharp, intense or first pain
  • Type 1: noxious mechanical
  • Type 2: noxious heat
  1. C-fibres - Unmyelinated (so slow) - dull, aching or second pain
    * Noxious thermal, mechanical and chemical stimuli (polymodal)

2)

  • A-beta - Large, myelinated - v.fast - inocuous mechanoreceptors
29
Q

Outline the pathway for the emotional component of pain (separate to the lateral spinothalamic tract sensory component)

A
  • The spino-reticular system
  • Spinal cord → parabrachial area (in brainstem) → limbic system (amygdala and hypothalamus)
30
Q

1) Where is the primary somatosensory cortex (SI) located?
2) Where is the secondary somatosensory cortex (SII) located?
3) What is the function of the posterior parietal cortex?

A

1) In the postcentral gyrus
2) In the parietal operculum
3) Spatial awareness of the body by sensory feedback giving us an idea of where we are in space

31
Q

When is the electrical perceptual threshold test useful, what is it, and why is it useful in this situation?

A
  • ​In spinal cord injury there is loss of sensation (thresholds increase)
  • Electrical current is passed through the skin, and you ask when the patient can feel it to map the sensation abilities in the patient to determine the site of the lesion because the lesion will be above the area where you lose sensory function
32
Q

What are the 6 types of pain, giving causes / explanations and examples where necessary?

A
  1. Nociceptive - tissue damage, typically acute pain (e.g. skin cut)
  2. Muscle - lactic acidosis, ischaemia (e.g. stretching, fibromyalgia)
  3. Somatic - well localised (e.g. inflammation, infection)
  4. Visceral - deep, poorly localised (e.g. stomach, colon, IBS)
  5. Referred - from an internal organ / structure (e.g. angina)
  6. Neuropathic - dysfunction of the nervous system
33
Q

What is the pain matrix, and how was it discovered?

A
  • fMRI showed a ‘cerebral signature for pain’
  • Activity in the SI, SII, Insula cortex, Anterior cingulate cortex, prefrontal cortex
34
Q

What NT is transmitted across the first synapse in the nociceptive pathway to the dorsal horn neurone?

A
  • Glutamate - excitatory
35
Q

Describe the gate control theory of pain

A
  • The inhibition of primary afferent inputs before they are transmitted to the brain through ascending pathways through superficial dorsal horn modulation
  • Aß fibres innocuous stimulation activates inhibitory interneurones which inhibit the signals that noxious stimulation via C-fibres to projection neurones to the brain send
36
Q

1) What are the 2 types of descending pain modulation (control) pathways?
2) What type of NT is released in these pathways - what are the 2 specific NTs and what neurones secrete these?
3) Which NT is used in each pathway?

A

1)

  1. PAG-RVM axis (periaqueductal grey - rostro ventromedial medulla)
  2. Locus cereleus

2)

  • Monoamines
  1. Serotonins - from serotonergic neurones (from medulla)
  2. NA - from noradrenergic neurones (originating from Pons)

3)

  • PAG-RVM - serotonin
  • Locus cereleus - NA
37
Q

Describe the mechanism for how the PAG-RVM axis modulates pain, including which specific receptors are involved

A
  • Contains serotonergic neurones which project to the dorsal horn and release serotonin
  • Here, serotonin can either dampen (inhibit glutamate release) or faciltate pain signals depending on which receptors are activated…
  • 5-HT1A - predominantly inhibitory
  • 5-HT3 - predominantly facilitatory
  • Remeber that the afferent neurones in the nociceptive pathway travel from the dorsal horn to the lateral spinothalamic tract - unlike other sensory pathways which may go through the dorsal column
38
Q

How does the locus cereleus pathway modulate pain transmission?

A
  • Noradrenergic nuclei secrete NA which dampens down nociception via the dorsal horn by binding to presynaptic alpha-2 adrenoreceptors on primary afferents and projection neurons, ultimately reducing excitability of neurones in the nociceptive pathway
  • Remember the dorsal horn → lateral spinothalamic tract in nociceptive pathway
39
Q

1) List 2 endogenous opioids
2) Describe the endogenous opioid analgaesic system

A

1)

  • Enkephalin
  • Dynorphin

2)

  • Endogenous opioids → bind μ opioid receptors which are high in concentration in PAG and RVM → thereby increasing serotonin release from the PAG-RVM axis so enhancing the PAG-RVM inhibition of glutamate release via the dorsal horn at the spinothalamic tract in the nociceptive pathway
40
Q

What is the evidence for placebo analgaesia?

