Abstract
Nociceptive pain is a critical physiological defense response triggered by stimuli of sufficient intensity to potentially lead to tissue damage. Central sensitisation is a form of spinal plasticity that represents an additional level of protection for an injured organism. This phenomenon is triggered when the first line of defense to detect potential harmful stimuli has failed and damage has occurred. Once the nociceptive neurons of the spinal cord are in a state of central sensitisation, they no longer transmit an information that reflects with precision the nature and intensity of environmental stimuli. Instead they transform any stimuli they receive into alert signals and convey a message that is uncoupled with its environment. Central sensitisation is characterised by an increase in excitability and response to noxious stimuli of the spinal nociceptive neurons; the enlargement of their receptor field; and an ability to respond to innocuous stimuli. When there is a transient injury, this hyperexcitability represents an extremely efficient way to maintain a whole body area protected from any stimuli until its full recovery. When those changes are permanent, however, pain becomes maladaptive and pathological. Central sensitisation provides a mechanistic explanation for many of the symptoms observed in chronic clinical pain settings and explains how changes in the fine balance between the excitatory and inhibitory regulatory controls of spinal nociceptive neurons can lead to persistent pain states.
Original language | English (US) |
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Title of host publication | An Introduction to Pain and Nervous System Disorders |
Publisher | Wiley Blackwell |
Pages | 35-87 |
Number of pages | 53 |
ISBN (Electronic) | 9781118455968 |
ISBN (Print) | 9781118455913 |
DOIs | |
State | Published - Mar 5 2016 |
Externally published | Yes |
Keywords
- Central sensitisation
- Disinhibition
- Heterosynaptic
- Homosynaptic
- Inflammatory pain
- LTP
- Neuropathic pain
- Nociception
- Pain
- Synaptic plasticity
ASJC Scopus subject areas
- Neuroscience(all)