Читать книгу Why It Hurts - Dr. Aneesh Singla - Страница 21

We now know that there is a clear link between pain and inflammation. In fact, the nervous system, including pain, and the immune system, which causes inflammation, coordinate their activities. When bacteria invade your body, they can directly cause pain when their work is detected by nociceptors, pain-sensing neurons. The immune system can also detect these invaders and respond by coordinating cells to fight them off. Both immune cells and sensory neurons lurk near the places bacteria commonly invade, ready to pounce when the nervous system sounds the alarm. The result? You guessed it: inflammation.

Peripheral sensitization occurs when the pain signal from the injury is amplified, driven by ongoing pain and inflammation. To explain this, think of an infected tooth, causing your entire jaw to hurt. The pain signal affects a larger area than just your tooth as a result of peripheral sensitization. The way this works might graphically look something like this:

Two important aspects contributing to peripheral sensitization are pain and inflammation. In particular, the two effects feed into each other, which I believe forms the circular feedback loop that drives this phenomenon. If the injury heals, then things return to normal in most cases. But in some instances, persistent pain causes wind-up, leading to central sensitization, which is how the body adjusts to the perception of ongoing pain. (For more on wind-up and central sensitization, see Chapter 1.) If your body is warning you of an ongoing injury, it will continuously sound the alarm, whether or not it is warranted. If your body senses that you will ignore the alarm, it will lower the threshold for the alarm, so with time, even the slightest pressure will elicit a painful signal. In effect, the pain alarm will become more sensitive, and you will become more sensitized to certain movements or stimuli.

To help explain wind-up and central sensitization, I will use an interesting case reported by D. W. Wheeler, et al., regarding a female patient with CIP. She became pregnant and, during childbirth, sustained multiple pelvic fractures. This meant that a C-section became necessary to prevent injury to herself or her baby. Due to injuries sustained during this fraught delivery, including injury to a nerve root in her spine, she began to experience pain for the first time in her life. Skin testing was used to determine her thresholds of sensitivity. This revealed that she was 10 times more sensitive to sensations than she had been prior to her pregnancy. Wind-up had dramatically restored the patient’s ability to feel pain.

Clearly, the nervous system is adaptive and can change. We call this trait neuroplasticity. Consider that wind-up was able to restore pain to someone previously incapable of feeling it. This should give you some sense of how excruciating wind-up can be for a person experiencing a ten-fold (or more) amplification of normal sensitivity to pain.

Inflammation can be driven by pain receptors in the skin. Pain receptors can drive the body’s inflammatory response, directly resulting in itching and discomfort. In a recent study published in Nature, scientists shut down the pain receptors in the skin of one group of mice. As a result, the mice had a lowered immune response.

This discovery fits with the observations I have made about my own patients. For example, after surgery patients often experience a stress response, similar to peripheral sensitization, with an increased level of inflammation. When we aggressively treat pain postoperatively, there is less inflammation and, in my belief, better postoperative recovery. My surgical colleagues at Mass General would routinely observe that the patients with epidurals for postoperative pain seemed to fare better after surgery, perhaps due to attenuation of the stress response and less inflammation.

Pain and inflammation are like a healthy marriage; when working well together, they are acting synergistically to maintain and protect us from outside invasion or threats. When there is an imbalance or lack of coordination, both can escalate until a pathological pain state occurs.

To interrupt the feedback loop, I treat patients with a dual approach: First, I administer steroids, which are anti-inflammatories. Then I use local anesthetics to numb the pain. This treatment approach breaks the feedback cycle at two points, more effectively than using either agent alone.

If we learn from adaptive pain, then it can serve a valuable purpose. But if we let pain spin out of control, it can become maladaptive. In that case, the feedback loop conditions a person to feel the pain in the absence of a physical cause. This poses the question: Can maladaptive pain be un-learned?

If you know that the problem generating the pain is not life threatening, you may have to simply adjust your routine around the pain, just as you adjusted your stride mid-way in your marathon. But when your body continues to sound the alarm and doesn’t respond completely to an anti-inflammatory or local anesthetic, you have to be careful not to ignore that pestering warning signal. If we fail to shut the pain alarm off with conservative therapy, it is possible that our body is desperately trying to indicate that there is a serious issue at hand (as is the case with appendicitis).

And so, once more we have discovered that the body has a way of fighting back to keep sending you the pain alarm when it senses something is wrong. When these rare, but serious events occur in our lives, I believe that we actually want to let our bodies continue to sound the alarm (i.e., continue to send the warning signal of pain). If we switch off the pain completely, through over-medication, we risk missing the serious problem that is occurring. Here again, I have observed that over-medicating patients rarely results in 100 percent pain relief. Again, this is the body’s natural intelligence preserving our ability to feel pain in the setting of a major systemic problem.