Pain Pt2

• Nerve Injury/ Compromise (peripheral neuropathic pain):

  • The nerve is the pathway for transmitting sensory information
  • Injury to the nerve can results in changes in structure and function which can cause pain
  • These changes can be long lasting and severe
• • The nerve connective tissue (epineurium) is itself innervated by nociceptors (the nervi nervorum)
  • So stress, strain or inflammation can cause nociceptive information to be generated and sent to the CNS, just like any other tissue
  • This pain is nerve related but not neuropathic as it does not reflect abnormal nerve function.

  
• Effect of mechanical stress on neural tissue:

  • Impaired blood flow – neural ischaemia
  • Impaired axoplasmic transport
  • Intraneural Oedema
  • Local demyelination
  • Neuroma formation
  • Hypersensitivity
  • Sympathetic changes
• Abnormal Impulse Generating Sites:

  • Possible local demyelination
  • Loss of myelin allows ion channels to present at the site
  • Ion channels allow depolarisation
  • Increased adrenoceptor channels keep membrane potential closer to activation and create a pathway for emotion/stress effect
• Gives rise to:

  • HYPERACTIVITY:
  • Nerve can become a pain generator
  • Neuroma formation - Ectopic Firing
  • Spontaneous activity and mechanosensitivity
  • Abnormal impulse generating sites (AIGS)
  • HYPOACTIVITY:
  • Blocked conduction - sensory/motor loss
• Abnormal Impulse Generating Sites:

  • Mechanosensitive
  • Thermosensitive
  • Chemosensitive
  • Adreno-sensitive
  • Often spontaneously active – ectopic firing
• Description and Behaviour: Peripheral Neuropathic Pain:

  • Burning
  • Pins & Needles
  • Numbness
  • Nocturnal pain
  • Dysaesthesia (‘crawling’)
  • Often affected by stress/emotional factors
  • Poor stimulus-response relationship
• Descending inhibition:

  • Nociceptive input isn’t just modulated by peripheral afferent input
  • The brain possesses endogenous mechanisms to modulate inputs
  • Electrical stimulation of various areas of the brain (eg the periaqueductal grey matter) causes analgesia
  • This mechanism is mediated by endogenous opioid (endorphin, enkephalin), serotonergic and noradrenergic pathways
• Placebo:

  • “A medicine having no therapeutic action” (Oxford Concise English Dictionary)
  • Perhaps “no specific active ingredient” would be a better definition
  • Placebo analgesia (the placebo effect) occurs in everyone
  • Expectation of pain relief leads to pain relief
• Implications for Physio

  • As well as the peripheral pain gate mechanism this is a possible mechanism by which manual therapy or movement might decrease pain
  • The positive emotional effects of treatment and reassurance may also stimulate inhibition from higher centres
  • But of course there are ethical aspects to the delivery of placebo in the clinic!
• Descending Pain Facilitation:

  • Higher Centres do not just suppress the pain experience – they may increase it
  • Stimulation of some brain areas causes excessive responses to nociceptive stimuli
  • This means that the CNS may not just filter nociceptive messages, it can also act as an AMPLIFIER
  • It is potentially possible for the CNS to generate pain without peripheral nociceptive input - WITHOUT INJURY or AFTER HEALING HAS OCCURRED
• Central Processing of Pain:

  • The dorsal horn is just the first site for processing
  • Conscious experience of pain is, in part, likely generated in a complex matrix of higher centres
  • Don’t underestimate this - no brain = no pain
• Nociception is not pain:

  • Nociceptive input does not necessarily mean pain will result
  • Pain is an experience generated by the brain after appraisal of a multitude of factors
  • It has been argued that pain is the result of the brains appraisal of threat, not actual threat: This is largely not a conscious process
  • But tissues, nerves and brains do not feel pain. PEOPLE feel pain.
• Is what goes in the same as what gets felt?

  • The experience of pain is incredibly variable
  • It changes between individuals, environment, context, cultures, gender, and past experience/beliefs
  • This isn’t just “all in the head” (i.e. psychological) it is fundamental to the experience
• Affective/Cognitive influences:

  • Injury/disease are potent stressors
  • Previous experience influences our reactions
  • Higher brain centres can facilitate or suppress the pain experience
  • Emotion and physiology are inseparable
• Psychological Factors:

  • People with persistent pain have been shown to more frequently demonstrate:
  • Anxiety/distress/depression
  • Catastrophising
  • External locus of control
  • These may be predictive of prognosis (more than measures of tissue damage or pathology)
• Nociplastic pain:

  • pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain
  • aka unexplained pain