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Pain is an extremely common symptom in patients with palliative illnesses. Patients and their families particularly associate advanced cancer with severe pain and fears about this can cause significant anxiety. Although opioids remain the a hugely important part of pain control, there are many other alternative pharmacological and non-pharmacological treatments that can play a role in minimizing pain and it is therefore extremely helpful if the pathology causing a pain can be identified and understood as this often helps determine what management is most useful.0

Definitions, Aetiology and Pathophysiology

the International Association for the Study of Pain defines pain as an "unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage."[1]

Pain is complex and not well understood. Perception of pain is influenced by the underlying pathology but also by individual patient factors such as psychological and spiritual concerns and the wider cultural context.

Pain pathways

The mechanism of pain is complicated and can be understood by thinking about the initial distal tissue insult and working proximally back to the pain centres in the brain. Damage to tissue results in a release of various mediators such as histamine, leukotrienes, prostaglandins substance P and TNF. These substances stimulate nociceptors. Various analgesic agents at at this level, including NSAIDs (which inhibit cyclo-oxygenase, an enzyme involved in production of prostaglandins.

Pain pathway mediawiki.jpg

  • Figure above - A diagram showing the stimulation of a nociceptor and following up the first order-nerve pathway into the dorsal horn.

Once activated the pain signal is transmitted along the "first-order" afferent nerve to the dorsal horn of the spinal cord where the neuron synapses with a "second-order" neurons that cross the midline and travel up the spinothalamic tract, as shown in the diagram below. There are additional modulating pathways involved as well. Various neurotransmitters and channels are involved including noradrenaline, GABA, NMDA, endogenous opioids and serotonin. Many analgesic agents are involved in modulating parts of this pathway, such as opioids, tricyclic antidepressants and gabapentinoids.

Ascending Pathways of Spinal Cord MediaWiki.jpg

  • Figure above - The ascending pathways of nerves as they enter the spinal cord and travel to the brain. The classical pain fibres cross the midline at entry of the spinal cord and ascend with temperature fibres in the lateral spinothalamic tract.

Neuropathic pain and nociceptive pain

Pain can be divided based on the pathophysiology into two major categories that tend to have different subjective qualities. The two categories are:

Nociceptive pain is pain that occurs when nerve endings are stimulated by noxious stimuli such as inflammatory mediators. When afferent somatic nerves are stimulated the pain is often sharp and localized. When visceral nerves are stimulated the pain tends to be dull and crampy and poorly localized.

Neuropathic pain is pain that occurs when nerves have been directly damaged, for example, by cancer invading into the nerve itself. Neuropathic pain often causes pain that feels burning or electric shock like, and sometimes pain that is described as numb or pins and needles. Allodynia, or pain on light touch, is sometimes a feature too.

Background pain, breakthrough pain and Incident pain

Pain varies in intensity over time. The term background pain is used to describe a baseline pain level that persists over hours and throughout the day and/or night. When the pain flares up, the term breakthrough pain is used. Incident pain is pain that predictably occurs by movement, weight bearing or activity.

Assessing pain - history, examination and investigations

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Pain management

Non-pharmacological measures

Simple analgesia


Adjuvant Agents

Interventional and procedural pain management

Anti-Cancer therapies


  1. Merskey H and Bogduk N. Classification of chronic pain. @nd edition. Seattle: IASP Press; 1994; 209-214.M


Graham Llewellyn Grove