Pain Pt1

• Pain definition:

  • unpleasant sensory or emotional experience associated with, or resembling that associated with, actual or potential tissue damage or described in terms of such damage
  • pain is always subjective
• Whats the point of pain:

  • early warning system
  • a learning tool
  • protection during recovery
  • all of the above in the context of survival
• The puzzle:

  • injury without pain
  • pain without injury
  • pain disproportionate to injury
  • pain without body parts
• Nociception:

  • there must be receptors sensitive to damage or threat in most structures of the body
  • these receptors are called nociceptors
  • present in skin, muscle, bone, ligaments, capsules, fascia, viscera, blood vessels, nerve sheaths
  • not found in hyaline cartilage, synovial membrane, brain, pericardium, lung parenchyma
• Characteristics of nociceptors:

  • Predominantly found as free nerve endings
  • Different classes of nociceptors are responsive to different types of noxious input
  • Other receptors respond to non noxious stimuli (eg light/ moderate touch/ pressure, mild heat/cold)
  • Nociceptors have the highest threshold for firing
• Cutaneous Receptors: A-Beta Mechanoreceptors:

  • Large diameter myelinated fibres
  • Have a low firing threshold
  • Sensitive to non-noxious mechanical/ thermal stimuli
  • Very Fast conductors
• Cutaneous Receptors: A-Delta Nociceptors:

  • Small Diameter thinly myelinated fibres
  • Have a high threshold for firing
  • Sensitive to noxious mechanical stimuli eg: sharp pricking stimuli
  • Relatively slow conductors
• Cutaneous Receptors: C fibres – Polymodal Nociceptors:

  • Small unmyelinated fibres
  • High threshold for firing
  • POLYmodal - responsive to many types of stimuli
  • Responsive to noxious heat, mechanical stimuli and irritant chemicals
  • Very Slow Conductors
  • There are SILENT nociceptors that may only become active in injured states
• Cutaneous sensory afferent fibres

  
• Muscle Nociceptors:

  • Group 3 Myelinated
  • Responsive to mechanical stimuli (mostly non-noxious)
  • Group 4 Unmyelinated
  • Responsive to mechanical, ischaemic, thermal and chemical stimuli
• Joint Nociceptors:

  • Found in capsule, ligaments, bone, blood vessels but NOT articular cartilage
  • A large number of afferent fibres are SILENT in normal joints
  • Normally joint afferents are only sensitive to high threshold mechanical stimuli
  • In inflammation joint afferents become sensitized
• Inflammation:

  • The “inflammatory soup” contains numerous chemicals
  • Many of these sensitize and activate nociceptors
  • C fibres are the main target for these chemicals as they are CHEMOSENSITIVE
• Hyperalgesia:

  • In the presence of inflammation free nerve endings become sensitized
  • This means that they have a lower threshold for firing
  • “Silent” nociceptors become sensitized and “speak up”
  • So we feel pain to things that were not previously painful and more pain to things that were
• Hyperalgesia - but why is the area of sensitivity BIGGER than the area of damage?

  • At the injured tissues there is an area sensitive to Thermal and mechanical stimuli (PRIMARY HYPERALGESIA)
  • A wider area of sensitivity is found surrounding the injury (only to mechanical stimuli) SECONDARY HYPERALGESIA
  • Primary hyperalgesia is due to peripheral nerve sensitization
  • Secondary hyperalgesia is due to sensitization in the CNS (Central Sensitization)
• The dorsal horn:

  • The Dorsal (posterior) horn of the spinal cord receives all sensory information from the periphery
  • It is the first site at which the CNS can process and integrate input from sensory nerves (like a switchboard!)
  • Sensory afferents synapse with neurones within the dorsal horn (DHC’s)
  • It is organised into layers called “laminae”
• Central Pain Processing: The Dorsal Horn

  • The CNS receives so much input it needs to prioritise
  • Processing filters out less important messages
  • The job of processing is to sort out the message from the noise
  • Nociceptive info has a tendency to be interpreted as IMPORTANT
• Interneurones:

  • Cells which extend from one cell to another are known as “interneurones”
  • Interneurones (excitatory and inhibitory) allow thousands of channels of communication between cells
  • This means activity in some cells can directly alter activity in other cells
  • It means that cells in different laminae can affect each other
• The pain gate:

  • Why does it help to rub it better?
  • Input competes for attention at the dorsal horn AND ABOVE
  • Nerves can have excitatory or inhibitory actions on their targets depending on the neurotransmitter they release
  • Interneurones mean that one type of input may suppress another
• The pain gate:

  • Think of the dorsal horn cell as a gate
  • When the gate opens the cell fires and we experience PAIN
  • When the gate is closed the cell is silent and we feel no pain
  • A delta and C fibre input will open the gate
  • A beta fibre input will close the gate
  • This model is grossly simplistic
• The Pain Gate:

  • Nociceptor input directly excites the Dorsal Horn Cell (DHC)
  • It also may activate excitatory interneurones which excite the DHC
  • A beta fibre input inhibits the DHC directly
  • It also excites inhibitory interneurones which also inhibit the DHC
  • A beta fibres are FASTER than nociceptors. They get there first
• Implications of the pain gate:

  • The amount of nociceptive information that reaches the brain can be amplified or suppressed by mechanisms remote from the damaged tissues
  • It gave us a first mechanism to explain pain variability and blew our understanding of pain wide open in the 1960s
  • It might represent a mechanism for the effect of some modalities such as manual therapies or TENS