Understand the essential concepts of pain pharmacology in a clinical approach and its role in pain management therapies.

Abstract: A Comprehensive Guide to Integrative Pain Management

Welcome to this in-depth educational post where we will embark on a comprehensive journey into the multifaceted world of pain management. From my perspective as a Doctor of Chiropractic, Advanced Practice Registered Nurse, and a certified functional medicine practitioner, I will guide you through the latest evidence-based pharmacological strategies, drawing upon the groundbreaking work of leading researchers in the field. This discussion is designed to be an easy-to-understand exploration of both common and novel treatment options, moving beyond traditional approaches to embrace a truly integrative model of care.

We will begin by establishing the critical importance of setting realistic patient expectations and adopting functional outcome measures beyond the standard 0-10 pain scale. The discussion will then transition to a detailed analysis of common over-the-counter and prescription medications, starting with acetaminophen and its associated risks of hepatotoxicity. We will conduct an in-depth review of non-steroidal anti-inflammatory drugs (NSAIDs), exploring their mechanisms, efficacy, and significant gastrointestinal and cardiovascular risks.

The post then provides a thorough analysis of topical agents, including diclofenac, lidocaine, and capsaicin, explaining how they target peripheral pain pathways and offer effective relief with a lower risk of systemic side effects compared to oral medications. We will move to neuropathic agents, focusing on anticonvulsants like gabapentin and pregabalin, detailing their mechanisms of action, evidence-based applications, and crucial safety warnings, including risks of respiratory depression, misuse, and new findings on cardiovascular risk. We will also delve deeply into the use of antidepressants for pain, clarifying that their efficacy is independent of mood disorders and discussing the roles of SNRIs like duloxetine and tricyclic antidepressants (TCAs) for conditions like chronic musculoskeletal pain and burning mouth syndrome.

Finally, the post critically evaluates the roles of benzodiazepines, muscle relaxants, and opioids, addressing topics such as the dangerous synergy between opioids and benzodiazepines, the nuances of cytochrome P450 metabolism, management of side effects like opioid-induced constipation (OIC), and the importance of naloxone. We will also explore emerging therapies like low-dose naltrexone (LDN) and the newly approved suzotrigine.

Crucially, this post will highlight the power of a multidisciplinary approach, showcasing how our practice, Injury Medical Clinic PA, integrates chiropractic care, functional medicine, and rehabilitation under the expert medical direction of Dr. Maria Guadalupe Cardenas, MD. We will explore how this collaborative model allows us to address the root causes of pain, reduce reliance on medication, and empower patients on their journey to recovery and optimal wellness. By the end of this post, you will have a profound appreciation for the complexities of pain and the sophisticated, patient-centered strategies required to manage it effectively.

Introduction: Our Collaborative, Multidisciplinary Approach to Care

Hello, I’m Dr. Alex Jimenez. Welcome to our educational series where we explore the complex world of pain management through the lens of modern, evidence-based research. With my background as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), board-certified Family Nurse Practitioner (FNP-BC), and certifications in Functional Medicine (CFMP, IFMCP), Advanced Technology Neurology (ATN), and Cranial Cervical Spinal Technology (CCST), my passion lies in bridging the gap between different medical disciplines to create a holistic and effective treatment plan for my patients.

This discussion is more than just a list of drugs; it’s a journey into understanding the “why” behind their use. We’ll explore the physiological mechanisms, the latest research findings from leading experts, and how these chemical interventions interact with our bodies. My goal is to empower you with the knowledge you need to be an active, informed participant in your own health journey.

A cornerstone of our practice at Injury Medical Clinic PA in El Paso, Texas, is our unique collaborative, multidisciplinary approach. I work alongside a phenomenal team, including our esteemed Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a Board-Certified Internist with over four decades of invaluable experience (NPI #1164426749, Texas MD License #J2933). Her extensive medical expertise provides essential oversight and a crucial perspective that complements our chiropractic, functional medicine, and rehabilitative services. This integrative model ensures that when medications are considered, they are prescribed and managed with the highest level of medical scrutiny, always in the context of your overall health and wellness goals.

