NEURO: Somatosensation II Flashcards
What happens when we get a lesion of the lower back (in terms of somatosensory systems)?
You would get reduced tactile sensation (DCML) on the same side, and reduced temperature and pain sensation (STT) on the opposite side.
What is pain?
It is a dual aspect model:
- SENSORY-DISCRIMINATIVE:
- location
- intensity
- duration
- quality - AFFECTIVE MOTIVATIONAL:
- unpleasantness (the painfulness of pain)
- effects on arousal, mood (affect) and behaviour
Pain relies on specific neurons.
What are they?
Examples?
Nociceptors
A-ẟ and C-fibres
Input into central somatosensory pathways
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
How can some people find hot chillies painful?
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.
What are the differences between A-δ and C fibres?
A-δ fibres:
- thinly myelinated
- transmit fast, sharp pain
- first sensation of pain
C fibres:
- non-myelinated
- transmit slow, dull pain
Receptor in A-ẟ and C-fibres
TRPV1 (vanilloid) receptor
- ion channel permeable to both Na+ and Ca2+
- involved in transduction of noxious heat
What stimulates TRPV1 (vanilloid) receptor?
Heat (e.g. Capsaicin from chille)
Acid (H+)
After a burn, why do you feel pain even after the stimulus has been removed?
How is the nociceptor activity maintained after injury?
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.
Define hyperalgesia and allodynia.
HYPERALGAESIA: increased sensitivity to pain
ALLODYNIA: maintenance of enhanced C-fibre activity during an inflammatory response
What pathway do A-ẟ and C-fibres stimulate?
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
The cortical representation of pain is complex.
Explain.
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.
What causes referred pain?
convergence of somatic nociceptive afferents with visceral afferents at the dorsal horn
Describe the dorsal horn interneurons.
- 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
How do afferents of the DCML and anterolateral system not converge at the thalamus?
because they project to different cells within the same thalamic nuclei
*pathways are parallel