There are different types of pain experience that are underpinned by a range of mechanisms. Remembering that pain is produced by the brain, we need to understand where the information about the perceived threat is coming from. Is it from the peripheral nerves sending danger signals or normal signals being modulated in the spinal cord or brain and then being interpreted as dangerous or a combination. With a skilled assessment we can identify the mechanisms and decide upon the best course of action.
Below are descriptions of the types of pain that we commonly see.
This type of pain is due to sensitivity in the nerves that detect danger in the tissues. These nerves are known as nociceptors and usually have a high firing threshold that means the stimulus must be strong or repetitive to trigger a response. The threshold is lowered by the release and production of chemicals that occurs after tissue damage (inflammation) and through disease states that may involve chronic inflammation (e.g. bradykinin, prostaglandins, serotonin, noradrenaline, immune mediators, neurotrophins). When the threshold is lowered it means that the nerve will be excited by a stimulus that would not usually do so. This manifests as sensitivity to mechanical, chemical and thermal stimuli, for example movement and touch (mechanical), exercise and inflammation (chemicals) and temperature change (heat or cooling).
Essentially this pain originates from a change in tissue state. The underpinning mechanisms can be inflammatory, ischaemic or mechanical. There may of course be a combination of mechanisms at play, and the assessment will provide information to determine which are pertinent.
Inflammatory pain produced from a tissue injury (e.g. ankle sprain) or disease (e.g. rheumatoid arthritis) as described above (also see pain explained page) can demonstrate signs such as redness, swelling (oedema) and heat. There is a good relationship between a stimulus and painful response, the pain can be worse at night and stiffness is a feature of the morning. Anti-inflammatory medication has a good effect. A further type of inflammation is known as neurogenic inflammation. This is caused by the release of chemicals (substance P and CGRP) into the tissues by the supplying nerves. These nerves are called C-fibres (type of nerve) and have a role in detecting ‘danger’. They send slow messages to the spinal cord from the periphery and also have a role in maintaining tissue health. However, the fact that C-fibres can release these chemicals into the tissues means that they can promote inflammation. Capillaries become leaky and plasma moves into the tissues (swelling) and substance P causes mast cells (these cells are involved in allergic reactions) to release histamine and serotonin in addition to promoting pro-inflammatory processes. Essentially the tissues become very sensitive and can be painful.
Ischaemic pain is caused by a rise in the acid levels in the tissues (lowered pH). With a lack of movement, persisting strain and tension in tissues (especially muscles), fluid is forced out and the pH drops. This causes pain in normal tissues, for example when sitting in one position for too long and developing pain and stiffness. When there is a state of sensitisation, this process can occur more readily. Commonly this is experienced in and around the neck and shoulders or low back when at a desk for a period of time. We have receptors (TRPV1) on the nerves mentioned earlier that detect changes in the acid levels and these are responsible for the increased signaling.
Mechanical pain is induced by activation of receptors that are mechanosensitive. For example pulling a finger back until it becomes painful, knocking your elbow on a door, moving an injured body part. Of course some of these pains are normal and would be expected as part of a protective response.
The International Association for the Study of Pain (IASP) definition: ‘pain initiated or caused by a primary lesion or dysfunction in the nervous system’ (2008) proposed definition (Treede et al., 2008): ‘pain arising as a direct consequence of a lesion or disease affecting the somatosensory system’
Characteristics of neuropathic pain (Baron & Tolle, 2008)
1. If a nerve in the periphery with a cutaneous branch (supplies the skin) or a central pathway (a nerve pathway that runs in the spinal cord to the brain) is affected, there will be an area of abnormal sensation (loss of sensation to painful and heat stimulation) in a similar location to the pain
2. Pins & needles (paraesthesia)
3. Spontaneous pain: ongoing, electric shock like feeling
4. Burning pain
5. Evoked pain: requires stimulation; sensitivity to mechanical strain, i.e. normal movement & pressure applied to the tissues causes pain, known as allodynia (painful response to non-painful stimuli; e.g. painful light brushing) and hyperalgesia (heightened painful response to a painful stimulus; e.g. very sharp pin-prick)
6. Summation: progressively worsening pain to stimulus; e.g., pain worsens with rubbing/massage
7. Cold allodynia: sensitivity to cold
8. Paroxysmal pain: shooting electrical pains
9. Mechanical deep somatic allodynia: sensitivity to pressure applied to deep tissues around joints
Many of these symptoms are caused by changes in the physiology of the nerve. It must be remembered that sensation is the realm of the nervous system, i.e. we only feel sensation because of the nerve supply to the tissues and the messages that they send to the brain. Some sensations can feel as if they are localised in a particular region but in fact originate in the peripheral nerves or central nervous system.
Pain as a result of an injury or inflammation is adaptive and protective whereas neuropathic pain represents abnormal activity in a damaged nerve. It is likely that after an injury there is a combination of inflammatory and neuropathic pain although in many cases the latter is not significant.
Managing neuropathic pain usually involves medication that helps the nerve to reduce in its excitability in addition to the techniques described on the treatment page. There are some conditions that are known to include neuropathic pain, e.g. diabetes (diabetic neuropathy) & post-herpetic neuralgia.