Chronic pain is defined as pain that persists past the healing phase following injury and in the absence of physical tissue damage. Chronic pain is a common problem affecting 15-20% of the population and leads to substantial productivity loss: $34.3 billion annually in Australia.
Pain is a normal physiological response to harmful stimuli and functions as a protective mechanism and initiates the healing process in the body. Acute pain usually settles once the underlying pathology (tissue injury) has resolved. This protective mechanism can be described as physiological pain. However, pain sometimes persists leading to pathological pain without any obvious biological meaning, which is possibly due to sensitisation of the nervous system.
Pain sensitisation, or central sensitisation, is associated with the development and maintenance of chronic pain. When central sensitisation occurs, the nervous system goes through a process called ‘wind-up’ and gets regulated in a persistent state of high reactivity. This persistent, or regulated, state of reactivity lowers the threshold for what causes pain and subsequently maintains pain even after the initial injury might have healed.
In short: pain itself modifies the way the central nervous system (brain and spinal cord) works, so that patients become more sensitive and get more pain with less provocation.
Central sensitisation is characterised by heightened sensitivity to pain (hyperalgesia) and sensation to touch (hyperesthesia). This can also lead to inappropriate pain response to non-harmful stimuli (allodynia). Although less common, central sensitisation can lead to heightened sensitivities across all senses, not just the sense of touch. Chronic pain patients can sometimes report sensitivities to light, sounds and odours. Central sensitisation is also associated with cognitive deficits, such as poor concentration and poor short-term memory. Central sensitisation also corresponds with increased levels of emotional distress, particularly anxiety.
What causes central sensitisation?
Sensitisation develops due to the presence of inflammatory mediators (substance P, histamines, cytokines) from injured tissue, which leads to allodynia and hyperalgesia. Central sensitisation develops in response to continual stimulation of particular fibres in the central nervous system called C fibres. This causes swelling and inflammation of a specific region of the spinal cord called the dorsal root ganglion, leading to a temporary decrease in blood flow to the tissues (ischaemia) and nerve tissue damage.
These changes cause the injured nerves to undergo neural plasticity (brain’s ability to reorganise itself by forming new neural connections throughout life), in which cells with very excitable membranes and enhanced synaptic efficacy (nerve cell interface) are reformed. The effect of this is the recruitment of nerves that are more responsive to stimuli and are more readily transmits nociceptive (pain) information to the brain.
The part of the nervous system responsible for regulation of pain (descending modulatory pain system) is then inhibited causing an increased sensitivity to pain and chronic pain. The effects of this process may persist beyond the duration of the initial noxious input resulting in pain hypersensitivity to normally innocuous stimuli and eventually neuropathic pain.