How and Why Pain Starts, Stays, and Spreads

What do these conditions have in common: rheumatoid arthritis, osteoarthritis, temporomandibular disorders (TMD), fibromyalgia, headache, complex regional pain syndrome (CRPS), and post-surgical pain? If you guessed “pain,” you were right. And not just pain but chronic (long-lasting) pain.

For the last 25 years, the National Institutes of Health (NIH) have contributed a great deal of money to research on the topic of pain. Trying to find out why pain starts, why it spreads, and why it doesn’t stop in some people has been a challenge. The most likely reason is something called central sensitization.

As much as 100 years ago, physicians realized that something gets turned on in the central nervous system that contributes to the start and spread of pain that doesn’t get turned off. The injury or local trauma has long since healed but the patient continues to experience daily, ongoing, and often very disabling pain.

That is the crux of central sensitization. Nerve cells called neurons in the spinal cord transmitting pain information from body part to brain don’t just pass the information along — they remain excited about the information. It’s too much (intensity) for too long (duration).

At the same time, the person’s threshold (level at which a response occurs) lowers so there’s a faster response to less input. Not only that but other nearby tissues get in on the act. They aren’t injured or damaged but they set up the same pain-inducing racket in the nervous system. That phenomenon is called field-expansion.

Other questions revolve around risk factors or predictive factors. In other words, why do some people become so sensitive and others do not? Are there environmental, social, genetic, and/or psychologic triggers? What is happening at the cellular and molecular levels? Are there separate mechanisms for what turns the pain on and what keeps it going or sustains it?

Scientists have been able to find out that it’s not just a matter of some pain switch getting turned on in the hand or foot (or other body part) that’s injured. There’s much more to it than that. It appears that in some people, the central nervous system is overly sensitive. Words like hypersensitive, exaggerated, or ramped up are used to describe it.

The question becomes, what can be done about it? If we can understand the mechanism, it may be possible to turn it off — or better yet, keep it from getting turned on in the first place. We know now that various parts of the nervous system from the individual cells to the message pathways (like a relay system) and brain are adaptable and changeable. That’s referred to as neural plasticity.

Now we come back to our original question: how is it that so many different physical problems like arthritis, fibromyalgia, migraines (or other headaches), and jaw pain (temporomandibular disorders) can create such similar pain patterns?

The answer is likely central sensitization. And if that theory is correct, then it means that scientists may be able to find a solution that could possibly work for all chronic pain problems.

Scientists may be able develop ways to work with neural plasticity. Right now, they are looking for ways to turn down the excitability of neurons in the central nervous system or even turn them off. If they are successful, it could give patients who have suffered chronic pain a new lease on life and keep others from suffering the same fate in the first place.