B. Peripheral and central sensitisation Flashcards
What is the protective mechanism related to pain ?
Protective mechanism leads to:
- Reflex
- Avoidance behaviour
What is the immediate motor response after noxious stimuli ?
Reflex
What is the meaning of innocuous stimuli ?
Light touch
What are the differences in pain experienced when inflammation sensitises the sensory system?
Innocuous pain becomes elicit pain
Response to noxious stimuli is enhances and prolonged
Threshold has lowered
What consequences can hypersensitivity have on neuronal damage ?
- Mechanical trauma
- Metabolic disease such as diabetes
- Neurotoxic chemicals (chemotherapy)
- Inflection
- Tumour invasion
- Spinal cord injury
- Stroke
Nerve damage can carry painful message without any noxious stimuli
What is the definition of allodynia ?
Pain in response to normally innocuous stimulus
what is the definition of hyperalgesia ?
Pain in response to a noxious stimulus with an exaggerated response
What is peripheral sensitisation?
- Nociceptor activation thresholds are lowered
- The nociceptor starts firing more and more and this is experienced as a pain
What is central sensitisation?
- Spinal cord (and brain) pain neurons are changed (anatomically, physiologically) so that they show increased responsivness to peripheral input
What happens when tissue damage and inflammation occurs ?
The chemical environment of nociceptor terminal changes
Many factors produced by numerous cell residing within or inflammatory into injured area
Generated an inflammatory soup
What neurotransmitters are in the ‘soup’?
Peptide:
Substance p
CGRP
bradykinin
Lipids: Prostaglandins Thromboxanes Leukatrienes Endocannabinoids
Neurothrophins Cytokines Chemokines Proteases Protons
How do these factors work ?
Factors bind to the receptor
Leads to depolarisation or alteration of the activation threshold.
This leads to increased nociceptor excitation
How does the binding of prostaglandins change nociceptor excitability ?
Prostaglandin E2 binds to PGE2 receptor
Activates Gs G-protein
Activates adenylyl cyclase which converts ATP into cyclic AMP
Cyclic AMP activates protein kinase A
This facilitates voltage gates sodium channels
Changes nociceptor excitability