How Our Team Works Together in Synergy

Our model is designed to be seamless and patient-centric. Here’s how the different components of our practice work in synergy:

• Medical Oversight and Direction (Dr. Cardenas, MD): Cardenas provides the essential medical framework for our practice. She oversees diagnostic protocols, reviews complex medical histories, and offers her extensive expertise in internal medicine to ensure that all underlying health conditions are appropriately managed. Her role is critical when pharmacological interventions are considered, as she ensures that prescriptions are medically necessary, safe, and integrated thoughtfully with other therapies. Her guidance is paramount in managing patients with comorbidities such as hypertension, diabetes, or cardiac issues, ensuring that their pain management plan does not compromise their overall health.
• Chiropractic and Biomechanical Care (Dr. Jimenez, DC): As a chiropractor, my primary focus is on the body’s structure and its relationship to function. I use manual adjustments, spinal decompression, and other biomechanical techniques to address the root structural causes of pain. For a patient with sciatica, for instance, I work to correct spinal misalignments or disc herniations that are compressing the sciatic nerve. This structural intervention can often provide significant pain relief without the need for medication, or it can work synergistically with medical treatments to enhance their effectiveness. By restoring proper alignment and motion, we reduce nerve irritation, decrease inflammation, and improve the body’s innate ability to heal.
• Functional Medicine Integration (Dr. Jimenez, CFMP, IFMCP): Functional medicine allows us to dig deeper and ask, “Why is this patient experiencing this pain?” We move beyond just treating symptoms to uncover the underlying root causes. This involves comprehensive lab testing to assess nutritional deficiencies, hormonal imbalances, gut health, and inflammatory markers. For example, chronic inflammation is a key driver of pain. Through functional medicine, we can identify and address the sources of that inflammation—whether it’s a pro-inflammatory diet, gut dysbiosis, or environmental toxin exposure. We then create personalized nutrition, supplement, and lifestyle plans to restore balance to these systems, thereby reducing pain from the inside out.
• Advanced Nursing and Pharmacological Management (Dr. Jimenez, APRN, FNP-BC): My role as a nurse practitioner allows me to bridge the gap between structural care and medical management. I am qualified to assess, diagnose, and, in collaboration with Dr. Cardenas, prescribe medications when necessary. This dual qualification is especially powerful. I can perform a chiropractic adjustment to alleviate nerve pressure. Then, if the patient is still experiencing acute inflammatory pain, I can consider prescribing a short course of an anti-inflammatory medication or recommend a topical agent, always with the comprehensive medical oversight of Dr. Cardenas. This ensures a cohesive treatment plan where every intervention is complementary.
• Rehabilitation and Personal Injury Care: Our clinic specializes in helping patients recover from personal injuries, such as those sustained in auto accidents or workplace incidents. Our rehabilitation programs are designed to restore function, strength, and mobility. We integrate physical therapies, corrective exercises, and soft tissue work with our chiropractic and medical treatments. This comprehensive approach ensures that patients not only get out of pain but also regain the functional capacity to return to their daily lives and prevent future injuries.

Together, we strive to provide a seamless continuum of care, from acute injury management to long-term wellness. Let’s begin this exploration together, aiming for that one key piece of information that might transform your understanding of pain and its management.

Setting the Stage: The Philosophy of Pain Management

Before we dive into the specifics of medications, it’s essential to address the foundational philosophy of effective pain management. For the past 25 years, first as a nurse and now for nearly two decades as an advanced practice provider, I’ve seen firsthand how pain permeates every aspect of a person’s life. It isn’t confined to a specific clinic or specialty; it is a universal human experience that all healthcare providers encounter.

My clinical observations at Injury Medical Clinic have consistently shown that the most crucial first step is managing patient expectations. This isn’t just about bedside manner; it’s a clinical necessity that profoundly impacts outcomes.

Pain Management is a Process, Not a Pill

I cannot emphasize this enough: pain management is a process, not a pill. While medications, which we will discuss at length, can be valuable tools, they are just one part of a much larger, more intricate puzzle. The expectation that a single pill, a single injection, or a single adjustment will provide a complete and permanent cure is a significant barrier to successful treatment.

Interestingly, research has illuminated a startling disconnect in patient expectations. A study revealed that when patients experience anything less than 100% pain relief, they often perceive it as a failure of care or even the withholding of effective treatment (Crombez et al., 2012). This all-or-nothing mindset is a disservice to both the patient and the provider. It sets an unrealistic standard that modern medicine, for all its advancements, cannot meet for chronic pain.

In the world of clinical research, a “clinically significant” improvement in pain is defined as a reduction of 30% to 50%. Think about that for a moment. If you were to purchase a service and were told you would only receive 30-50% of the promised benefit, you would likely feel short-changed. It’s understandable why patients might feel frustrated.

This is precisely why we advocate for a multimodal approach. If we can achieve a 30% improvement from a well-chosen medication, another 20% from a targeted chiropractic care plan, perhaps 15% from nutritional changes guided by functional medicine, and another 25% from a specific rehabilitation program, suddenly we are accumulating benefits. We are chipping away at the pain from multiple angles, leading to a much more substantial and sustainable improvement in quality of life.

