What is the definition of pain?

Pain is defined by the International Association for the Study of Pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.’

How does pain differ from nociception?

Nociception is the process by which noxious signals are encoded as action potentials and transmitted from the periphery to the central nervous system (CNS). Pain results from the brain’s interpretation of these nociceptive signals, resulting in the perception of an unpleasant sensory and emotional experience.

How is pain classified?

Traditionally, pain has been classified as either acute or chronic based on a duration of <12 weeks or >12 weeks, respectively. This arbitrary distinction has been replaced, and chronic pain is now defined as pain that extends beyond the expected period of healing following tissue injury.

Pain may be arbitrarily classified as nociceptive (caused by stimulation of nociceptors) or neuropathic (caused by damage to the neurons themselves). Nociceptive pain may be classified as:

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  Superficial or cutaneous pain due to skin damage and characterised by sharp, well-localised pain.

  
  
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  Deep pain, a dull, aching and poorly localised pain arising from structures such as muscles, tendons and ligaments.

  
  
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  Visceral pain, a dull, diffuse and poorly localised pain arising from the viscera; for example, spasm or overdistension of a hollow viscus.

What is a nociceptor?

A nociceptor is a free, unmyelinated nerve ending capable of generating action potentials in response to a variety of stimuli that are generated by cellular damage. For example:

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  K⁺ is released from damaged cells.

  
  
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  Histamine is released from mast cells near to the site of tissue damage.

  
  
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  Bradykinin is increased at the site of injury as a result of inflammation.

  
  
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  Leukotrienes and prostaglandins are synthesised in response to cellular damage as part of the inflammatory process.

  
  
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  Serotonin is released by platelets in response to vascular injury.

What nerve fibre types carry pain sensation?

There are two types of nociceptor fibre, classified by fibre structure (see Chapter 52):

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  Type Αδ fibres carry impulses produced in response to mechanical and thermal stimuli. These neurons have myelinated axons of large diameter and have a relatively high conduction velocity of around 20 m/s. As a consequence of the higher conduction velocity, nociceptive impulses carried by type Αδ fibres produce the first sensation of pain, often perceived as being sharp and well localised in character.

  
  
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  Type C fibres carry impulses produced in response to thermal, mechanical and chemical stimuli. These neurons have unmyelinated axons of small diameter, which results in a relatively low action potential conduction velocity (0.5–4.0 m/s). Firing of their associated nociceptors produces a sensation of dull, poorly localised pain that often follows the early sharp pain mediated by Αδ fibres.

What are the pathways by which pain signals are relayed to the brain?

As discussed in Chapter 50, the afferent neurons that relay nociceptive impulses from the peripheries travel in the spinothalamic tract:

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  A first-order neuron (C or Αδ fibre) relays action potentials from a nociceptor to the substantia gelatinosa (Rexed lamina II) or nucleus proprius (Rexed laminae III, IV and V) in the dorsal horn of the spinal cord. Here, the first-order neuron synapses with a second-order interneuron, with substance P as the neurotransmitter.

  
  
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  The second-order interneuron decussates in the anterior commissure, before ascending the length of the spinal cord in the spinothalamic tract. The second-order neuron synapses with a third-order neuron in the thalamus.

  
  
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  The third-order neuron relays nociceptive action potentials to the somatosensory cortex.

Sensation from the face is relayed to the brain through the trigeminal pathway:

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  A first-order neuron (C or Αδ fibre) relays action potentials from the face to the trigeminal nucleus. Most of this sensory information is relayed to the brain through the trigeminal nerve, but a small number of sensory afferent neurons from the oropharynx and ear travel in the facial, glossopharyngeal and vagus nerves. Irrespective of the cranial nerve, all sensory afferent fibres synapse with second-order neurons in the trigeminal nucleus, the equivalent of the dorsal horn of the spinal cord. Again, substance P is thought to be the neurotransmitter at this synapse.

  
  
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  The trigeminal nucleus (also known as the Gasserian ganglion) is large, extending from the medulla to the midbrain. Three parts of the trigeminal nucleus receive different sensory modalities:

  
  
  
  
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     – The spinal trigeminal nucleus receives pain and temperature information.

     
     
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     – The main trigeminal nucleus receives touch and proprioception information from the face and mouth.

     
     
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     – The mesencephalic trigeminal nucleus receives proprioceptive information from the jaw.

  
  
  
  
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  Like the spinothalamic pathway, the second-order neurons immediately decussate and ascend through the brainstem to the thalamus, where they synapse with third-order neurons.

  
  
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  The third-order neurons relay action potentials to the somatosensory cortex.