Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
The mechanism by which a damaging stimulus in the body is perceived as painful by the brain is a complex one which is not yet fully understood. The complexity of the process results from the nervous system not being a ‘hard wired’ system, but exhibiting plasticity that enables it to modify its function under different conditions.
As shown by the definition, pain serves the purpose to prevent tissue damage and protect the body while it is healing. Under certain conditions, pain can become maladaptive and persist as chronic pain. This pain serves no protective function and is described as pathological pain as opposed to physiological pain; it is then no longer a symptom of another disease, but a disease in its own right. Another term for pathological pain has been suggested recently: dysfunctional pain.
In order to adequately treat physiological, but even more pathological pain, an understanding of pain mechanisms is required.
Painful stimuli are detected by nociceptors, which are free nerve endings located in tissues and organs. They have high thresholds and, under normal circumstances, only respond to noxious stimuli.
There are two distinct types of nociceptors
High threshold mechanoreceptors which stimulate small myelinated Aσ-fibres and transmit a well-localised sharp or pricking sensation that lasts as long as the stimulus.
Polymodal nociceptors that stimulate small unmyelinated slowly conducting C fibres. As well as responding to mechanical stimuli they are activated by thermal and chemical stimuli e.g. hydrogen ions, potassium ions, bradykinin, serotonin, adenosine triphosphate and prostaglandins.