chronic pain
Pain is not just a signal from injured tissue. It is a subjective sensory and emotional experience produced by the brain, influenced by biological, psychological, and environmental factors. Two people can have the same injury but very different pain experiences because pain is shaped by factors such as beliefs, fear, stress, mood, sleep, previous experiences, and the nervous system’s sensitivity.
Types of pain
Acute pain
Acute pain is short-term pain after injury, surgery, trauma, or illness. It acts as a warning signal to protect the body and prompt help-seeking.
Subacute pain
Subacute pain is the transition phase between acute and chronic pain. This is an important window where appropriate management may reduce the risk of chronic pain developing.
Recurrent pain
Recurrent pain occurs in cycles, such as migraine or pelvic pain.
Chronic pain
Chronic pain persists beyond the expected time for healing. It may continue even after the original injury has healed, and sometimes there is no clear ongoing tissue damage. Chronic pain can become a condition or disease in its own right, because the nervous system itself becomes sensitised.
Nociceptive pain — “tissue warning pain”
Nociceptive pain starts when specialised nerve endings called nociceptors detect actual or potential tissue damage.
The pathway is:
- Tissue injury or threat activates nociceptors.
- Pain signals travel through peripheral nerves.
- Signals enter the spinal cord through the dorsal root.
- They synapse in the dorsal horn.
- Signals travel upward to brain regions including the thalamus, hypothalamus, reticular system, and cortex.
- The brain interprets the signal as pain.
The page 1 diagram shows this pathway from nociceptors in muscle, through the spinal cord, and up to brain regions involved in pain perception, emotion, sleep, and stress responses.
Examples include pain from:
- fracture
- sprain
- burn
- inflammation
- post-operative tissue injury
- arthritis flare
Neuropathic pain — “nerve injury pain”
Neuropathic pain occurs when there is injury or dysfunction in the peripheral or central nervous system itself.
It can be difficult to recognise because pain may occur in an area with reduced sensation, or in an unusual distribution. Patients may describe:
- burning
- shooting
- electric shock-like pain
- pins and needles
- numbness with pain
- pain from normally non-painful stimuli, such as light touch or breeze
Examples in the fact sheet include trigeminal neuralgia, postherpetic neuralgia, diabetic neuropathy, central pain after stroke or spinal cord injury, phantom limb pain, and post-surgical neuropathic pain.
How acute pain can become chronic
Untreated or undertreated acute pain can lead to changes in the nervous system through neuroplasticity.
After ongoing tissue or nerve injury:
- peripheral nociceptors become more sensitive
- spinal cord neurons become more reactive
- the brain and spinal cord can develop a “pain memory”
- pain signals may continue even after the original injury has healed
This is called pain sensitisation. The nervous system becomes over-responsive, so pain is produced more easily and may persist unnecessarily.
Gate Control Theory
The Gate Control Theory explains that the nervous system is not just a passive cable carrying pain signals to the brain.
At the spinal cord level, pain signals can be amplified or inhibited before reaching the brain. The “gate” can be more open or more closed depending on competing nerve inputs and descending signals from the brain.
In chronic pain, the gate may remain more open, allowing pain messages to continue even with normal daily activity. The brain also sends descending signals back to the spinal cord, which can either dampen or amplify pain.

Why chronic pain is more than just ongoing injury
Chronic pain is often not proportional to visible tissue damage. It may reflect a sensitised nervous system rather than ongoing structural injury.
Important concept:
Hurt does not always equal harm.
A patient may have severe pain even when investigations show minimal findings, because the pain system itself has become overactive. This does not mean the pain is “imaginary”; it means the nervous system is producing a real pain experience through altered processing.
Clinical takeaway
Pain should be understood using a biopsychosocial model:
Biological factors
- tissue injury
- inflammation
- nerve injury
- central sensitisation
- sleep disruption
- deconditioning
Psychological factors
- fear
- anxiety
- depression
- catastrophising
- previous trauma
- beliefs about damage
Social/environmental factors
- work stress
- family stress
- compensation issues
- reduced activity
- isolation
- cultural beliefs
- access to care
The RACGP First Do No Harm guidance
– https://www.racgp.org.au/clinical-resources/clinical-guidelines/key-racgp-guidelines/view-all-racgp-guidelines/first-do-no-harm/gp-resources/opioids-to-treat-chronic-non-cancer-pain
The RACGP First Do No Harm guidance says chronic non-cancer pain is multifactorial, influenced by biological mechanisms, culture, previous pain experiences, beliefs, expectations, mood and resilience. It aligns with the PainAustralia concept that pain is a subjective brain-and-nervous-system experience, not simply a direct measure of tissue damage.
