Session 4 Flashcards
(29 cards)
What is pain?
An unpleasant sensory and emotional experience, associated with actual or potential tissue damage.
What is chronic pain?
Pain/discomfort persisting continuously/intermittently for more than 3 months.
What are nociceptors?
Free, branching, unmyelinated nerve endings that signal that body tissue is being damaged or is at risk of being damaged. Present in most body tissues, except the brain.
What stimuli are able to activate nociceptors?
- Strong mechanical stimulation
- Chemical exposure
- Extremes of temperature
- Damaged cells at the site of injury can also release a number of chemicals that cause nociceptor membranes to open. E.g. proteases, ATP etc.
What would make nociceptors polymodal?
Able to respond to more than one modality, e.g. hot and spicy food. In this case, Capsaicin activates TRPV1 ligand-gated ion channels, which then fires an action potential.
What is the indirect pain pathway?
Involved in the affective aspect of pain. Much slower pathway, and involves 4 main pathways:
1) Spinoreticular
2) Spinomesencephalic
3) Spinotectal
4) Spinohypothalamic
How are nociceptors activated?
Tissue damage releases serotonin, bradykinin and prostaglandins, which all activate nociceptors. This results in a release of Substance P, which increases vascular permeability and histamine release from mast cells.
How are painful stimuli transducted?
- C-nociceptors are unmyelinated and associated with dull, aching pain. They have a larger receptive field.
- A-delta nociceptors are myelinated and associated with sharp pain. They are mechano-heat fibres and have smaller receptive fields.
Where do nociceptive primary afferents terminate?
Dorsal horn of the spinal cord
How does referred pain come about?
Nociceptor axons from the viscera enter the spinal cord by the same route as the cutaneous nociceptors, and converge in Rexed laminae V. Within the spinal cord there is substantial mixing of information from these two sources of input.
What is modulation of pain?
Means that pain is perceived differently by individuals and it is the gate control theory that allows for this modulation to occur.
What is the role of the substantia gelatinosa?
Acts negatively on lamina 1 and V to inhibit nociceptive impulses.
How does modulation occur?
A-delta and C-fibres entering lamina 1 and V synapse on the 2nd order neurone to pass impulse to the thalamus. They also act on the substantia gelatinosa to inhibit its inhibitory signal (therefore there’s a positive effect on the pain impulse).
How do mechanoreceptors affect pain stimuli?
Act via A-beta fibres on the substantia gelatinosa to increase its inhibitory effect, hence rubbing a damaged area may reduce the pain felt by the individual.
What is the role of descending inhibitory neurones?
Act to inhibit lamina 1 and V, both directly and via the substantia gelatinosa. They use endogenous opiods (5-HT and enkephalin). These descending neurones arise from the periaqueductal grey mater of the brain.
What is the function of the periaqueductal grey?
Stimulates the nucleus raphe magnus to send their inhibitory neurones down to lamina 1 and V of the dorsal horn of the spinal cord. (Hence depressing activity of nociceptive neurones).
What is a mixed nerve?
Contains a variety of different nerve fibres.
Describe a compound action potential.
A-wave: fastest nerves, large myelinated neurones.
C-wave: small, unmyelinated neurones.
B-wave: intermediate.
What is hyperalgesia?
A reduced threshold to pain, an increased intensity of painful stimuli or even spontaneous pain.
What is allodynia?
Pain from stimuli which are not normally painful, or pain which occurs in an area not stimulated.
What causes allodynia?
Process called wind-up, which occurs in persistent activation of pain afferents. Persistent activation and upregulation of NMDA receptors, and increased glutamate release, causing excessive second order neurone firing. Hence nociceptive neurones become hyperexcitable.
What is neuropathic pain?
Pain of neuronal origin, hence no nociceptors involved. E.g. diabetic neuropathy, cancer and trigeminal neuralgia. This can occur in the brain, spinal cord or peripheral nerves. Burning, electric, pins and needles kind of pain.
What can sensitisation of a peripheral nerve lead to?
- Decreased threshold of nociceptor activation
- Increased receptive field of nociceptor
- Allodynia and hyperalgesia
- Prolonged post-stimulus sensations (hyperpathia)
Describe the two pathological mechanisms of neuropathic pain.
1) Ectopic activity - upregulation of voltage gated sodium channels, hence increased excitability of the nerve and ectopic APs fire.
2) Ephaptic activity - ectopic beats cause action potentials that have been sent to activate adjacent nerve fibre bundles, causing receptor field expansion.
