Pain injury was first suggested in 1965

Pain perception is the way in which pain is experienced to an individual, how much or little pain that is felt by the individual is determined by ‘gates’ which allow or block pain from being processed by the brain. There are many other ways in which pain can be perceived differently from what should occur from the physical injury, including pain felt being less than what should be expected



Until the 20th Century, it was understood that perceived pain was directly dependant on the amount of physical injury caused to the body, this was known as the ‘specificity theory’ (René Descartes, cited in The Open University, 2018a). However, it was not until 1956 that Dr Henry Beecher published his scientific observations he had made during World War II detailing if narcotics, such as morphine, were required to treat pain by soldiers who had been severely injured during the war against a similar group of 150 male civilian patients. Beecher found that although the soldiers had extensive wounds, only 32 out of the 150 men observed requested narcotics as opposed to 83 out of 150 of the civilian men. From this data, Beecher concluded that it is not possible to judge how much pain an induvial is in according to the amount of physical injury perceived by another and that the amount of pain felt by the individual is largely dependent on their own experiences and thoughts (Henry Beecher, cited in The Open University, 2018b).

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Leading on from Beecher’s observations, one of the current theories that also suggests pain perception is not entirely dependent on physical injury was first suggested in 1965 by Ronald Melzack and is known as ‘The gate control theory’ This theory suggested that there are ‘little cells’ in the spinal cord that acted as a gate, these cells could shut or open and therefore preventing or allowing nerve impulses continuing along the spinal cord to the brain. The brain can then process this signal depending on the individual’s current emotions or previous experiences, the signal then travels back down the spinal cord to establish the type and amount of pain felt (Melzack and Wall, cited in The Open University, 2018c).

When Melzack first proposed this theory, there was no way to prove the existence of these ‘little cells’, however now there is sufficient evidence to suggest that the theory was correct.

The ‘little cells’ also known as the spinal interneuron produces enkephalin when the cell becomes excited by an action potential, enkephalin then binds to the nociceptor which reduces the release of glutamate. It also binds with transmission cell receptors, inhibiting this cell and cancelling the excitation caused by any remaining glutamate, no action potential is caused and therefore information about the noxious stimulus is not passed to the brain.

Enkephalin can be released from the interneuron via two methods, the first of which is caused by an action potential being released from a touch neuron, this causes the release of an excitatory neuron transmitter to be released into the synapse which in turn binds to receptors on the spinal interneuron. This cell becomes excited triggering the release of enkephalin.

The second method occurs when an action potential travels from the brain to the spinal cord, this stimulates the release of an excitatory neuron transmitter which also binds to receptors on the spinal interneuron, in turn exciting the interneuron causing the release of enkephalin (The Open University, 2018d).