For chronic non-cancer pain, the RACGP position is:
- Long-term opioids should not be common.
- There is limited evidence supporting opioids for chronic non-cancer pain.
- There is no evidence of long-term benefit for chronic pain outcomes.
- Opioids can cause significant harm, so use must be cautious and based on individual risk–benefit assessment.
What not to do
Do not initiate or escalate opioids for chronic non-cancer pain unless all of the following have been done:
- comprehensive biopsychosocial assessment
- clear diagnosis
- careful risk–benefit assessment
- shared decision-making management plan
- plan for regular clinical monitoring
Do not initiate or escalate opioids in patients with comorbid alcohol use disorder, substance use disorder, or polydrug use.
Do not abruptly stop opioids in patients already taking them for chronic non-cancer pain. Tapering should be planned, staged, and collaborative.
What to do instead
Use non-drug interventions first, and consider non-opioid analgesia where appropriate. RACGP specifically supports psychological therapies, physical therapies, return to activity, and multidisciplinary care.
Examples include:
- pain education
- pacing and graded activity
- physiotherapy or exercise physiology
- strengthening programs
- hydrotherapy, yoga, Tai Chi
- CBT, ACT, behavioural therapy
- sleep optimisation
- mood and trauma-informed care
- occupational therapy
- multidisciplinary pain service referral when pain continues to reduce function or quality of life
If the patient is already on opioids
RACGP recommends:
- prescribe the lowest effective dose
- monitor pain and function regularly
- use real-time prescription monitoring
- review sedating co-medications, especially benzodiazepines, antipsychotics, gabapentinoids, alcohol
- develop a deprescribing plan through shared decision making unless opioids are being used for end-of-life pain or dyspnoea
- consider naloxone access if overdose risk is present
Main harms of long-term opioids
Common harms include:
- nausea
- constipation
- itch
- sedation
- dental caries
- sexual dysfunction
- low mood
Serious harms include:
- falls
- impaired driving
- overdose
- respiratory depression
- cardiac arrhythmias
- worsening sleep apnoea
- death
Long-term use can also cause tolerance, dependence, withdrawal, opioid-induced hyperalgesia, and diversion-related harms.
Red flags for specialist or multidisciplinary review
Consider pain specialist or multidisciplinary review if there is:
- opioid plus benzodiazepine use
- two or more psychoactive medicines
- complex mental health comorbidity
- substance use history
- suicidality or previous overdose
- unexpected dose escalation
- high distress
- new patient requesting opioids without an established therapeutic relationship
- correctional/forensic history
- possible high-risk medication behaviour
Patient explanation
“Chronic pain is real, but it often behaves differently from acute injury pain. In long-term pain, the nervous system can become sensitised, like an alarm system that keeps ringing too easily. Opioids may help short-term severe acute pain, but for chronic non-cancer pain they usually do not improve long-term function or quality of life and can cause serious harm. The safest approach is to focus on function, movement, sleep, mood, pacing, education and multidisciplinary support.”
Resources and information for patients
- NSW Government Agency for Clinical Innovation, self-management of pain resources
- Pain Australia, The nature and science of pain
- Pain Australia support groups and help lines
- The Royal Australian College of General Practitioners, Opioids to treat long-lasting pain
- University of South Australia, Professor Lorimer Moseley discusses his experience with pain for Feeling Human at MOD
Resources for GPs
- RACGP, Prescribing drugs of dependence in general practice, Part C1 – Opioids
- RACGP, Prescribing drugs of dependence in general practice, Part C2 – The role of opioids in pain management
- RACGP, Handbook of non-drug interventions (HANDI)
- RACGP, AOD clinical advisory service and S8 prescribing in your state or territory
- The University of Sydney, Evidence-based clinical practice guideline for deprescribing opioid analgesics
