Pain

Question 1

What is the difference between pain and nociception

Answer 1

Pain is an unpleasant sensory motor experiences associated with actual or potential tissue damage. Nociception is the neural process of encoding noxious stimuli. Meaning that nociception may not always result in pain.

Question 2

What are the three main types of pain

Answer 2

Nociceptive - pain that arises from actual or threatened dmaage to non neural tissue (activation of nociceptors)
Neuropathic - lesion or disease of the somatosensory nervous system (normally chronic)
Nociplastic - altered nociception despite no clear evidence of actual or threatened tissue damage causing activation of nociceptors

Question 3

Two types of pain processing

Answer 3

Central and peripheral. These can often overlap. Nociceptive seen as peripheral while the other pain types seen as central.

Question 4

What causes peripheral sensation

Answer 4

Damage to tissue causes inflation resulting in an influx of inflammatory cells. Histamine is released and blood vessel release plasma causing oedema and nerves also release inflammatory chemicals. Meaning the tissue environment around the nerve becomes very acidic and thus increasing its sensitivity.

Question 5

What are the effects of peripheral sensation

Answer 5

Decreases in threshold of nociceptor fibre activation, increases in responsive at end of nerve fibres and the activation of silent nociceptors.

Question 6

Two different peripheral nociceptive fibres

Answer 6

A delta fibres - larger diameter and myelinated (fast response time, received first). Only have a small receptive field meaning they’re quite precise making them more situated to localised/sharp pain. Mechanical or thermal stimuli
C fibres - small diameter and unmyelinated (secondary perception of input). Larger receptive field meaning it is often dull or burning pain. May only be silent nociceptors (need peripheral sensitisation). Mechanical, thermal or chemical.

Question 7

What is hyperalgesia

Answer 7

Increases in pain from a stimulus that would normally evoke pain. Primary hyperalgesia occurs at the site of an injury due to sensitisation from inflammation

Question 8

Allodynia

Answer 8

Pain due to a stimulus that would normally not produce a painful response.

Question 9

Clinical features of referred pain

Answer 9

Deep and aching. Margins hard to define. Lacks cutaneous quality and rarely refers distal to elbow or knee.

Question 10

Clinical features of radicular pain

Answer 10

Sharp shooting pain in a relatively narrow band (dermatome)

Question 11

What causes nociceptive pain with minimal inflammation

Answer 11

Ischemia is when fluid moves out of tissues. With little movement this can occur and pH will change causing a nociceptive response.

Question 12

Why are ion channels replaced on axons and where are they created

Answer 12

Created in the DRG and are replaced to ensure afferent nerve maintains sensitivity.

Question 13

What is an AIGS

Answer 13

This is when the axon its self becomes an impulse generating site and does not just transmit.

Question 14

Causes of central pain (pain persistence)

Answer 14

• Ongoing or recurrent tissue damage (acute injury)
• Chronic inflammation
• Peripheral sensitisation
• Central sensation (changes in spinal cord and brain, nociplastic pain)
• Red flags (cancer)

Question 15

Central sensitisation vs peripheral sensitisation

Answer 15

peripheral - increased responsiveness and reduced threshold of responsiveness in periphery

central - increased responsiveness of nociceptive neurons in CNS. Can occur due to increased responsiveness due to dysfunction of endogenous pain control systems or peripheral structures are functionally normally and changes in functions are present in central neurons.

Question 16

Changes in spinal cord for central pain

Answer 16

Normal state - Substance P and glutamate are released from C fiber which then activate specific receptors. Small inhibitory neuron input meaning C fiber input = WDR output

Suppressed state - both inhibitory neuron and inhibitory interneuron release neurotransmitters. These can act presynaptically on the C fiber meaning less glutamate and substance P are released. Can also act on WDR meaning there is less activity in WDR.

Excited state - Barrage of C fiber input leads to more excitable neurotransmitters released. Pre and post NDMA receptors are activated which causses increased calcium in WDR resulting in phosphorylation. Meaning the NMDA channel stays open for longer allowing for WR neuron to be depolarised more easily.

Opening of dormant receptors

Pain system has lower activation threshold, input from low threshold afferents can evoke pain.

Question 17

Secondary hyperalgesia

Answer 17

Secondary hyperalgesia is a feature of central sensitisation and develops in uninjured tissues surrounding the injury site. Caused by enhanced responsiveness in CNS and sites may be quite far apart. Signals from non-nociceptive afferents give rise to pain.

Question 18

Changes in the dorsal horn with central pain

Answer 18

Rerouting - C fibres (light touch and vibration) go away from lamina 2 allowing beta to sprout into gaps left behind, majority of WDR also arise here which is why nonnoxious stimuli is perceived as painful.

Death of interneurons in dorsal horn due to high concentration of excitatory neurotransmitters, means need to rely more on descending input from brain

Question 19

Changes in the brain with central pain

Answer 19

Most important is the changes in receptive field in cortex referred to as cortical smudging, brain areas specific to sensory areas begin to overlap and long the pain persists the worse the change becomes.

Cell death due to neurotransmitter, upregulation of receptors, altered levels of neurotransmitters, immune responses.

Question 20

Clinical features of central pain

Answer 20

Pain may not have anatomical boundary, any original pain may have spread (secondary hyperalgesia), sudden stabs of pain, pain with all movements, may be linked to traumatic event (cyclical), unpredictable or inconsistent, pain when they think about it.

Question 21

Acute nociception

Answer 21

Noted as normal pain, in response to injury and associated with tissue healing. 0-12 weeks. Primary hyperalgesia

Question 22

Peripheral neurogenic pain

Answer 22

May be hyperactive (pain, burning, feelings of cold, crawling, tightness, prickling) or hypoactive (muscle or sensory loss). May have night pain. Symptoms arise along a neural zone (dermatome) or along nerve trunk and are well localised. Pain evoked by movement of nerve or surrounding issues (often have antalgic postures to deal with this)