Neuropathic pain

Neuropathic pain is not pain that originates as part of ‘normal’ pain pathways. It has been described as pain related to abnormal processing within the nervous system (Mann [134]). Nerve injury or dysfunction can be caused by a range of conditions such as infection, trauma, metabolic disorder, chemotherapy, surgery, radiation, neurotoxins, nerve compression, joint degeneration, tumour infiltration and malnutrition (Mann [134]).
The following are currently thought to contribute to the mechanisms by which neuropathic pain is generated and maintained (Baron et al. [9], Mann [134], Nickel et al. [157]).
  • Damage or abnormalities in the nerves change the way in which nerves communicate with each other.
  • Pain receptors require less stimulation to initiate pain signals both in peripheral nerves and the central nervous system, where it is often referred to as central sensitization.
  • Pain transmission is altered from its normal sequence.
  • There may be an increase in the release of chemical neurotransmitters.
  • There can be increased and chaotic firing of nerves.
  • Damaged nerves spontaneously generate impulses in the absence of any stimulation.
  • The descending inhibitory systems may also be reduced or lost.
The nervous system changes its structure and function in response to the input it receives throughout an individual's life course and this is termed neuroplasticity, also known as brain plasticity or neural plasticity. Neuroplasticity is evident at all levels from the nociceptor to the brain (cortex). Individuals who suffer from persistent pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. These mechanisms result in increased activity or transmission of pain signals despite less input from the peripheral nervous system, and even become responsive to innocuous stimuli. Pain can be spontaneous, may be triggered by non‐painful stimuli such as touch (allodynia) or may be an exaggerated pain response (hyperalgesia); patients may also experience non‐painful sensations such as pins and needles and tingling (paraesthesias).