Chronic Pain and Central Sensitisation: When the Volume Won’t Turn Down
Acute pain is one of evolution’s most important inventions. It is a warning system — tissue is damaged, stop using it, protect it, let it heal. Short-term, specific, and purposeful. Chronic pain — pain persisting beyond three months, often long after tissue healing is complete — is a different phenomenon entirely. It is not a louder version of acute pain. It is the nervous system stuck in a different mode.
Understanding this distinction changes everything about how chronic pain can be helped.
What Central Sensitisation Is
In response to sustained pain signalling (from injury, surgery, infection, or chronic stress), the central nervous system can undergo neuroplastic changes that lower its pain threshold. Normally, a certain level of input is required to cross the threshold and register as pain. In a sensitised system, that threshold drops: minor stimuli that previously wouldn’t register as painful now do. Touch, temperature, movement, even sound or light can become painful.
This is central sensitisation. It is not imagined pain. It is real pain generated by a nervous system that has been recalibrated at a more reactive set point. The original injury or stimulus may be long resolved. The amplified signalling persists because the nervous system has learned a new pattern.
Conditions characterised by central sensitisation include: fibromyalgia, chronic low back pain, chronic headache/migraine, temporomandibular pain, irritable bowel syndrome, and complex regional pain syndrome.
The Evolutionary Context: Why Does This Happen?
Central sensitisation evolved as a protective mechanism. After a severe injury or threat, heightened pain sensitivity made sense — protect the area until full recovery. The problem is that the “off switch” requires sufficient safety signals. Pain resolves when the nervous system is convinced that the threat has passed.
In chronic pain states, several factors prevent this: ongoing psychological stress keeps the threat system activated; sleep deprivation amplifies pain processing; social isolation removes co-regulatory nervous system input; fear-avoidance keeps the nervous system in threat mode; and often, the original structural contributors have never been fully addressed.
Osteopathy and the Sensitised Nervous System
The osteopathic approach to chronic pain works on multiple levels simultaneously.
Structural: Addressing residual restriction, tension, or asymmetry that maintains nociceptive input to the spinal cord, even at low levels that a non-sensitised system would ignore.
Neurological: Hands-on treatment activates mechanoreceptors that compete with and inhibit pain signals at spinal cord level (gate control theory). Safe, therapeutic touch is a direct input of “no threat here” to the nervous system.
Autonomic: Normalising autonomic balance — reducing sympathetic overdrive, supporting vagal tone — shifts the nervous system toward the state in which pain down-regulation is possible.
FAQ
Does chronic pain mean my body is still damaged?
Not necessarily. Pain is produced by the brain as a protective response — it does not require ongoing tissue damage. In central sensitisation, the nervous system generates pain from sensitised circuits, not active injury. This means the treatment target is the nervous system, not damaged tissue.
Why does stress make chronic pain worse?
Stress activates the sympathetic nervous system and elevates cortisol, both of which lower the pain threshold and amplify central sensitisation. Pain and stress are physiologically bidirectional — each worsens the other.
Can osteopathy help with fibromyalgia?
Yes. Osteopathic treatment addresses the musculoskeletal tension, autonomic dysregulation, and sleep disruption that characterise fibromyalgia. It doesn’t cure the condition, but many patients experience significant pain reduction and improved function.
Chronic pain that hasn’t responded to treatment? There may be neurological dimensions that haven’t been addressed yet. Book →