A client relays this conversation with her primary care provider:

Mrs. Smith: No matter what I do, it hurts all the time. It hurts when I rest, and when I work. It hurts when I eat healthy, and when I eat junk. It hurts whether I sleep or not. It hurts all the time. I don’t remember what it’s like to not hurt. What am I supposed to do?

Doctor: I can’t imagine why you’re having so much pain, Mrs. Smith. Your tests show hardly any …

Finish the sentence: arthritis, disc damage, whiplash injury. For women, add endometriosis; for men, add prostate enlargement. The unspoken assumption? This person is a drug-seeker, or a malingerer, or a little nutty. But often, this client is simply experiencing chronic pain.

She is not alone. According to a recent article in Massage & Bodywork (Diana Thompson’s “The Epidemic of Pain,” May/June 2012, page 48), up to 116 million Americans have chronic pain. Deaths from the misuse of pain-killing drugs have tripled in the last decade. We are desperately in need of some better options for treating chronic pain, but to achieve that, we need to understand what is really happening.

The phenomenon behind Mrs. Smith’s chronic pain may be a fairly recently explored dysfunction of central nervous system (CNS) processing called central sensitization. And the reason massage therapists might be interested is that careful manual therapy may have a profoundly positive effect on this situation that is termed by one specialist as a “prevalent, promiscuous pain plasticity.”¹ In other words, this is a common condition, where pain is perceived out of proportion to the input the system receives. 

Definition of Central Sensitization

In its simplest terms, central sensitization is the result of synaptic changes in the spinal cord that occur after injury or irritation, with the consequence of a persistent, yet possibly reversible, perception of pain. 

Synapses, the junction point where signals jump from one neuron to the next, can vary greatly in their activity levels and efficiency. Seldom used or unused synapses can degenerate, but highly sensitized ones can become overactive. This ability of synapses to change according to demand is called synaptic plasticity. 

In central sensitization, a triggering problem or trauma causes sensory neurons to release a flood of pain-promoting chemicals at the synapses in the dorsal horn. The signals transferred by these chemicals can outlast the actual trigger by minutes, hours, or longer. If this environment is prolonged, painful signals are triggered with much less intense stimuli: the pain threshold is lowered, and synaptic plasticity allows the pain-sensing neurons in the spinal cord to become more excitable. At the same time, the inhibitory signals that would ordinarily limit or interrupt the perception of pain are essentially locked out of the loop. Soon, only minimal sensory input (or sometimes none at all) is needed to maintain the perception of damage, and the person enters a persistent state of constantly high reactivity: this is a type of chronic pain.

The chronic pain related to central sensitization has traditionally been associated with a CNS injury, like a stroke or a spinal cord injury. This makes sense since damaged neurons, plus inflammation, means the ongoing transmission of massive pain signals. More recently, we have realized that this pain pattern can be initiated by tissue damage or inflammation anywhere in the body.

The most consistent characteristics of central sensitization are: 

• Allodynia: even normally nonpainful stimuli produce a sensation of pain. 

• Hyperalgesia: normally painful events cause pain that is out of proportion to the stimulus. 

• Enlarging areas of perceived pain: if pain begins in a foot, for instance, the painful area seems to expand, possibly spreading up the leg; this is sometimes called secondary hyperalgesia. 

• Wind-up and temporal summation: these are similar phenomena that occur in different CNS locations. The basic principle is that stimuli that are repeated at a consistent intensity lead to progressively more pain perception.

Many people who live with central sensitization also experience problems with short-term memory and concentration, and amplification of all senses (light is brighter, odors are stronger, textures are rougher, noises are louder, and so on). These other sensory misunderstandings are termed dysesthesias, which essentially means incorrect perceptions. This suggests that similar synaptic plasticity changes can occur throughout the CNS. 

Central sensitization is a normal function of the nervous system, in place to help us resolve problems as they develop. This is important, because it means that nothing is really wrong with the nervous system—the situation is reversible. Problems occur, however, when those heightened pain perceptions become ingrained. Some people appear to be especially susceptible to this problem. Genetics may predispose some people, and a prior history of anxiety or depression is also predictive, because the nervous system is already vulnerable to dysfunction. In addition, central sensitization easily leads to anxiety, depression, and poor sleep—all of which can exacerbate pain. The result is an endless loop of pain and reactive behaviors that reinforce pain. 

Mechanisms of Central Sensitization 

You may remember from anatomy classes that all of the peripheral sensory neurons enter the spinal cord via the dorsal aspect. Within the dorsal horn of the spinal cord, short sensory axons have synapses with tracts of neurons carrying messages up to the thalamus and cortex, where sensation is perceived. 

