Chronic pain perception: understanding the neurology
Central sensitisation of pain: the mechanisms
According to the International Association for the Study of Pain (IASP), central sensitisation is an increase in the reactivity of nociceptive neurons of the central nervous system to normal or sub-threshold afferent inputs. This amplification of pain, responsible for chronic pain, is particularly problematic because it contributes to a state of suffering and disability in patients, affecting their quality of life and generating major economic and social costs. Recognised as a disease by the World Health Organization (WHO), chronic pain is one of the most widespread disorders, creating complex diagnostic and therapeutic challenges.
The mechanisms of central sensitisation
Acute pain has a protective function: it helps to detect and avoid harmful stimuli and to promote the healing of damaged tissues. However, the transition to a chronic state modifies the adaptive nature of pain and can lead to central sensitisation. Several mechanisms participate in this sensitisation:
- Increased neuronal excitability: Neurons of the CNS (spinal cord and brain) become hypersensitive, requiring fewer stimuli to be activated. This hyperreactivity, often persistent, explains why some patients experience disproportionate pain, even after an initial lesion has healed.
- Synaptic plasticity and neuronal reorganisation: Central sensitisation leads to lasting modifications in pain circuits, thereby increasing the "memory of pain" in the CNS. This plasticity can render the nervous system hypersensitive, triggering painful responses even in the absence of harmful stimulation.
- Modification of receptor expression: Pain receptors, notably NMDA receptors, increase in number and sensitivity, which worsens the perception of pain.
- Reduced inhibition of pain pathways: Normally, inhibitory mechanisms in the CNS moderate pain signals. In central sensitisation, this inhibition is impaired, allowing more intense and persistent pain signals to traverse the CNS.
Allodynia and hyperalgesia
Central sensitisation will lead to an exaggeration of the painful sensation, described in two forms: allodynia and hyperalgesia.
Allodynia is a type of pain where a stimulus that would not normally be painful becomes painful. For example, a simple brush of the skin, a light contact with clothing or even a breeze on the skin can provoke pain in some people with allodynia. This can be particularly disabling, as the pain occurs without apparent reason or following benign stimulation, making everyday gestures difficult. Allodynia is often associated with conditions such as fibromyalgia, neuropathies, or certain forms of migraine. It frequently manifests in areas where the pain threshold is lowered.
Hyperalgesia, for its part, is an increase in sensitivity to pain provoked by normally painful stimuli. In people suffering from hyperalgesia, the painful response is exaggerated. For example, light pressure that would provoke moderate pain becomes intensely painful. Unlike allodynia, where non-painful stimuli are perceived as painful, hyperalgesia intensifies the pain felt in response to stimuli that are, at baseline, painful.
Nociplastic pain
Central sensitisation has led to a rethinking of pain treatment and to the introduction of a new category of pain: nociplastic pain. This term, established by the International Association for the Study of Pain (IASP), complements the classification of pain by adding to the existing categories — nociceptive pain (injury from excess nociception) and neuropathic pain (lesion of the nervous system). Nociplastic pain is defined by increased sensitisation in the CNS and plays an essential role in conditions such as fibromyalgia, functional colopathy and chronic low back pain.
Conclusion
Central sensitisation represents a key domain in the understanding of chronic pain. It helps to explain pain that is not directly associated with peripheral lesions, and orients towards combined therapeutic approaches, including interventions centred on the CNS and the treatment of peripheral factors. This understanding is essential in order to offer care adapted to patient profiles, particularly in the context of precision medicine.
Frequently asked questions (FAQ)
What is central sensitisation in chronic pain?
Central sensitisation is a neurobiological phenomenon in which the central nervous system becomes hypersensitive after prolonged exposure to painful stimuli. It amplifies pain signals, even in the absence of tissue damage, explaining the persistence of chronic pain.
How does osteopathy act on central sensitisation?
Osteopathy modulates the nervous system via descending inhibitory mechanisms (endorphins, serotonin), reduces peripheral nociceptive inputs and improves proprioception. These effects contribute to normalising central pain circuits.
Can the perception of pain be modified by treatment?
Yes, neuroplasticity allows the brain to restructure its pain circuits. Therapeutic education, osteopathy, physical exercise and cognitive-behavioural therapies produce lasting changes in the perception of chronic pain.
Why do some people have a higher pain tolerance?
Pain tolerance depends on genetic, psychological (anxiety, catastrophising), contextual factors and the person's history with pain. These factors modify the activity of the descending inhibitory systems that regulate pain perception.