Moving Beyond the 0-10 Pain Scale

Another critical component of managing expectations is how we measure success. The ubiquitous 0-10 numeric pain rating scale, while a required metric in many clinical settings, is a deeply flawed and often misleading tool when used in isolation.

Pain is not just a number; it is an experience that impacts function, mood, sleep, and social engagement. The number “10” can mean vastly different things.

• Is the patient a “10” while lying motionless on the couch, unable to move?
• Or are they a “10” after spending a wonderful afternoon walking through the mall with their granddaughter, an activity they haven’t been able to do in years?

These are two entirely different clinical scenarios. The second “10” represents a massive victory in functional improvement, even if the subjective pain score remains high. This is why we must shift the focus from a simple number to functional goals.

To achieve this, we can use validated tools like the Brief Pain Inventory (BPI). The BPI is a short questionnaire that assesses not just pain severity but also how pain interferes with general activity, mood, walking ability, work, relationships, sleep, and enjoyment of life. By averaging the scores from these functional domains, we get a much richer, more meaningful picture of the patient’s experience and our treatment’s true impact.

Alternatively, and often more powerfully, we can work directly with the patient to identify their personal goals. What do they want to be able to do again?

• “I want to be able to sleep through the night without waking up from pain.”
• “I want to be able to walk my dog around the block.”
• “I want to sit through a family dinner at a restaurant without having to get up and stretch constantly.”
• “I want to attend my child’s dance recital and be present in the moment.”

These become our new metrics for success. We document them, we track them, and we celebrate them. This investment by the patient in their own functional goals is what sustains motivation and provides a tangible measure of progress when the 0-10 scale fails to capture the full story. This approach is central to how we structure our integrated care plans at our clinic.

The Journey of a Pain Signal: From Periphery to Brain

I often find that my patients feel more empowered and engaged in their treatment when they understand why we are choosing a particular therapy. A crucial part of this education is explaining the journey of a pain signal. When I discuss pain management regimens, I don’t just hand over a prescription; I talk about how pain is generated and transmitted through the body.

I’ll often use a simple analogy. Imagine you accidentally smash your hand in a door. The pain doesn’t just magically appear in your brain. That initial injury triggers a complex cascade of events right there in your hand, at the periphery. This first stage is called transduction.

When the tissues in your hand are damaged, they release a cocktail of inflammatory chemicals. This is the body’s natural alarm system. These chemicals start a process that converts the physical injury into an electrical signal —an impulse that travels from the periphery (your hand) to your spinal cord. This second stage is called transmission. Once in the spinal cord, the signal is relayed up to the brain. The brain then processes this information in a stage called perception, and only then do you consciously “feel” the pain.

The reason it’s so important to understand this pathway is that it reveals multiple opportunities for us to intervene. We can try to block the signal at its source in the periphery, intercept it along the nerves leading to the spinal cord, or modulate how it’s processed in the spinal cord and brain. Logically, it makes perfect sense to start where the pain impulse originates: at the periphery.

A Deeper Look at Peripheral Activation and the “Chemical Soup”

To truly grasp why certain medications are so effective, we need to look closer at the “chemical soup” released during an injury. Imagine a nail piercing your skin. This injury, or any tissue damage from a chemical burn, infection, or ischemia (lack of blood flow), triggers the release of several key substances:

• Prostaglandins: These are lipid compounds that are fundamental players in inflammation. As I’ve mentioned in discussions about anti-inflammatory medications, prostaglandins don’t directly cause pain, but they sensitize the nerve endings, making them much more responsive to other pain-producing stimuli. They essentially lower the pain threshold.
• Histamine: Released from specialized immune cells called mast cells, histamine is well-known for its role in allergic reactions, causing itching and swelling. In the context of injury, it also contributes to the inflammatory response and sensitizes nerve endings.
• Bradykinin: This is a powerful pain-producing peptide. Once prostaglandins and histamine sensitize nerve endings, bradykinin directly activates them, causing a strong pain signal.
• Serotonin: Released from platelets, serotonin also contributes to the inflammatory process and pain signaling.
• Substance P and Calcitonin Gene-Related Peptide (CGRP): These are neuropeptides released from the sensory nerve endings themselves. They are powerful vasodilators, meaning they cause blood vessels to widen. This leads to the redness and swelling we associate with inflammation. More importantly, Substance P is a key pain-sensitizing compound that amplifies the signals being sent to the spinal cord.

All of these chemicals work together to open up ion channels on the sensory nerves, known as nociceptors (pain receptors). This influx of ions generates the electrical impulse that travels up the nerve fiber to the dorsal root ganglion, which is a cluster of nerve cell bodies located just outside the spinal cord, and then into the spinal cord itself. From there, it’s a direct route to the brain.