Nociceptors (pain receptors) release excitatory neurotransmitters to stimulate the next neurons in the pathway. When enough nociceptors are signaling loud enough to pass the message to the neurons of the ascending tracts, those postsynaptic neurons may also become highly sensitized. Studies show that even a short-term stimulus can cause a long-lasting change in the chemical environment of the dorsal horns. This allows the CNS to distort and amplify the severity and duration of pain. Further, remember that each dermatome has some amount of overlap of nerve root supply; the same is true to an even greater extent for myotomes and sclerotomes. As neurons from multiple levels are recruited to relay messages about pain, the brain perceives that the pain is spreading.

But what starts the whole process of this type of chronic pain? And what maintains it? Consider a typical sprained ankle. The initial injury leads to inflammation and the secretion of potassium ions, substance P, bradykinin, prostaglandins, and other pro-inflammatory chemicals that support and prolong inflammation and the sensation of pain. Nociceptors that might otherwise have been silent may be activated in this chemical environment. So far, this is a healthy process. Pain tells us about damage—that we need to treat this part of the body carefully. Under normal circumstances, we heal, the pain signals stop, and all is well.

But if the injury or problem is severe, all the sensory neurons—not just the nociceptors—can begin to behave like pain sensors. They pour pain-related excitatory neurotransmitters into the dorsal horn, the ascending tracts become highly sensitized, and the brain interprets it all as pain. Meanwhile, mechanisms that would limit pain sensation languish: inhibitory interneurons stop working, and the secretion of gamma-aminobutyric acid, an inhibitory neurotransmitter, is suppressed.

Chronic pain is such a common and serious problem that the National Institutes of Health present it as a freestanding disorder, rather than as a complication of some underlying condition. Nonetheless, many other problems list chronic, hard-to-treat pain as a major symptom, including:

• Complex regional pain syndrome.

• Fibromyalgia.

• Neuropathic pain, including diabetic neuropathy and postherpetic neuralgia.

• Postsurgical complications.

• Rheumatoid arthritis and osteoarthritis.

• Temporomandibular joint disorder.

• Tension-type, migraine, and cluster headaches.

• Visceral pain, including irritable bowel syndrome, pancreatitis, angina, chronic pelvic pain syndrome, and endometriosis.

• Whiplash.

Conventional Treatment Options

Central sensitization is a challenge for pharmacological treatment because it’s a problem of perception, more than of specific damage. Unfortunately, the most effective drugs for this are ketamine (a strong tranquilizer) and its chemical equivalents, which carry unacceptable risks of dangerous side effects that include amnesia and psychosis.

Other centrally acting analgesics have some efficacy, but many patients find them insufficient. These include some antidepressants and antiseizure drugs that alter both pain perception and reactivity. Cognitive behavioral therapy that explores solutions to problems that predictably cause pain events can be helpful as well.

Research suggests that mild aerobic exercise can reverse some of the synaptic plasticity that causes this problem, and reduce pain.² Anti-inflammatory medications can be useful, but they usually work only when the trigger for the initial damage involved some kind of inflammation, and this is not always the case. 

Where Does Massage Fit?

The most important takeaways about central sensitization are these:

• The pain is real, not imaginary.

• The pain was triggered by some event outside the CNS.

• The pain is common.

• The pain can be reversible—and manual therapy may help.

Most of us often go through some kind of trauma or problem that could start a central-sensitization cycle, but most of us don’t end up with persistent pain. Besides good luck, the main reason is probably that our normal healing mechanisms resolve the irritation before the pain pathways become deeply ingrained. 

But for those people who do go through this ordeal, it is important to remember that if the source of the problem can be eliminated, we can work to reduce the pain signals, and allow the CNS to return to its normal, functional state. 

It is a fairly new idea to link peripheral injury to CNS dysfunction, and recognizing and locating the peripheral sources of the problem can be challenging. Among many possibilities, we can consider scar tissue, adhesions that irritate nerve endings in fascia, trigger points, gait patterns that reinforce pain, or inefficient postural habits. Another intriguing possibility is that the pain signals may be generated by systemic, but extremely subtle, inflammation or oversecretion of pro-inflammatory chemicals. If we are patient, imaginative, and sensitive to our clients’ needs, we have the opportunity to beneficially interfere in their chronic-pain cycle and help them come to a highly satisfactory resolution. 

Thank you to Geoffrey Bove, DC, PhD, who provided input and significant help during the development of this article. If you get a chance to take a course with him about pain, I highly recommend it. Find him on Facebook—Geoffrey Bove, DC, PhD, Bove Pain Diagnosis and Therapy.

Notes

1. C. Woolf, “Central Sensitization: Implications for the Diagnosis and Treatment of Pain,” Pain 152 (2011): S2–S15.

2. M. Curatolo et al., “Central Hypersensitivity in Chronic Pain: Mechanisms and Clinical Implications,” Physical Medicine & Rehabilitation Clinics of North America 17 (2006): 287–302. 

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