Everything You Need to Know About the Evolving Science of Chronic Pain.
I'm tired of the pain. I'm tired of hurting all the time. I'm tired of feeling tired. I'm tired of being tired. I'm just tired of all this. I'm tired of bothering my doctor. I'm just simply exhausted from feeling this way. For once...just for once in my life, I want to feel a sense of normalcy...even for just a bit. I do what I can. I keep going. I push myself. I'm trying my best to still be here for my kids and do what they want. I miss the "old me" that didn't hurt all the **** time. I'm trying to change all this pain, but so far, it's not working, but I'm determined to change that. And those who know me know that I am one hell of a determined and stubborn woman. (Excerpt from social media, edited)
Introduction
Chronic pain is not an extended version of acute pain. It is a different entity that results from changes in the structure and function of your nervous system at multiple levels. Injuries, infection, inflammation, and nerve damage from medicines, poisons, surgery, radiotherapy, or diseases like diabetes, among other causes, can trigger these changes.
In this review, we will look into the mechanisms and processes contributing to developing and maintaining chronic pain. This is the pathophysiology of chronic pain. Other than knowing what is happening to you, understanding these mechanisms will help you make informed treatment decisions. It will also help you prevent the deterioration of your overall well-being.
Pain mechanisms
Nociceptive pain
Nociceptive pain is the pain that results from the activation of your pain sensors (nociceptors). These sensors are found in nearly all body parts and organs. Examples of nociceptive pain include pain after a cut, a burn, and exposure to extreme cold. Inflammatory and ischemic pain (pain from poor blood supply to body tissue or organs) are subsets of nociceptive pain. Pain from arthritis, infections, or surgery is an example of inflammatory pain. The pain of heart attack and leg pain from diseases of blood vessels are examples of ischemic pain.
Nociceptive pain can be acute or chronic, depending on how long it lasts and the duration of stimulation of the pain sensors. In biological terms, acute nociceptive pain (as opposed to chronic nociceptive pain) is a protective mechanism that alerts us of potential or actual threats to our organs and survival.
Chronic nociceptive pain includes knee arthritis, hip arthritis, bursitis, facet joint arthritis, osteoarthritis, rheumatoid arthritis, inflammatory bowel disease, tendonitis, plantar fasciitis, and sacroiliitis.
Neuropathic pain
Neuropathic pain is commonly referred to as nerve pain. It is a pain primarily caused by an injury to the nerves or a disease involving individual nerves or parts of the nervous system (spinal cord and brain). Neuropathic pain is often described as a burning, tingling, shooting, stabbing, or electric shock-like painful sensation. It can be accompanied by a massively increased magnitude of response to painful stimuli (hyperalgesia), elicitation of pain by non-painful stimuli like touch (allodynia), and spontaneous unprovoked pain.
Common causes of neuropathic pain include diabetes, shingles, effects of chemotherapy or radiotherapy, entrapment of nerves, injury of nerves or spinal cord, multiple sclerosis, and complex regional pain syndrome.
Nociplastic pain
Nociplastic pain is a relatively new term introduced by the International Association for the Study of Pain (IASP) in 2017 to describe a third category distinct from nociceptive and neuropathic pain.
Nociplastic pain arises from changes in pain signal detection and generation and its processing in the nerves, spinal cord, and brain. These changes may include the following:
Increased triggered or spontaneous activity of the pain signal-transmitting (nociceptive) nerves that convey pain signals to the spinal cord and brain.
Reduced activity of the body's inbuilt pain-relieving system (inhibitory nerves) that modulates pain signals in the spinal cord and brain.
Changes in regions of the brain that participate in pain perception, emotion regulation, attention, memory, and reward.
Increased levels of neurotransmitters and inflammatory mediators leading to increased and more efficient pain transmission.
Nociplastic pain can occur in isolation or combined with nociceptive or neuropathic pain, affect any body part, or be widespread. It is often accompanied by other symptoms such as fatigue, sleep problems, mood changes, brain fog, learning and memory difficulties, and sensitivity to light, sound, or touch.
Examples of nociplastic pain conditions include fibromyalgia, irritable bowel syndrome, chronic fatigue syndrome, and chronic pelvic pain.
We do not fully understand the exact causes of nociplastic pain, but the following factors are contributory:
Genes:
Some people may have a genetic makeup that makes them more prone to developing nociplastic pain.
Environmental triggers:
Certain events or conditions such as infections, injuries, surgeries, stress, trauma, or emotional distress may trigger or worsen nociplastic pain.
Psychological factors:
Negative emotions such as anxiety, depression, fear, anger, or guilt may amplify nociplastic pain or interfere with its management.
Behavioral factors:
Unhealthy habits such as poor sleep hygiene, physical inactivity, substance abuse, or social isolation may aggravate nociplastic pain.
The diagnosis of nociplastic pain is based on a comprehensive clinical assessment, as there are no specific tests for nociplastic pain.
Have you heard of neuroplasticity?
Neuroplasticity is the phenomenon that occurs when the nervous system can adapt and reorganize itself in response to stimuli. In pain processing, neuroplasticity makes your nervous system more sensitive and responsive to pain signals. It is a key feature of chronic pain.
Neuroplasticity is not limited to pain processing and can be beneficial, such as when we learn new skills or recover from an injury.
The results of the neuroplasticity associated with chronic pain development and persistence include:
Peripheral sensitization: This occurs when the pain sensors (nociceptors) are easily excitable and send more signals to the spinal cord and brain. The intensity of pain is magnified.
