LECTURE 8 - pain Flashcards
Define pain
“an unpleasant sensory and emotional experience associated with actual or potential tissue damage”
- combination of sensory (discriminative) and affective (emotional) components
pain is always subjective
Describe the peripheral perception of pain
- free nerve endings in skin, muscle, viscera
- activated by intense (noxious) stimuli - sufficient to cause tissue damage
- generates AP
pain generating stimuli: injury, heat, cold, inflammation, pH
What are the two kinds of nociceptor?
- Mechanical nociceptor
- activated bu strong shearing force in skin e.g. cut, strong blow
- sharp pain
- a delta fibres - Polymodal nociceptor
- respond to many stimuli e.g. sharp blow, damaging heat (>46°C)
- chemicals released by damaged tissue (means we only feel pain when we should)
- dull burning pain
- C fibres
How is pain detected by primary sensory neurone?
(cell body in dorsal root ganglia, single axon that splits and has a peripheral end and central end)
- AP generated in peripheral nerve ending
- NT released in dorsal horn of spinal cord
- all are excitatory primary afferent fibres
How quickly is noxious information carried by primary afferents?
- A delta fibres are myelinated => fast transmission of a sharp pain
- C fibres are unmyelinated => slower transmission of a dull, burning pain
How are nociceptive inputs received in the dorsal horn?
- laminar organisation
- synapse with second order neurones
- directly to indirectly make contact with protection neurones
AB fibres: III-V
Ad, C:
cutaneous I-II (topographic)
viscera I, V, X
What do the interneurones in the dorsal horn do?
- vastly made up of local interneurons
- interneurons modulate activity of projection neurones
- majority of interneurones are major inhibitory, without them we would feel unnecessary pain (some are spontaneously active, some stimulated by 1° afferent input
- pain signal must overcome inhibition to be sent to brain
What is the Gate Theory of Pain?
Wall and Melzack, 1965
- gatekeeper neurone (inhibitory interneuron) with cell body in substantia gelatinosa
- inhibiting output neurone in deeper lamina
- output neurone getting signals from AB mechanoreceptors (non-noxious signals therefore gate closed to AB input)
- excitatory AB fibre also directed to a different inhibitory interneurone to make sure threshold not reached in response to AB input
- when a noxious stimulus arrives (from AD/C fibres) gate needs opening
- done when the new excitatory neurone is fed to another population of inhibitory neurones to inhibit the inhibitory neurone that is keeping the gate closed (disinhibition -ve onto a -ve)
How is the gate closed to prevent a further pain signal?
- rubbing the skin activates AB fibres
- sensory input sent to spinal cord
- interneurones activated to stop signals being sent
How can the gate control system be used clinically and how does it work?
Increased non-noxious afferent input to spinal cord for analgesic effect
Examples:
- acupuncture
- TENS = transcutaneous electrical nerve stimulation
What happens in the ascending spinothalamic pathway?
- afferent synapses in thalamus
- pain localised when signal reaches cortex (you know where its coming from)
- pain perceived at subcortical level in brain
- limbic system feeds in affective component
What does the descending spinothalamic pathway do?
- able to modify and modulate ongoing pain
- allows ability of brain to signal back down to spinal cord
- in dorsal horn, 5-HT, noradrenaline and enkephalin (endogenous opioid) released in response to pain
- spinal gate can be closed => analgesic effect i.e. by swearing
- this is called the intrinsic analgesia system and allows for situations like battlefield soldiers to carry on even after severe injuries
What is facilitated pain?
normal physiological pain
- sensation of pain = afferent input
- duration and intensity of pain felt is directly equal to the afferent input
facilitated pain
- persistent/ chronic pain states => increased sensitivity to pain, allows for protection e.g. knowing not to flop around a broken arm
- process of peripheral and central sensitisation modify neurotransmission. this is neural plasticity
Define hyperalgesia
Primary hyperalgesia = increased pain sensitivity that occurs directly in the damaged tissue
Secondary hyperalgesia = increased pain sensitivity distant from the site of injury
Define allodynia
- central pain sensitisation following normally non-painful, but repetitive stimulation
- can lead to triggering of a pain response from stimuli which do not normally provoke pain
E.g. repeatedly having foot stood on (from friends)
