NEURO: Somatosensation II Flashcards

1
Q

What happens when we get a lesion of the lower back (in terms of somatosensory systems)?

A

You would get reduced tactile sensation (DCML) on the same side, and reduced temperature and pain sensation (STT) on the opposite side.

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2
Q

What is pain?

A

It is a dual aspect model:

  1. SENSORY-DISCRIMINATIVE:
    - location
    - intensity
    - duration
    - quality
  2. AFFECTIVE MOTIVATIONAL:
    - unpleasantness (the painfulness of pain)
    - effects on arousal, mood (affect) and behaviour
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3
Q

Pain relies on specific neurons.

What are they?

Examples?

A

Nociceptors

A-ẟ and C-fibres

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4
Q

Input into central somatosensory pathways

A

Spinothalamic Tract/Anterolateral System:

  • input from thinly/unmyelinated afferents (small)
  • A-ẟ and C-fibres
  • detect coarse touch, pain, temperature

Dorsal Medial-Column Lemniscal System:

  • input from large myelinated afferents
  • A-⍺ (proprioception) and A-β (tactile) afferents
  • detect discriminative touch, pressure, vibration
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5
Q

How can some people find hot chillies painful?

A

Capsaicin is a protein found in hot chilli peppers. It activates the TRPV1 receptors, which activate the A-δ and C fibres of nociceptors.

This gives the feeling of pain when eating the chillies.

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6
Q

What are the differences between A-δ and C fibres?

A

A-δ fibres:

  • thinly myelinated
  • transmit fast, sharp pain
  • first sensation of pain

C fibres:

  • non-myelinated
  • transmit slow, dull pain
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7
Q

Receptor in A-ẟ and C-fibres

A

TRPV1 (vanilloid) receptor

  • ion channel permeable to both Na+ and Ca2+
  • involved in transduction of noxious heat
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8
Q

What stimulates TRPV1 (vanilloid) receptor?

A

Heat (e.g. Capsaicin from chille)

Acid (H+)

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9
Q

After a burn, why do you feel pain even after the stimulus has been removed?
How is the nociceptor activity maintained after injury?

A

The inflammatory response involves local signalling molecules (cytokines, prostaglandins, signalling molecules) which act on the vanilloid receptors in the C-fibres and maintain depolarization in the absence of the noxious heat stimulus.

Although the C-fibre axon projects back to the spinal cord from the skin, there are peripheral branches that can release transmitter substances such as substance P which further promotes the inflammatory cascade that maintains the nociceptor activity after injury.

It can also cause hyperalgesia and allodynia.

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10
Q

Define hyperalgesia and allodynia.

A

HYPERALGAESIA: increased sensitivity to pain

ALLODYNIA: maintenance of enhanced C-fibre activity during an inflammatory response

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11
Q

What pathway do A-ẟ and C-fibres stimulate?

A

Spinothalamic Tract/Anterolateral System

  • axons arrive in the dorsal column and synapse in the dorsal horn (grey matter)
  • second-order neurones cross to the other side of the spinal cord
  • ascend in anterolateral white matter to ventral posterior nuclear complex or midline nuclei of the thalamus
  • third-order thalamic neurones project to S1/S2 via the lateral system or anterior cingulate/insular cortex via the medial system
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12
Q

The cortical representation of pain is complex.

Explain.

A

STT projects to S1 via ventral posterior nuclei of the thalamus (like the DCML system). However, STT and DCML axons do not converge on the same thalamic neurons - their pathways are parallel.

S1 is necessary for the localisation of pain, but stimulation of S1 gives rise to referred tactile, not painful, sensations. So, additional areas are involved in pain sensations.

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13
Q

What causes referred pain?

A

convergence of somatic nociceptive afferents with visceral afferents at the dorsal horn

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14
Q

Describe the dorsal horn interneurons.

A
  • located in the superficial and deep layers of the dorsal horn
  • receive synaptic input from C- and A-δ fibres
  • axons cross and ascend in anterolateral white matter
  • some are multi-modal (receive convergent nociceptive and non-nociceptive inputs)
  • some receive convergent input from visceral afferents, which can explain the phenomenon of referred pain
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15
Q

How do afferents of the DCML and anterolateral system not converge at the thalamus?

A

because they project to different cells within the same thalamic nuclei

*pathways are parallel

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16
Q

The function of the primary somatosensory cortex

A

stimulation gives rise to referred tactile sensations, not painful sensations
-however necessary for localisation of pain via somatotopic mapping

17
Q

Divergence of anterolateral system/spinothalamic tract

A

Diverges at the thalamus, producing two systems involved in central pain processing:

  • Lateral system (sensory discriminative)
  • Medial system (affective-motivational)

*can dissociate from one another

18
Q

The lateral system of Spinothalamic Tract

A

Sensory Discriminative

> target ventral posterior (VP) nuclear complex of thalamus (in parallel with tactile afferents of the DCML system)

> project via specific thalamic nuclei to the primary and secondary somatosensory cortex (SI and SII), where localisation of sensations/pain is made possible

19
Q

Medial system of Spinothalamic Tract

A

Affective-Motivational

> axons diverge medially and target midline nuclei of the thalamus (intralaminar)

> onward thalamic projection neurones don’t project to SI, but to other cortical regions such as the anterior cingulate cortex and insular cortex (non-specific)

20
Q

Different hypothalamic and cortical areas of the brain are involved in central pain processing. There are two systems that diverge at the level of the thalamus.

Explain.

A

There are two systems:
LATERAL SYSTEM (do not confuse with anterolateral system):
- ventral posterior nuclei of the thalamus, in parallel with DCML system
- primary and secondary somatosensory cortex (SI and SII)

MEDIAL SYSTEM:

  • midline nuclei of thalamus (intralaminar)
  • anterior cingulate and insular cortex
21
Q

Describe the information processed through the lateral and medial pain systems.

A

LATERAL:

  • sensory discriminative
  • project via specific somatosensory thalamic nuclei

MEDIAL:

  • affective-motivational
  • project to different cortical areas via (non-specific) midline thalamic nuclei
22
Q

How do we get dissociation of the two aspects of pain?

A

We get that dissociation in, for example, a postcentral lesion, where we see the pain affect without the pain sensation.

An anterior cingulotomy has been used for decades as a last resort for intractable pain. It’s a targeted lesion to disconnect the anterior cingulate cortex on both sides.

23
Q

Describe the descending modulation of pain pathways.

A
The analgaesic properties of opium have been known for centuries.
Endogenous opioids (such as enkephalins and endorphins) and opioid receptors were discovered in the 1970s-80s. They act on the pain pathways to block it, providing an analgaesic effect.
24
Q

Describe the treatment of treating pain.

A

We are successful at treating pain as a neurophysiological response to tissue damage.

Some examples of substances used are NSAIDs and opiate drugs.

25
Q

Describe when pain is dissociated from tissue damage.

A

This involves the tissue damage model of pain.
Doctors are trained in this, and they will look for tissue damage, and quite plausibly, find it. The problem is that the tissue damage is not correlated with the level of pain, when you compare across individuals.

If you have pain in a tissue that hasn’t existed for years, this alone suggests that pain is in the mental image of the body rather than the body itself.

26
Q

What is chronic pain?

A

It is the persistence of pain for more than 3 months. Most of the time, there is very little or no tissue damage, so how would we treat it?
It has an alarmingly high prevalence.

We don’t fully understand them, it may be due to the dysfunction of the pain pathways.

Neuropathic pain is normally associated with nerve damage.