This detailed understanding reveals our therapeutic targets. We can directly interfere with this peripheral chemical cascade. We can block the production of prostaglandins, counteract the effects of histamine, or even deplete Substance P right at the site of injury.

Balancing Body and Metabolism- Video

A Closer Look at Common Over-the-Counter Analgesics

With that foundational understanding in place, let’s begin our review of specific pharmacological agents. We will start with some of the most common medications that patients often use before ever seeking specialized care.

Acetaminophen: The Deceptively Complex Analgesic

Acetaminophen, widely known by the brand name Tylenol, is one of the most-used drugs in the world. What I find truly mind-blowing, and a testament to the complexities of pharmacology, is that even after all these decades, the precise mechanism of action of acetaminophen is not fully understood. The leading theory suggests it works primarily in the central nervous system (brain and spinal cord) to inhibit cyclooxygenase (COX) enzymes, particularly a variant known as COX-3. It may also interact with the body’s own cannabinoid and serotonergic systems (Ghanem et al., 2016). However, its effects are distinct from NSAIDs, as it has very weak anti-inflammatory properties in the rest of the body.

The Hidden Dangers of Acetaminophen

The most critical information to convey to patients about acetaminophen is the risk of hepatotoxicity, or severe liver damage. It is well-established that doses exceeding 4 grams (4,000 milligrams) per day can be toxic to the liver.

The danger lies in the unintentional overdose. A staggering 30,000 people are hospitalized annually in the United States for acetaminophen-induced liver toxicity. Even more concerning is that half of all acetaminophen overdoses are unintentional (Yoon et al., 2016).

Why does this happen? Because acetaminophen is a hidden ingredient in hundreds of over-the-counter products. It’s in combination pain relievers, cold and flu remedies, and sleep aids. A patient might take the maximum dose of Tylenol for their back pain, then later take a dose of NyQuil for a cold, not realizing they are consuming a dangerous amount of the same drug.

This is why patient education is paramount. The “Know Your Dose” campaign is a valuable resource that aims to raise public awareness about this issue. We must have explicit conversations with our patients, teaching them to read labels and track their total daily intake of acetaminophen from all sources.

Clinical Application and Evidence for Acetaminophen

Despite these risks, is there a place for acetaminophen in pain management? The evidence is mixed. For acute low back pain, a large randomized controlled trial found that acetaminophen was no more effective than a placebo (Williams et al., 2014). This has led many guidelines to de-emphasize its use for this condition.

However, clinical experience tells a more nuanced story. I have had patients with significant, “terrible-looking” findings on their MRI scans—severe spinal stenosis, large disc herniations—who report meaningful relief from taking just two regular-strength acetaminophen tablets twice a day. On the other hand, some patients are terrified to take even a single dose, believing it will immediately harm their liver, even with no other risk factors.

My approach is this: If a patient with chronic pain, particularly something like osteoarthritis, has not had an adequate trial of scheduled acetaminophen, it is a reasonable, low-risk option to try, provided they are well educated on the maximum daily dose and are not consuming it from other hidden sources. It is often about finding that balance between unfounded fear and a lack of awareness of real danger.

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): Potent but Risky

We now move to another cornerstone of pain management: non-steroidal anti-inflammatory drugs (NSAIDs). This class includes over-the-counter medications like ibuprofen (Advil, Motrin) and naproxen sodium (Aleve), as well as a host of prescription drugs. Patients often believe NSAIDs are the “safe” alternative. While they can be incredibly effective, particularly for pain driven by inflammation, their side effect profile is significant and warrants a deep, respectful understanding.

The primary mechanism of action for NSAIDs is the inhibition of cyclooxygenase (COX) enzymes. These enzymes are responsible for producing prostaglandins. Prostaglandins drive inflammation, pain, and fever. Still, they also perform crucial protective functions, most notably maintaining the protective mucosal lining of the gastrointestinal tract and regulating blood flow to the kidneys.

There are two main types of COX enzymes:

• COX-1: Is “constitutively” expressed, meaning it’s always active. It’s responsible for the “housekeeping” functions, like protecting the stomach lining and supporting platelet function (which is essential for blood clotting).
• COX-2: Is “inducible, meaning its levels increase dramatically at sites of injury and inflammation. It is the primary driver of inflammatory pain and fever.

Most traditional NSAIDs (ibuprofen, naproxen, diclofenac) are non-selective, meaning they block both COX-1 and COX-2. This is why they are effective at reducing pain and inflammation (by blocking COX-2) but also why they carry significant risks of gastrointestinal bleeding and kidney issues (by blocking the protective COX-1).

