Somatosensation II Flashcards
Why is it important that DCML and STT cross the midline at different sites?
DCML and STT cross the midline at different sites
This is significant
If a lesion damaged the left side of the spinal column we lose both temperature and pain AND fine tactile discrimination
Differential loss of temperature/pain vs fine tactile discrimination
What is pain?
Dual aspect model: Sensory-discriminative - Location - Intensity - Duration - Quality Affective-motivational - Unpleasantness – the painfulness of pain - Effects on arousal, mood (affect), behaviour
What’s the difference between temperature and pain receptors?
Nociceptors are neurons specialised for detection of painful stimuli
Gentle heat will stimulate thermoreceptors
We have separate neurons for non-nociceptive thermoreception and nociceptive thermoreception
A nociceptor doesn’t respond until the temperature reaches the threshold for painful stimuli
NB a temperature sensitive nociceptor is a specific type of nociceptor
How do A-delta and C fibres produce different effects?
A-delta and C-fibres contribute different aspects of pain sensation
A delta fibres produce the initial first pain and the slower conducting C fibres produce the following second pain
What is the function of the TRPV1?
The TRPV1 receptor is involved in transduction of noxious heat
The peripheral axons of Adelta and C fibres are bare nerve endings underneath the skin (not associated with any special structures)
Transduction mechanisms involve opening of ion channels in the peripheral axonal endings of the sensory neurons in response to external stimuli
Example, the thermal nociceptor has an ion channel called the TRPV1 receptor, present in both Adelta and C fibres.
The TRPV1 allows entry of sodium and calcium resulting in depolarisation
Capcaisin acts on this receptor and opens in
This happens to be the active ingredient in chilies
Why does pain persist after initial injury?
‘Inflammatory soup’ of cytokines, prostaglandins and small signalling molecules maintains depolarisation and sensitivity of C-fibre terminals after original stimulus (so they keep the nociceptor depolarised)
A peptide that is synthesised and secreted by the C fibres called substance P also contributes to this (acts on mast cells or neutrophils to release histamine to act on depolarising C fibres)
Collateral branches of the C fibres would induce local release of substance P to keep the cycle up as well as promoting vasodilation to increase blood flow as part of the inflammatory response
This gives rise to two phenomena:
Hyperalgesia- increased sensitivity to pain
Allodynia- painful response to a response that would normally be innocuous (like touching the place you got cut)
What is the spinothalamic tract pathway?
Dorsal horn interneurons
Located in superficial and deep layers of dorsal horn
Synaptic input from C- and A-δ fibres
Axons cross and ascend in anterolateral white matter
Some are multi-modal (receive convergent input from nociceptive and non-nociceptive inputs)
Some receive convergent input from visceral afferents as well as afferents from the skin
Visceral afferents don’t have their own set of spinal interneurons to signal which results in poorly localised visceral pain, this leads to referred pain in the internal organs
Why do we have referred pain?
Heart pain is expressed on the chest, back and sometimes the arm due to convergence of visceral afferents onto the secondary interneurons receiving their C and A delta fibres from other regions of the body
What are the two systems involved in central pain processing?
Diverge at level of thalamus
Lateral system (do not confuse with anterolateral system)
- Projection to the VP nuclei of thalamus, that is the one in parallel with DCML system
- Primary and secondary somatosensory cortex (SI and SII)
Medial system
- Midline nuclei of thalamus (intralaminar nuclei)
- These project to the anterior cingulate and insular cortex
How do the lateral and medial pain systems differ?
Lateral
- Sensory-discriminative
- Project via specific somatosensory thalamic nuclei
Medial
- Affective-motivational
- Project to different cortical areas via (non-specific) midline thalamic nuclei
The periaqueductal brain in the midbrain is a major pain modulating site and happens to be the site that contains the endogenous opioid
What are opioids and how do they work?
Analgesic properties of opium known for centuries
Opium and its derivatives are the most powerful painkillers known
Endogenous opioids (enkephalins, endorphins) and opioid receptors discovered 1970s-80s
The main source of enkephalins is in the periaqueductal grey and this sends projections to many different parts of the brain
These structures are all associated with particular neuromodulator substances particularly serotonin and noradrenaline
The somatic sensory cortex interacts with these opiate containing neurons and these systems such as serotonergic neurons from the raphe system project all the way down to the dorsal horn of the spinal cord where the Abeta, Adelta and C fibres synapse
The way this works in the raphe nuclei
In the spinal cord these activate local spinal cord interneurons and these are opioid neurons, they are enkephalin containing
They pre-synaptically inhibit the incoming C-fibres by synapsing onto the synaptic terminal of a C fibre
So incoming action potentials arriving at the C-fibre terminals will be less effective at inducing transmitter release
This is for example how an epidural works
What are the different ways you can treat pain?
Successful at treating pain as neurophysiological response to tissue damage
- NSAID
- Opiate drugs
Chronic pain
- antidepressants (e.g., amitriptyline, duloxetine)
- At lower dosage and in absence of diagnosis of clinical depression
What is chronic pain?
> 3 months
Alarmingly high prevalence
May be due to nerve damage from prior injury: neuropathic pain
However, increasingly accepted that pain can be dissociated from tissue damage
(What could that mental image be? Well we have substrates for the location and identification of pain and also for the affective aspects of pain, if even if they’re not proven. But the principle that pain could be a sort of hallucination (real pain for all that) follows from any representational view of the mind.
What is phantom limb pain?
Pain dissociated from tissue damage
Following amputation most people experience phantom limb
Phantom limb pain
This is an example of central pain as the somatosensory cortex still contains a representation of the missing body part
Why does it happen?
We don’t know
(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 a 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.)
What is an anterior cingulotomy?
Anterior cingulotomy for intractable pain
Targeted lesion to disconnect anterior cingulate cortex on both sides
Used for decades as last resort to treat truly intractable pain
“Importantly, the patients described that although pain was present, it was ‘less bothersome’ or ‘separate from them’, playing into the affective role of the ACC. ” Farrell et al (2018)
