TENS (TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION)
It is at this level that the pain gate first postulated by Melzack and Wall in 1965 operates. They proposed the existence of a gating mechanism at the spinal level that could alter ascending transmissions of nociceptive input.
The mechanism by which the gate influences afferent transmission is based on the quantity of input between A
and C fibres to the dorsal horn of the spinal cord.
The substantia gelatinosa consists of a group of cells located in the dorsal horn of the spinal cord.
and C fibres project to, and synapse on, both the substantia gelatinosaand the first central
transmission (T) cells
in the dorsal horn.
It was thought that the T cells, when sufficiently stimulated, activated an actionsystem that is responsible for response and perception.
The T cells are, in turn, excited by the A
and C fibres.
Melzack and Wall felt that
the substantia gelatinosa modulated the transmission from peripheral (A
& C) fibres to central (T) cells by presynaptically inhibiting the fibres from stimulating the T cells
The gate is “closed” by high levels of activity in the A
Using the negative feedback system, the A
fibres exert presynaptic on the T cells via facilitation of the substantia gelatinosa.
The gate is “opened” with high levels of activity from the C fibres, preventing the substantia gelatinosa from exerting its inhibition on the T cells.
This results in T cell excitation by either spatial or temporal summation.
The net result is the perception of pain.
If nociceptive information is allowed through the gate then this traffic willcontinue up the lateral spinothalamic tract of the spinal cord to the thalamus, andfrom here to the cerebral cortex.
As this stimulus passes through the brainstem it may cause an interactionbetween the
periaqueductal area of grey matter (PAG)
These nuclei form part of the descending pain suppression system and theirdescending neurons can release an endogenous opiate substance into thesubstantia gelatinosa at the spinal cord level.
The chemical nature of this endogenous opiate, which may be
, is such as
to cause inhibition of transmission in the nociceptive circuit synapses
This is achieved y blocking the release of the chemical transmitter (substance P) in the pain circuit.