A

There is increased activity in the PAG and RVM - indicating PAG-RVM axis involvement

41
Q

1) What is neuropathic pain?
2) Give some examples of the pain sensations felt in neuropathic pain
3) Give some examples when neuropathic pain can arise

A

1) Pain caused by lesion or disease of the somatosensory nervous system

2)

  • Stabbing
  • Electric shock
  • Pins and needles
  • Numbness
  • Throbbing
  • Shooting
  • Burning

3)

  • Radicular low back pain (sciatica)
  • Diabetic neuropathy
  • Post-herpetic neuralgia
  • Post-surgical pain
  • HIV-induced neuropathy
  • Chemotherapy induced neuropathy
  • Complex regional pain syndrome
42
Q

Define Allodynia?

A

Pain due to a stimulus that does not normally provoke pain

43
Q

Define Hyperalgaesia?

A
  • Increased pain from a stimulus that normally provokes pain
  • Primary hyperalgaesia - in the region of damaged tissue
  • Secondary hyperalgaesia - in the region immediately surrounding the damaged tissue
44
Q

Define Parasthesia

A

Abnormal sensation whether spontaneous or provoked

45
Q

What is central sensitisation?

A

Mechanism that occurs in the dorsal horn where when you repeat a stimulus it becomes more painful

46
Q

1) Describe the pathophysiological mechanism for how neural plasticity leads to central sensitisation and thus chronic pain?
2) How does central sensitisation via neural plasticity give rise to allodynia and hyperalgaesia?

A

1)

  1. Repeated stimulus
  2. NMDA receptors activation
  3. Results in massive post-synaptic depolarisation - Ca2+ enters the neurone
  4. Ca2+ mediated neural plasticity in dorsal horn neurones
  5. Increases synaptic strength (efficacy) and neural sensitivity
  6. Inhibitory interneurons also become less influential - leading to increased sensitivity
  7. This increased sensitivity in the pain pathway leads to chronic pain
  • Therefore excessive NMDA stimulation can lead to chronic pain via central sensitisation

2)

  • The increased sensitivity in the pain pathway as aforementioned leads to hyperalgaesia
  • Inhibitory internuerones normally prevent Aß fibres (innocuous stimuli) from causing pain. Reduction in influence of the inhibitory interneurones therefore results in allodynia (pain from stimuli which do not normally provoke pain)
47
Q

1) What is the neuropathic phenotype useful for?
2) Give 5 examples of neuropathic phenotypes

A

1) A way to describe the type of pain the patient is feeling

2)

  • Heat hyperalgaesia
  • Cold hyperalgaesia
  • Mechanical hyperalgaesia
  • Mechanical allodynia
  • Loss of sensation
48
Q

List 4 treatments for neuropathic pain that target descending modulation pathways, giving example drug names where applicable

2) What has better analgaesic efficacy - TCAs, SNRIs or SSRIs?

A

1)

  1. Opioids - work in PAG and RVM
  2. SSRIs (fluoxetine, cetalopram)
  3. SNRIs (duloxetine)
  4. TCAs (amitryptiline)

2)

  • TCAs and SNRIs have better efficacy than SSRIs which have very low analgaesic efficacy
49
Q

How do SNRIs enhance descending noradrenergic inhibition of pain, and therefore what existing descending pain modulation pathways do they act on?

A
  • Binds to the pre- or post-synaptic nerve terminals in the dorsal horn and increase synaptic [NA]
  • Therefore enhances the locus cereleum effects on pain inhibition
  • By enhancing [NA] in synapse - more NA binding presynaptic and post-synaptic α2 receptors - which when bound inhibit signalling within the pain neurones in the pain pathway
50
Q

How can we measure the degree of descending control in patients, and why can this be useful clinically?

A
  • Conditioned pain modulation is used to measure the degree of descending modulation
  • Greater descending control = better SNRI (e.g. duloxetine) efficacy
  • SNRIs (e.g. duloxetine) are useful in treating neuropathic pain
  • So can be used for ‘personalised medicine’

Y2 - NMH (12 decks)

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