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Pathophysiology of chronic pain

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Andrew Muirhead-Smith

on 21 November 2012

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Transcript of Pathophysiology of chronic pain

Ouch! Pathophysiology of
Chronic Pain Chronic Pain Normal pain pathway DEFINITION

'Chronic pain is continuous, long-term pain of more than 12 weeks or after the time that healing would have been thought to have occurred in pain after trauma or surgery.'

- British Pain Society What is pain? Interpretation of nociception in context of personality, circumstance, emotional state, etc

Caused by a noxious stimuli - heat, pressure, inflammation, etc

3 main types
- Nociceptive
- Neuropathic
- Inflammatory HIGH THRESHOLD
Thinly myelinated Ad fibres - 'fast pain'
Unmyelinated C fibres - 'slow pain'

Myelinated Ab fibres - light touch, vibration, pressure

High threshold fibres have 'free' nerve endings

These respond to substances released by damaged tissues e.g. peptides, prostaglandins, histamine, etc

Synapse in Dorsal Horn of spinal cord

Lamina I-II and V Wind-up Central sensitization Defined as an increased central reponse to a normal peripheral stimulus

Mediated by amplification of CNS signalling in response to nociceptive or other stimulus

> Described by Clifford Woolf in 1983

Leads to changes in synaptic connections and reduction of inhibitory neurons and transmitters

Both spinal and cerebral Central sensitization Two main phases:

1. CNS terminals of nociceptors release signal molecules inc. glutamate, substance P and BDNF
- these act on spinal neuron receptors eg NMDA/AMPA
- receptors are phosphorylated
- these lower channel opening threshold and therefore increase excitability
- this results in more action potentials in dorsal horn Central sensitization Two main phases:

2. 'Transcription dependent' phase
- increased levels of protein production
- proteins increase neuronal excitability
- upregulated proteins include Dynorphin and Cox-2
- minimal stimulus is therefore needed to activate neurons Repetitive or prolonged stimulation of C fibres leads to increased discharge of dorsal horn cells

> Increased perception of pain despite reduced APs in C fibres

Progressive increase in number of action potentials elicited per stimulus occurring in the dorsal horn

Can precipitate long-term potentiation (LTP)
- long-lasting increase in efficacy of synaptic transmission

LTP thought to last at least 1 hr to months NMDA receptor Critical in 'synaptic plasticity'

NMDA activation results in opening of ion channels
- Na + Ca flow into cell, K flows out

This triggers a 'cascade of events' leading to sensitisation of dorsal horn WDR neurones
> ie increasing excitability of neurons

Increases spinal phospholipase and NO synthetase
- these stimulate further release of excitatory AAs from primary afferent pain fibres Chronic pain models Peripheral sensitisation

Central sensitisation

NMDA receptors

Wind-up Conclusion Multiple modalities of pain sensitisation

> Central and peripheral sensitisation

> Wind-up

Multi factorial

social, emotional factors important Peripheral sensitization changes in peripheral ends of nociceptors
> reduction in threshold
> increase in responsiveness

Occurs at site of tissue damage or injury

Due to inflammatory markers
> some act directly
> can activate cells such as neutrophils >> COX2 >> PGE2 >> sensitising nerve ending

Can be a normal response, eg sunburn
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