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( Referred pain)
Referred pain is a term used to describe the phenomenon of pain perceived at a site adjacent to or at a distance from the site of an injury's origin. One of the best examples of this is during ischaemia brought on by an angina pectoris, or heart attack. Even though the heart is directly affected the pain is often felt in the neck, shoulders and back rather than the chest. The International Association for the Study of Pain, as of 2001, has not officially defined the term; hence several authors have defined the term differently. Despite an increasing amount of literature on the subject there is no definitive answer regarding the mechanism behind this phenomenon.[1] There are several proposed mechanisms for referred pain. Currently there is no definitive consensus regarding which theory may be correct. This represents one of the earliest theories on the subject of referred pain. It is based on the work of W.A. Sturge and J. Ross from 1888 and later TC Ruch in 1961. This theory proposes that afferent nerve fibers from tissues converge onto the same spinal neuron. This theory explains why referred pain is believed to be segmented in much the same way as the spinal cord. Additionally, experimental evidence shows that when local pain (pain at the site of stimulation) is intensified the referred pain is intensified as well. Criticism of this model arises from its inability to explain why there is a delay between the onset of referred pain after local pain stimulation. Experimental evidence also shows that referred pain is often unidirectional. For example stimulated local pain in the anterior tibial muscle causes referred pain in the ventral portion of the ankle; however referred pain moving in the opposite direction has not been shown experimentally. Lastly, the threshold for the local pain stimulation and the referred pain stimulation are different, but according to this model they should both be the same.[1]
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