Central sensitization: implications for the diagnosis and treatment of pain
Synopsis
What has central sensitization taught us about the nature and mechanisms of pain in patients, and what are the implications of central sensitization for pain diagnosis and therapy? Before doing this though, it is important first to understand exactly what central sensitization represents, how it has changed our general understanding of pain mechanisms, as well as reviewing the substantial data on central sensitization derived from studies on experimental pain in human volunteers. (from Woolf, 2011)
Key Points
A couple of questions to keep in mind:
1. What is central sensitisation?
2. Is central sensitisation present in people with pain?
First of all, what is central sensitisation?
– prolonged but reversible
– increase in the excitability and synaptic efficacy
– of neurons in the central nociceptive pathways
– which manifests as pain hypersensitivity
How is it induced?
– volunteers are subjected to various experimental noxious conditioning stimuli – applied to skin, muscles and viscera
What happens to these volunteers?
– they’re tested with various sensory stimuli before and after the conditioning stimuli
– if central sensitisation is present they manifest with pain hypersensitivity
What is pain hypersensitivity?
– pain on normally non-painful stimuli (allodynia)
– increased pain on normally painful stimuli but outside of the area of damage (secondary hyperalgesia – receptive field expansion)
– pain that continues after the stimulus (aftersensations)
– when a painful stimuli is repeated it gets more painful (enhanced temporal sensation)
What did this do to our understanding of pain?
“Pain we experience might not necessarily reflect the presence of a peripheral noxious stimulus.”“Central sensitisation represents an uncoupling of the clear stimulus response relationship that defines nociceptive pain.”“..noxious stimulus while sufficient was not necessary to produce pain.”
So, central sensitisation can be robustly and readily produced in volunteers in response to noxious stimuli.
Is the hypersensitivity that is seen in many pain states attributable to central sensitisation?
To answer these questions we need to know what measures accurately demonstrate the presence of central sensitisation. In the laboratory researchers commonly used the nociceptive withdrawal reflex and imaging as objective markers.
However, it is unlikely that clinicians will be able to use these.
Are there specific subjective measures that suggest the presence of central sensitisation? Does the spreading of symptoms or elicitation of pain on normally non-painful stimuli suggest central sensitisation is present? Some interesting questions to have in mind whilst reading through this interesting review.
Enjoy!