Gate control method

The Gate Control Model

The gate control model begins with the idea that pain signals
enter the spinal cord from the body and are then transmitted
from the spinal cord to the brain. In addition, the
model proposes that there are additional pathways that
influence the signal sent from the spinal cord to the brain.
The central idea behind the theory is that the signals from
these additional pathways can act to open or close a gate,
located in the spinal cord, which determines the
VL 3 strength of the signal leaving the spinal cord.
Figure 14.23 shows the circuit that Melzack and Wall
(1965) proposed. The gate control system consists of cells
in the spinal cord called the substantia gelatinosa (Figure
14.23a). These cells are represented by SG_ and SG_ in the
gate control circuit in Figure 14.23b. We can understand
how this circuit functions by considering the following
facts about its operation.
Input to the gate control system occurs along three
pathways:
■ S-fibers. The small-diameter fibers (S-fibers) are associated
with nociceptors—fibers or receptors that fire
to damaging and potentially painful stimuli. Activity
in the S-fibers increases the activity of the transmis-
Pain 345
T-cell
Pain
Gate-control system
SG–
Central
control
Gate closes
Gate opens
SG+ +
+
+
+
+
+
–
L-fiber
(a)
(b)
S-fiber
(from
nociceptors)
Dorsal root
Substantia gelatinosa
Figure 14.23 ❚ (a) Cross section of the spinal cord showing
fibers entering through the dorsal root and the location of the
substantia gelatinosa. (b) The circuit proposed by Melzack
and Wall (1965, 1988) in their gate control model of pain
perception. See text for details.

sion cell (T-cell). The intensity of pain is determined

by the amount of T-cell activity, with more activity
resulting in more pain. You can see how this works
by following the paths along which signals from the
S-fibers travel and noting that all of the synapses are
excitatory. Thus, signals from S-fibers always excite
T-cells, and therefore increase pain.
■ L-fibers. The large-diameter fibers (L-fibers) carry information
about nonpainful tactile stimulation. An
example of this type of stimulus would be signals sent
from rubbing the skin. Activity in the L-fibers can
send inhibition to the T-cells. This occurs because
signals that pass through SG (dashed line) activate
an inhibitory synapse. This closes the gate, which decreases
T-cell activity and decreases pain.
■ Central control. These fibers, which contain information
related to cognitive functions such as expectation,
attention, and distraction, carry signals down
from the cortex. As with the L-fibers, activity coming
down from the brain also closes the gate, decreases
T-cell activity, and decreases pain.
Since the introduction of the gate control model in
1965, researchers have determined that the neural circuits
that control pain are much more complex than what
was proposed in the original model (Perl & Kruger, 1996;
Sufka & Price, 2002). Nonetheless, the idea proposed by the
model—that the perception of pain is determined by a balance
between input from nociceptors in the skin and nonnociceptive
activity from the skin and the brain—stimulated
research that provided a great deal of additional evidence
for the idea that the perception of pain is influenced by more
than just stimulation of the skin (Fields & Basbaum, 1999;
Sufka & Price, 2002; Turk & Flor, 1999; Weissberg, 1999).
We will now consider some examples of how cognition can
influence the perception of pain.