Physiology of Pain Flashcards
Where are nociceptors found?
Everywhere in the body except the brain
Where do nociceptor axon afferents terminate?
At the spinal level of entry - part of the (lateral) spinothalamic tract so the primary nociceptor afferent only reaches the spinal cord and then secondary afferent takes over.
What are the two broad classes of nociceptors?
- A-delta fibres
- C fibres
Describe A-delta fibres
- NT = glutamate
- Axon thin and myelinated
- Stimulated by mechanical trauma / noxious heat
- Immediate, sharp “1st pain”
- Synapses in laminae I, II, V
- Anterolateral (spinothalamic) tract
Describe C fibres
- NT = glutamate, Sub P
- Axon thinner and unmyelinated
- Stimulated by mech trauma, noxious heat/cold, inflammatory mediators
- Delayed, aching, “2nd pain”
- Synapses in laminae I, II, V
- Anterolateral (spinothalamic) tract
How do (C-fibre) nociceptors contribute to inflammation?
C-fibres are sensitive to inflammatory mediators, so when inflammatory mediators are released at a site of injury (histamine, bradykinin, prostaglandin), the C-fibre nociceptor becomes depolarised, and then releases its own pro-inflammatory peptides eg. Sub P which results in further depolarisation AND inflammation
What is the difference between the reflexes produced by A-delta and C fibres?
They’re both protective reflexes. A-delta fibres get to the spine quicker, so initiate crossed/uncrossed intersegmental reflexes eg. withdrawal from what caused the injury.
C-fibres come later where they also initiate crossed/uncrossed intersegmental reflexes such as immobilisation -> freezes you to prevent you putting weight on injury.
What is the point of pain perception apart from protective reflexes?
It’s for aversion - to take remedial actions to prevent injury happening again, learning process.
Why aren’t viscera represented on the sensory homonculus? How does this lead to referred pain?
Afferents from the body surface are mapped somatotopically in the cortex but the viscera aren’t.
The input from somatic nociceptors is somatotopically organised; that from certain visceral organs is not. Instead, visceral nociceptors converge on nociceptive projection cells that relay nociceptor information from the body surface.
What roles do the two different medial and lateral pain pathways play? How are they different in function?
The lateral pain pathway (neospino) is vital for the discrimination and localisation of pain, although pain can be felt even in the absence of somatosensory cortex.
The medial pain pathway (paleospino) structures mediate the emotional and motivational responses that are associated with pain, also sympathetic responses.
What areas of the brain are responsible for fear, distress and avoidance?
Anterior cingulate, hypothalamus, amygdala, insula, etc
What is the importance of descending control of pain?
The periaqueductal grey (PAG), which projects to the RVM release serotonin and noradrenaline to the dorsal horn of the spinal cord, via the dorsolateral funiculus. They activate interneurones in layer II, the substantia gelatinosa, which inhibit activity in the ascending pain pathways.
So descending pathways are important to damp down the pain sensation.
Descending pathways result is to suppress the transmission of nociceptor input via both presynaptic inhibition and hyperpolarisation of the projection cells. Is this on C or A-delta fibres, or both?
These effects are selective, targeting C fibre pain while leaving the fast Aδ withdrawal reflexes and other somatosensory signalling intact.
What are other methods apart from opioids to trigger the descencing pain pathway control to inhibit ascending pain?
- Good coping
- CBT
- Placebos
- Survival
Chronic pain is often associated with depression. How does treatment of antidepressents affect pain?
Often said to reduce pain by improving mood + coping ability, but also increase serotonergic and noradrenergic pathways in the descending anti-nociceptive pathways -> this also helps ease pain and in turn, depression.
