The pain gate theory, also known as the gate control theory of pain, was first proposed in 1965. This theory suggests that pain is not solely determined by the extent of tissue damage or perceived injury, but also by the interaction between two types of nerve fibers – A-delta fibers and C fibers – and specialized cells in the spinal cord known as “gate cells”.
According to the theory, A-delta fibers and C fibers transmit pain signals from the site of perceived injury to the spinal cord. These fibers are activated by the tissue injury, sending signals through the dorsal root ganglia (DRG) to the spinal cord, where they synapse with gate cells in the substantia gelatinosa of the dorsal horn.
Gate cells act as a kind of “gatekeeper”, either allowing or blocking pain signals from reaching the brain. When activated by A-delta and C fibers, the gate cells open the “gate” and allow pain signals to pass through to the brain, resulting in the perception of pain.
However, other sensory inputs such as touch, vibration or heat can also activate different nerve fibers (A-beta fibers) which can compete for space with the A-delta and C fibers to activate the gate cells, reducing the amount of pain signals that pass through.
Therefore, the pain gate theory suggests that non-painful sensory inputs can be used to modulate or reduce the perception of pain by closing the gate and inhibiting the transmission of pain signals from the injury site to the brain. This is why techniques like massage, acupuncture and transcutaneous electrical nerve stimulation (TENS) are often used as non-pharmacological approaches to managing pain, by stimulating A-beta fibers to activate the gate cells and reduce the amount of pain signals that can pass through.