Explain the Gate control theory of Pain
Substantia gelatinosa is constantly inhibiting any pain neurons. C and A(delta) pain fibres work by inhibiting SG and transmitting pain to the thalamus
Why does rubbing the skin result in reduction in the pain response?
Rubbing the skin activates the A(beta) receptors which activates more inhibition via the substantia gelatinosa
What is hyperalgesia and how does it occur?
Hyperalgesia - increased pain at normal threshold stimulation.
Can occur due to persistent tissue or nerve damage which reslts in excess glutamate release, excess NMDA receptor activation and excess 2nd order firing. This results in long term changes in nociceptive neurones which become hyperexcitable.
Pain from a stimulus that isnt normall painful or which occurs in an area other than that stimulated
Allodynia =/= Referred pain
Define nociceptive pain.
Sharp stabbing pain
Activation of nociceptors stimulates the nociceptive signalling along the Aδ and C-fibres.
Define neuropathic pain
Pain of neuropathic origin. Does not involve stimulation of nociceptors to cause pain.
Burning, tingling, or shooting pain.
What are the 2 mechanisms which underlie the pathophysiology of neuropathic pain?
Ectopic activity - upregulation of Voltage gated Na channels occurs distal to damage, causing increased excitability of the nerve and ectopic APs to occur along pain fibre
Ephatic activity - ectopic beats cause AP sent to activate adjacent nerve fibres, causing receptor field expansion
Give examples of neuropathic pain
Phantom limb pain, complex regional pain syndrome
How do opioids act to treat chronic pain?
Act on opioid receptors. Close VOCC, open K+ channels to hyperpolarise membrane, inhibit cAMP formation - Overall inhibiting neurotransmitter release
What are the side effects of opioids?
Resp depression, N&V, constipation, antitussive
Which type of pain are opioids better suited to treating?
Bad at treated neuropathic pain
What adjuvant analgesics can be used?
NSAIDs, paracetemol, cannabinoids, ketamine, capsaicin, tricyclics, anticonvulsants
What are the effects of sensitisation of nerves to pain?
- Decreased threshold
- increased receptive field
- Prologned post stimulus sensations - hyperpathia
- Emergence of spontaneous activity
What physical changes allow the sensitisation of nerves to pain?
- Abnormal sodium channels - fire off dysfunctionally and have different depolarisation properties.
- Afferent nerves sprout from lamina 3 to lamina 1 and 2 which gain access to spinal regions involved in transmitting high intensity noxious signals.
What is type 1 and type 2 complex regional pain syndrome?
Type 1 - no identifiable lesion
Type 2 - Identifiable nerve lesion (causalgia - severe pain in limb caused by damage to peripheral nerve)
What factors can trigger Chronic Regional Pain Syndrome (CRPS)?
Trauma, bone fracture, surgery, stroke, MI
What are the symptoms of CRPS?
Sensory - severe continuous burning pain, hyperalgesia, allodynia
Vasomotor - Temp asymmetry, skin colour changes, skin colour asymmetry
Motor - decreased ranbge of motion, motor dysfunction (ie weakness, tremor, dystonia), changes in hair, nail or skin.
What is the Mechanism of CRPS?
- Injury to limb
- Injury initiates a pain response to the CNS
- Pain impulse triggers activation of SNS to the injury
- SNS triggers inflammation causing vessels to swell an dincreased pain
- Pain triggers another response, establishing a cycle of pain and swelling
Describe stage 1 of CRPS?
- Pain in limb following or w/o a cause
- oedema, throbbing pain, sensitivity
- Altered colour and temp,
- X-rays may show patchy demineralisation of involved bones
Describe stage II of CRPS
- Soft tissue oedema
- thickening of skin and articular soft tissues
- Muscle wasting
- Skin, nail, bone, and muscle changes
Describe stage III of CRPS