Debunking 5 Traditional Beliefs About Pain with Cutting-Edge Science

One hundred million Americans experience chronic pain, contributing to an estimated 560 to 635 billion dollars annually in medical costs. This is a fast-growing problem; importantly, not all pain is the same.  Pain is a complex and subjective experience that keeps us away from injury and harm. It is both a sensory and emotional experience and is incredibly individual.

As a frontline clinician, you need access to up-to-date science to understand, integrate, and unlearn some of the outdated science formally learned in academic training. It is critical to inform yourself and recognize that what we may have learned may not be consistent with our current understanding of neuroscience, neurobiology, and immune function.

To illustrate how far pain science has come, we’re debunking five traditional beliefs about pain with cutting-edge science:

Myth #1 Pain is a 1:1 relationship between stimulus and pain.

René Descartes, a French scientist and philosopher, was the first to suggest that pain came from the brain. The theory states that pain is a direct sensory readout of damaged tissues. A physical stimulus, like fire, sends a message to the brain, then the brain sends pain back down. In this model, pain is an input.

Centuries later, science has flipped, and current research shows that pain is different than we once thought.

1. Pain starts with a stimulus (like a kink in the neck or shoulder after working out.) Nociceptors, sensors in our skin, soft tissue, and deep tissue, sense different types of stimuli (temperature, pressure, and PH changes due to inflammation) and send signals via nerve fibers.

There are two nerve fiber types: 1) A-delta, which transmits fast, for example, a sharp jolt when one steps on a tack or touches a hot stove, and 2) C fiber, which transmits slowly and is responsible for dull, achy pain.

2. The message travels along the nerves to the spinal cord, changes a bit, and then goes to the brain.

3. The brain receives and evaluates these messages, telling the body to move away, send endorphins, start the process of healing, etc. This becomes the experience of pain.

What goes on in the periphery (neck, shoulder, foot, etc.) is not pain; it is nociception (electrical signals) that becomes the experience of pain.

Myth #2 The brain has a “pain matrix.”

Pain is a conserved phenomenon. It is necessary for survival, yet pain represents major clinical challenges, and throughout history, humans have sought to control and manage pain. It was once thought that there was a dedicated area of the brain for pain. This so-called “pain matrix” represented areas such as the insula cortex, anterior cingulate, and amygdala, i.e. regions that served specific functions.

While some may have hoped for a dedicated area of the brain for pain when you knock out one pathway going to the brain, others will carry the system forward, and you’ll still experience pain.

We are moving away from this “pain matrix” model because every year or so, we pick up another region of the brain that contributes to this network of pain. Pain is a distributed network of different brain systems. That said, there are common brain networks that represent the experience of pain. This gave rise to the newer development of brain-based biomarkers that hold the potential for objective means of determining if someone is in pain and predicting pain.

The holy grail would be to combine brain imaging biomarkers with inflammatory markers and with genetic markers to determine what the right treatment for each individual is under these particular systems. Due to the pioneering work of PAINWeek faculty Sean C. Mackey MD, Ph.D., CPE, precision, patient-tailored pain care is coming!

Myth #3 All Pain is in the brain.

It’s time to unravel the link between pain and emotion. Pain is complex and the nuanced interplay of social, emotional, and cognitive components contribute to pain.

Our brain serves many functions (cognition, emotions, memory) that shape the signals coming into the body, creating your unique experience of pain that is different from everyone else. This has two important implications for clinicians:

1.      We have a hard time understanding what others are experiencing, and the converse is true, when we are in pain, we assume others understand our pain. A great example is fibromyalgia or chronic pain, where outwardly, we don’t see anything wrong, so we have a hard time understanding it. In other words, we bring in our history of pain and put that on other people. This challenge underscores the need for up-to-date and practical strategies to talk with patients in pain.

2.      While all pain is real and manifests through the lens of the brain and nervous system, there are two types of chronic pain: 1) Primary pain describes a condition that’s not caused by a different medical condition, here pain itself being the problem. 2) Secondary pain is a consequence of another condition.

Primary pain is most chronic pain. Since the brain actively protects us from pain, it will respond to pain signals even when there is no damage in the body. Moreover, with unconscious feelings, the brain recognizes the danger and uses pain to get attention. In many cases, there is no structural damage, yet the pain stays real even if the trigger is only a prediction that something could be dangerous.

Primary pain is driven by the fear-pain cycle, and clinicians can use the latest research and practical strategies to interrupt the cycle of catastrophizing and fear!

Myth #4 Improving patient communication using the 0-10 pain scale.

The 0-10 pain scale is the most used in healthcare and it can be helpful in some situations; however, there are serious limitations of the 0-10 scale. This numerical scale asks patients to self-report their pain with 0 being no pain and 10 being the worst pain you ever felt.  It is far too simplistic and doesn’t consider the qualities of pain from stabbing to throbbing to aching. It also fails to capture changes in pain which can vary hour by hour. Finally, pain is highly subjective, and a simplistic pain scale can lead doctors to treat the numbers.

While there remains a place for the stand-alone tools, and the scale is quick and easy to use, pain is complex and nuanced. A one-size-fits-all approach will not work for everyone. Today, we are moving away from pain scales in favor of questions that assess the whole patient, not a number. Providers can ask patients in pain about what’s important to them: is it going to work? Sleeping? Playing catch with their kid?

Chronic pain requires a comprehensive and detailed assessment as the foundation for a personalized treatment plan - using a mix of pharmacological and nonpharmacological evidence-based approaches.

Myth #5 Treat all pain.

Pain is adaptive and very important. Pain is essential information coming into the brain from the body and environment, which helps us predict whether we’re safe or in danger. The resulting response, such as inflammation, is part of healing. This raises a key question: what is the threshold that one should treat the pain?

Lack of protection

If you increase pain medication too much, the patient may not protect that injured area and make it worse. The threshold is when it’s impacting daily life (ability to interact with friends, go to work, sleep).

Historically, in sports, if a player fractured their ankle, they may have been treated with potent opioids (or another analgesic painkiller) so they can continue playing. This is NOT safe.

After an injury, we get inflammation which sensitizes the injured area – sending out a message to protect. NSAIDS (antihyperalgesic drugs) reduce some of that sensitization out on the periphery, then on the spinal cord, and back in the brain. This desensitization, as well as the anti-inflammatory effect, is at the root of the current controversy of NSAIDs for acute injury. 

Delaying healing

Inflammation is also part of the healing process, and medications for pain can intervene in this natural biological process.

NSAIDs and COX-2 inhibitors, a selective NSAID, reduce inflammation and pain. COX-2 inhibitors block prostaglandin when we introduce these drugs to restore normal functioning and living. Research shows that by blocking inflammation we may be blocking the normal healing process, leading to delays in fracture and tissue repair.

The short answer is to have patients take the lowest dose possible that allows for restoring normal functions and sleep at night, which is critical to the healing process. Overall, we need more data on this healing message, and this remains a nuanced and complex problem!

Love learning about pain with PAINWeek and looking for more opportunities to expand your knowledge of pain management? On September 3-6, 2024, gain insights from leading experts, engage in thought-provoking discussions, and connect with peers who share your commitment to advancing pain management. Register now and join us in Vegas this fall for the #1 US pain conference – PAINWeek 2024! 

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• pathophysiology of pain