physical therapist treating hip pain gate control

Physiotherapist Shin Iwayoshi works with a patient with hip pain. (Photo courtesy of Shin Iwayoshi)

 

If you have bumped your elbow against a table, you probably have instinctively massaged your elbow to reduce the pain. But why do you feel less pain when you rub it?

And speaking of rubbing, why do many people tend to get short-term pain relief after a massage session?

Based on previous pain theories, the gate control theory of pain suggests that the spinal cord has a neurological “gate” that either blocks or reduces nociceptive signals to pass to the brain from the skin or internal organs. These signals are blocked at the first synaptic level in the spinal cord that connects nociceptors in the skin to nerves that send signals to the brain (ascending interneurons).

Also, the gate can be closed by stimulating afferent nerves by touching at or near the site that is causing the pain. Such touching and rubbing behavior could be seen in humans and various animals, such as mice.

In other words, when you massage or rub the painful area, it stimulates a different set of nerves that block the nociceptive signals to the spinal cord. 

However, how we sense pain isn’t just a one-way street of nerve impulse flow. Pain researchers Dr. Ronald Melzack and Dr. Patrick Wall have found that our pain experience is also the accumulation of how we perceive the stimulus, our environment, context of the stimulation, and emotions.

To understand how this works, let’s take a closer look at how the gate control theory works.

In their book The Challenge of Pain, second edition (1988), Melzack and Wall described five stages on which they formulated the gate control theory.

The gate control theory starts with Descartes’ specificity theory of pain where small, peripheral nerves (S) send impulses to transmission cells in the spinal cord (T). The nerves are small, myelinated A-delta fibers and the unmyelinated C fibers. From the T, impulses are transmitted to reflex circuits in the spinal cord and to the brain. (Images by Nick Ng)

Stage 1: Small-diameter peripheral nerves (myelinated A-delta fibers, unmyelinated C fibers) are stimulated by an injury. They deliver impulses to the transmission cells in the dorsal horn of the spinal cord. Then they travel to the local reflex arc and to the brain.

Facilitatory cells (orange) in the T cell region “gate” the input signals.

Stage 2: All synaptic regions include cells that facilitate or inhibit the impulses, which includes wide-dynamic range cells (WDRs). These cells in the dorsal horn fire prolonged bursts of impulses after the initial impulse arrives at the spinal cord.

Facilitatory cells (orange) in the T cell region “gate” the input signals.

Large, low-threshold, unmyelinated nerves (L) can also trigger the T cells. These large nerves respond to a full range of inputs, from gentle touch and pressure to nociceptive input (e.g. heat, puncture, cut).

Stage 3: WDRs are also stimulated by large, low-threshold myelinated fibers. Melzack and Wall proposed that pain would be triggered if the firing rate of any cell group exceeded a critical level determined by the brain.

WDRs can both inhibit and facilitate nociception, depending on how the afferent nerves are stimulated.

Since large afferents can excite and inhibit T cells, nerves in the central area tend to excite the cells while those around the edges suppress their activity. This later led to suggest the substantia gelatinosa, a dense cluster of cells in the spinal cord, also plays a key role in both exciting and inhibiting signal transmission.

Stage 4: Every synapse has both inhibitory and excitatory systems that regulate how impulses pass through, depending on their overall balance of activity. Large nerve fibers can excite and inhibit these signals. Fibers located in the central area tend to activate the cells while those around the edges suppress their activity. The substantia gelatinosa, a dense cluster of cells in the spinal cord, also plays a key role in both exciting and inhibiting signal transmission.

The brain can modulate the input signals, such as stimulation in the midbrain and medulla areas inhibit the firing of T cells.

Stage 5: The brain can modulate sensory information in the spinal cord, too. The midbrain and medulla oblongata inhibit the spinal cord cells from firing. Ascending messages to the brain can influence descending controls. This completes a loop from the spinal cord to the brain and back to the spinal cord.

Gate control theory updates

The gate control theory underwent a few updates since its debut in 1965. While the theory can explain acute pain, it doesn’t explain chronic pain and pain without peripheral input, such as phantom limb pain and CRPS, completely.

First, Melzack and Wall wrote that local inflammation of damaged tissues releases prostaglandins that sensitize nerve endings, while nociceptors lower their activation threshold. Nociceptors also release substances that cause swelling and vasodilation, and they can become reactive to noradrenaline from the sympathetic nervous system. These effects explain why treatments like ice, compression, and aspirin can help.

However, the widespread and persistent nature of pain and movement changes after an injury suggests that something more happens in the central nervous system. Melzack and Wall wrote that earlier theories suggested “reverberating circuits,” or ongoing nerve activity, but they wrote there is no evidence of this idea.

The substantia gelatinosa (SG) represents the gate area where it can facilitate or inhibit input signals. When there is an increased activity coming from large afferents, it inhibits activity in the SG, which lowers the input coming from the small afferents. The action system originally refers to the behavioral response to the input, but it is later further described by the interactions of the sensory, cognitive, and affective brain regions that produce this behavior.

They suggested that when a peripheral nerve is injured or cut, a series of changes spreads through the nervous system over days or weeks. These changes alter the chemistry and behavior of the dorsal root ganglion cells, motor neurons, and sensory terminals in the spinal cord. As a result, inhibition decreases, receptive fields expand, and neurons become more excitable.

