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?
Nociceptors are neurons specialised for the detection of painful stimuli.
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:
- myelinated
- transmit fast, sharp pain
C fibres:
- non-myelinated
- transmit slow, dull pain
How is the nociceptor activity maintained after injury?
There is an ‘inflammatory soup’ of cytokines , prostaglandins and small signalling molecules that maintain the depolarisation and sensitivity of C-fibre terminals after the original stimulus.
It can also cause hyperalgaesia and allodynia.
Define hyperalgaesia and allodynia.
HYPERALGAESIA: Hyperalgesia is a condition where a person develops an increased sensitivity to pain.
ALLODYNIA: Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain.
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 reffered pain
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.
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.
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
Describe the information processed through the lateral and medial pain systems.
LATERAL:
- sensory discriminative
- project via specific somatosensory thalamic nuclei
MEDIAL:
- affective-motivational
- project to different cortical areas via (non-specific) midline thalamic nuclei
How do we get dissociation of the two aspects of pain?
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.
Describe the descending modulation of pain pathways.
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.
Describe the treatment of treating pain.
We are successful at treating pain as a neurophysiological response to tissue damage.
Some examples of substances used are NSAIDs and opiate drugs.
Describe when pain is dissociated from tissue damage.
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.
