Pain Flashcards
What is the difference between pain and nociception
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.
What are the three main types of pain
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
Two types of pain processing
Central and peripheral. These can often overlap. Nociceptive seen as peripheral while the other pain types seen as central.
What causes peripheral sensation
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.
What are the effects of peripheral sensation
Decreases in threshold of nociceptor fibre activation, increases in responsive at end of nerve fibres and the activation of silent nociceptors.
Two different peripheral nociceptive fibres
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.
What is hyperalgesia
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
Allodynia
Pain due to a stimulus that would normally not produce a painful response.
Clinical features of referred pain
Deep and aching. Margins hard to define. Lacks cutaneous quality and rarely refers distal to elbow or knee.
Clinical features of radicular pain
Sharp shooting pain in a relatively narrow band (dermatome)
What causes nociceptive pain with minimal inflammation
Ischemia is when fluid moves out of tissues. With little movement this can occur and pH will change causing a nociceptive response.
Why are ion channels replaced on axons and where are they created
Created in the DRG and are replaced to ensure afferent nerve maintains sensitivity.
What is an AIGS
This is when the axon its self becomes an impulse generating site and does not just transmit.
Causes of central pain (pain persistence)
- Ongoing or recurrent tissue damage (acute injury)
- Chronic inflammation
- Peripheral sensitisation
- Central sensation (changes in spinal cord and brain, nociplastic pain)
- Red flags (cancer)
Central sensitisation vs peripheral sensitisation
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.
Changes in spinal cord for central pain
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.
Secondary hyperalgesia
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.
Changes in the dorsal horn with central pain
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
Changes in the brain with central pain
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.
Clinical features of central pain
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.
Acute nociception
Noted as normal pain, in response to injury and associated with tissue healing. 0-12 weeks. Primary hyperalgesia
Peripheral neurogenic pain
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)
