Pain Mechanisms

The IASP defines pain as an ‘unpleasant sensory and emotional experience associated with actual or potential tissue damage – or described in terms of such damage’.

In the 1960s Melzack and Wall proposed that pain was not a hard-wired warning system but in fact highly modifiable via the CNS, especially at the dorsal horn and brain. Receptors are constantly being removed and replaced allowing for a highly adaptable dynamic system (Kandell et al 2000).

Some receptors have a higher stimulation threshold and require a greater stimulus for them to be activated. Nociceptors are receptors which respond to noxious stimuli and are detected by receptors on the slower conducting Aδ and C nerves. The nociceptive information indicates the dorsal horn that something (possibly) damaging is happening to the tissues. Aβ nerves are low threshold and transmit messages relating to non-threatening or innocuous stimuli.

Pain is a sensation that is produced by the brain. The nociceptive messages are processed with other factors such as knowledge, belief, emotional state and past experiences to result in sensations such as pain.

The pain gate theory provides us with the idea that if the site of injury is rubbed, therefore using the Aβ nerves, the feelings of light touch and pressure presynaptically inhibit the noxious messages and therefore decrease the sensation of pain.

In a therapeutic setting, this explains why treatments such as massage and manual therapy have been effective in reducing pain. Transcutaneous Electrical Nerve Stimulation (TENS) is a small, battery powered unit which delivers small electrical pulses that stimulate the Aβ nerves and therefore reduce the nociceptive input reaching the brain.

However the pain gate theory is still unable to explain all cases, there are still examples where light touch is excruciating and TENS does not have an effect.

Nociceptive Pain

Nociception is the neural process of encoding and processing tissue damage. It is an afferent activity from the CNS and PNS by stimuli that have the potential to cause tissue damage. It is initiated by nociceptors (pain receptors) that detect mechanical, thermal or chemical changes above a set threshold. (Note there are no nociceptors in the articular cartilage or intervertebral discs). Mechanical receptors respond to pressure and stretch, thermal receptors respond to temperature changes and chemical respond to chemical release, especially those released during inflammation or ischaemia. Nociception triggers a variety of autonomic responses that can result in the experience of pain.

Nociceptive pain is the everyday pain; bruises, burns, strains and sprains. Nociceptive messages generated following an injury or pathology in the tissues result in the feeling of pain. Afterwards, the body undergoes the normal healing process to repair during which nociception from the healing tissue should reduce and disappear within the expected healing time.

Symptoms that may indicate the presence of nociceptive-mediated pain include:

·         Specific movements aggravate pain whilst others ease the pain

·         Clearly defined borders of pain

·         On/off pattern with specific postures or activities

·         Physical examination tests have consistent findings.

·         The pain reduces in line with the healing time.

·         Responds well to manual and electrical treatments

·         Responds well to analgesics (painkillers)                               (van Griensven 2005)

As time passes from the initial injury, local and central changes can affect the clinical presentation. Sensitisation in the dorsal horn may result in allodynia (other pain), which may cause false positives in the clinical tests.

Peripheral Neurogenic Pain

Peripheral neurogenic pain is pain generated due to damage of the peripheral nerves. It may also be termed as neuropathic pain if it lasts longer (IASP 2009).

Damage to the nerve can range from a quick compression (e.g. banging your funny bone) to forcefully stretching or cutting it. Damage at any point along the nerve can cause action potentials to be generated at the point of injury, which can then travel both up and down the nerve i.e. either towards the dorsal horn as normal or out towards the periphery.

Action potentials that travel down towards the periphery cause the release of calcitonin gene related peptide (CGRP) and substance P, which encourage an inflammatory response. This neurogenic inflammation can be maintained by these chemicals even in the absence of local tissue damage.

Symptoms of pain mediated by a peripheral neurogenic source include:

·         History of trauma to a nerve, including surgery

·         Continuation of pain beyond the normal healing time

·         Sudden bursts of pain with no obvious reason

·         Pain that does not fit with the normal on/off pattern and aggs and eases

·         Difficulty in describing the pain

·         Numbness or altered sensation

·         Increased pain when stressed

·         Lack of response to analgesics (e.g. paracetamol)          (van Griensven 2005)

Although simple analgesics often don’t dull the pain, other medications such as antidepressants and anticonvulsants can be extremely useful in the control of peripheral neurogenic pain when prescribed in lower doses.

Central Sensitisation

Central sensitisation is when the neurones in the dorsal horn become sensitised to input from the periphery. This leads to a reduction in pain thresholds, hyperalgesia (heightened sensitivity to pain) and allodynia (pain due to a stimulus which does not normally provoke pain) adjacent to the original injury (Ji et al 2003).

Common features which help to identify central sensitisation are:

·         Continuation of pain beyond the normal timescale of healing

·         Pain that doesn’t fit an normal on/off pattern with aggs and eases

·         Exaggerated pain response to a given stimulus or pain to a normally non-painful stimulus

·         Difficulty in describing the pain

·         Lack of response to simple analgesics

·         Pain expanding into areas adjacent to the original site of injury