These delayed effects aren’t caused by nerve impulses because the effects persist even when impulses are blocked or when similar injuries are created. Instead, the timing and pattern of these changes suggest that they are driven by chemical signals transported within sensory nerve fibers, especially unmyelinated C fibers.

“[These mechanisms] operate within a range of variability that is determined by the demands of the environment and the needs of the brain,” Melzack and Wall wrote. “We must take into account, in understanding a response to injury, that the state of other tissue is important, and the state of the brain is equally important.Its job is to assess priorities of behaviour. In our motor performance, we are not puppets driven by strings; similarly, in our sensory world, we seek and select that information relevant to our needs, rather than being the passive recipients of whatever happens in our world.”

Further reading: Bridging Descartes to Melzack and Wall, specificity to gate control theory of pain

Applying gate control theory with massage

Massage therapy interacts with several mechanisms described in the gate control theory.

First, massage stimulates large, fast-conducting A-beta afferents that respond to touch and pressure signals. These signals compete with the smaller, slower afferents (A-delta and C fibers) at the first synaptic gate in the spinal cord.

When non-painful stimuli dominate, they “close the gate,” reducing the amount of nociceptive input that is passed to the brain. (This goes back to why rubbing or touching an injured area can dull the pain.)

Depending on the type of massage, massage therapy can keep the gate closed with rhythmic and/or sustained mechanical stimulation, such as Swedish massage and deep tissue massage with sustained compression, respectively. This also promotes inhibitory interneurons in the dorsal horn to dampen nociception.

Beyond the spinal cord, massage influences descending pathways from the brain that regulate pain. Pleasant touch and relaxation activate the periaqueductal gray, nucleus raphe magnus, and other brainstem regions are involved in descending inhibition. These areas release serotonin, noradrenaline, and endogenous opioids, which suppress nociceptive transmission.

This descending control is one of the features that Wall and Melzack emphasized as essential to the gate control model—it explains why context, mood, and expectation matter. Massage enhances these effects by promoting relaxation, reducing anxiety, and altering attention away from pain, all of which increase descending inhibition.

Massage can also reduce ongoing nociceptive input from sensitized tissues by interrupting central sensitization. After an injury or period of stress, unmyelinated C fibers from muscles and fascia can maintain long-lasting excitability in the spinal cord, making normal touch or movement feel painful. 

Massage may help by improving local circulation, reducing inflammation, and normalizing muscle tone, which decreases the barrage of C-fiber impulses that keep the spinal neurons hyperactive. At the same time, the repeated non-painful stimulation during massage may help retrain the nervous system to interpret touch as safe, which may gradually shrink the expanded receptive fields that sustain tenderness and hypersensitivity.

While massage does not directly alter the long-term chemical and structural changes after a nerve injury or widespread pain, such as CRPS, it may indirectly benefit by improving overall sensory input and reducing stress and anxiety.

Rise of the neuromatrix theory

The gate control theory sets the stage for Melzack’s neuromatrix theory that includes cognition and emotions as contributors to pain. In Challenge of Pain, Melzack and Wall described the limbic system and the reticular structures of the brainstem are “powerful motivational” drivers that trigger an organism into action when responding to pain.

A conceptual model of the neuromatrix theory of pain that arises from the gate control theory. Melzack and Wall state that the output from transmission cells (blue) projects to the sensory-discriminative and motivational-affective systems in the brain. Both systems communicate with higher functional parts of the brain and provide a feedback loop back to the gate control system. Eventually, the interactions of these systems lead to a movement behavior that responds to the stimulus. (Image by Nick Ng)

These “emotional” structures—called the “motivational-affective system”—determine how distressing the pain feels, how much attention it demands, and how you respond to it. For example, you can cry, call for help, change your movement pattern or posture. This system can open or close the gate indirectly by changing descending impulses from the brain.

The motivational-affective system interacts with the “sensory-discriminative dimension of pain,” which is where the somatosensory pathway runs from the spinal cord up to the brain’s thalamus. Then the pathway goes into the primary and secondary somatosensory cortices, which tells you where you are hurt, how much it hurts, and what kind of pain it is (sharp, burning, throbbing, etc.)

Combined with higher processing areas of the brain that evaluates past experiences and the context of pain, Melzack and Wall wrote, “The complex sequences of behaviour that characterize pain are determined by sensory, motivational, and cognitive processes that act on motor mechanisms,” which means any behavior that responds to pain.

“Even ‘simple’ reflexes, which are generally thought to be entirely spinal in their organization, are now known to be influenced by cognitive processes,” they wrote. “If we pick up a hot cup of tea in an expensive cup, we are not likely to simply drop the cup, but jerkily put it back on the table, and then nurse our hand.”

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Nick Ng is the editor of Massage & Fitness Magazine and the managing editor for My Neighborhood News Network.

An alumni from San Diego State University with a bachelor’s degree in graphic communications, Nick had completed his massage therapy training at International Professional School of Bodywork in San Diego in 2014. In 2021, he earned an associate’s degree in journalism at Palomar College.

When he gets a chance, he enjoys weightlifting at the gym, salsa dancing, and exploring new areas in the Puget Sound area in Washington state.