Central sensitization: This occurs in the spinal cord and brain, and pain signals from the pain sensors are amplified, further intensifying the pain perceived (hyperalgesia). Non-painful signals are also interpreted as pain (allodynia).
Wind-up: This occurs when repeated or prolonged stimulation of pain sensors leads to a more profound increase in the response of spinal cord neurons, resulting in enhanced pain perception.
Cold hyperalgesia: This is present when cold temperatures/breezes trigger or worsen the pain.
Neuropathic pain:
Sensitization
Sensitization, as discussed earlier, is the process that makes your nervous extremely sensitive and responsive to pain. Sensitization can occur at the peripheral (nerves outside the spinal cord and brain) or central (within the spinal cord and brain) level.
Peripheral sensitization is caused by inflammatory chemicals, such as prostaglandins, bradykinin, histamine, serotonin, and cytokines released from injured tissues or immune cells. These chemicals increase the firing rate of pain sensors (nociceptors), resulting in increased pain sensitivity (hyperalgesia) and pain perception in response to non-pain stimuli like touch (allodynia).
Central sensitization is caused by increased transmission of pain signals and the diminished influence of inbuilt pain-relieving mechanisms in the spinal cord, amplifying the pain signals and responsiveness. Hyperalgesia, allodynia, and spontaneous pain signify the presence of central sensitization.
Modulation
Your body has ways of changing how much pain you feel. Sometimes, you can feel pain even when there is no injury, or you can feel less pain than you expect from an injury. This process is called pain modulation, which happens at different levels of your nervous system.
Modulation is the basis of the Ticked Bucket List, using travel as a tool for pain management and a catalyst for overall well-being.
Some specialized nerves function at the spinal cord as gates controlling how much pain signals can pass through to your brain. Different factors can open or close these gates, such as signals from nerves that carry other sensations (e.g., touch, temperature, or pressure), emotions, attention, expectations, and medications. This is why rubbing a sore spot can relieve pain. When stressed or anxious, the gates may open more and let more pain signals pass to your brain. If you are distracted or relaxed, the gates may close more and let fewer pain signals through; therefore, you feel less pain.
It is the brain that finally processes and interprets pain signals. A pain-modulating mechanism originating in the brain is called the descending pain-modulatory pathway. This is the body's inbuilt pain-relieving system. This system releases natural opioids (endorphins and enkephalins), serotonin, and norepinephrine that block the transmission of pain signals. This system can be activated by other influences such as joy, positive messages, a sense of accomplishment, focus tasks, and well-being activities, resulting in better pain relief and pain treatment/management success.
However, stress, anxiety, fear, depression, grief, and bad memories shut or slow down the inbuilt pain-relieving system. This results in worse pain and pain treatment/management failure.
Changes in the structure and function of nerves
Pain-transmitting nerve fibers can be damaged by injury, compression, inflammation, or disease, altering their structure and function, leading to abnormal firing and increased excitability. An example is sciatica, pain from the compression of the roots of the sciatic nerve by a prolapsed disc in your lumbar spine or pinched by your piriformis muscle.
Other body functions and systems involved in chronic pain conditions.
Chronic inflammation and the immune system:
Chronic inflammation can lead to persistent activation of nociceptors and contribute to peripheral and central sensitization.
The immune system can also interact with the nervous system and modulate pain through various mechanisms. For example, immune cells can release pro-inflammatory chemicals that stimulate pain sensation generation and transmission. They can also produce anti-inflammatory chemicals that reduce pain sensation generation and transmission.
Endocrine system:
The endocrine system comprises the glands that secrete hormones that regulate the body's processes and functions. However, hormones can also affect pain perception and modulation through multiple mechanisms. For example, cortisol (a stress hormone) can suppress inflammation and reduce pain sensitivity. Estrogen (a female sex hormone) can enhance inflammation and increase pain sensitivity.
Psychological factors:
These mental processes and emotions influence how we perceive and cope with pain. Psychological factors can have both positive and negative effects on chronic pain. For example, positive aspects (such as optimism, coping skills, and social support) can reduce stress, enhance mood, increase self-efficacy, and improve quality of life. Conversely, negative factors (such as anxiety, depression, and catastrophizing) can increase stress,
Social factors:
Chronic pain can affect interpersonal relationships (family, friends), occupational functioning (work performance, disability), and quality of life (satisfaction and well-being). These factors can modify pain perception through social support, validation, empathy, feedback, and expectations.
The science-influenced chronic pain treatment.
A pain science-influenced chronic pain treatment is based on the idea that different types of pain have other underlying mechanisms and require specific interventions. For example, neuropathic pain may respond better to drugs that modulate nerve activity, such as pregabalin, gabapentin, duloxetine, and amitriptyline. On the other hand, inflammatory pain will respond better to drugs that reduce inflammation, such as nonsteroidal anti-inflammatory drugs (NSAIDs – celecoxib, naproxen, ibuprofen, etc.) or steroids.
A pain science-influenced chronic pain treatment approach also considers the biopsychosocial factors influencing pain perception and coping, such as emotions, beliefs, expectations, and social support.
By identifying the specific mechanisms and factors contributing to your pain, a tailored, science-influenced chronic pain treatment plan can be instituted.
In conclusion
Our understanding of the complex science of chronic pain is still evolving even though we already know a lot. We have information and scientific evidence to translate to day-to-day care for better pain relief. The elusive universal treatment and cure for chronic will eventually be realized once we gain a complete understanding of the science of chronic pain.