Key Clinical Pearls for NSAID Use

Let’s discuss some important practical points about using NSAIDs that you might not be aware of.

1. No Single NSAID is Superior: In large-scale clinical trials, no single NSAID has been consistently proven to be more efficacious than another for pain relief. Patient response, however, is highly individual. A person might fail to get relief from ibuprofen and naproxen but find that a third option, like meloxicam, works wonders. Therefore, if the first choice isn’t effective, it’s reasonable to try a trial of one or two others before abandoning the entire class.
2. An Adequate Trial is Key: For an NSAID to be deemed ineffective, it needs a proper trial. This isn’t just one or two doses. Clinical studies that have demonstrated efficacy looked at consistent dosing for at least four days. We need to set this expectation with patients: “We’re going to try this for several days at a consistent dose to see if it helps. If it doesn’t, we have other options.”
3. The Celecoxib Exception for Anticoagulants: We are all taught to avoid NSAIDs in patients on anticoagulants (blood thinners) like warfarin or newer agents like apixaban (Eliquis). This is because blocking COX-1 inhibits platelet aggregation, creating a “double-hit” on the body’s clotting ability and dramatically increasing bleeding risk. However, celecoxib (Celebrex) is a COX-2 selective inhibitor. Because it largely spares the COX-1 enzyme, it does not have the same antiplatelet effect. It is considered a safer option (though not risk-free) for patients on anticoagulants who require an anti-inflammatory (Schjerning Olsen et al., 2015). This is a critical piece of information that can make a real difference for complex patients with both pain and cardiovascular conditions.

The Profound Gastrointestinal (GI) Risks of NSAIDs

The GI side effects of NSAIDs are widely known, but the underlying physiology is often misunderstood. Many patients believe that if they take their NSAID with food, they are protected. While taking medication on a full stomach can reduce local irritation, the most dangerous GI effects are not local; they are systemic.

As we discussed, NSAIDs work by blocking the production of prostaglandins throughout the body. The same prostaglandins that are blocked to reduce joint inflammation are also blocked in the stomach wall, where they are essential for stimulating the production of the protective mucus layer and bicarbonate, and for maintaining healthy blood flow to the tissue. When this protective mechanism is disabled, the stomach lining becomes vulnerable to damage from its own acid.

The consequences can be severe and surprisingly rapid. One study in healthy volunteers taking 800mg of ibuprofen three times a day—a dose many people might consider standard for a bad flare-up—found that evidence of GI bleeding could appear within just three to five days (Lanza et al., 1999). This underscores the danger of the “it’s just Advil” mindset.

Furthermore, combining even low-dose aspirin (often taken for cardiac protection) with a non-selective NSAID can double the risk of a significant GI bleed.

It is also important to note that while COX-2 selective inhibitors like celecoxib have a significantly lower risk of GI complications compared to traditional NSAIDs, the risk is not zero. Even in studies comparing celecoxib to the combination of a traditional NSAID plus a proton-pump inhibitor (PPI) like omeprazole, celecoxib demonstrated a better GI safety profile (Chan et al., 2017).

One final, crucial point: PPIs are not a panacea. While they are very effective at protecting the stomach by reducing acid production, they offer no protection against NSAID-induced damage to the small intestine. NSAID enteropathy (damage to the small bowel) can lead to ulceration, bleeding, and protein loss, and PPIs do not prevent this.

The Cardiovascular and Renal Risks of NSAIDs and COX-2 Inhibitors

In the early 2000s, the cardiovascular risks of NSAIDs came into sharp focus with the withdrawal of rofecoxib (Vioxx). Since then, we have learned that this risk is not unique to Vioxx but is a class-wide effect for all NSAIDs, with the possible exception of naproxen at certain doses, though this is still debated (Nissen et al., 2016). Even celecoxib, which is safer for the gut, carries the same cardiovascular risk as other NSAIDs.

The mechanism is thought to relate to an imbalance between prostacyclin (a vasodilator and platelet inhibitor, primarily from COX-2) and thromboxane A2 (a vasoconstrictor and platelet activator, primarily from COX-1). By blocking COX-2, we may be tipping the scales toward a pro-thrombotic, vasoconstrictive state, increasing the risk of heart attack and stroke. A major concern is the increased risk of severe cardiovascular events, including:

• Heart Failure: These medications can cause fluid retention and increase blood pressure, placing a substantial burden on the heart and increasing the risk of developing or exacerbating heart failure.
• Myocardial Infarction (Heart Attack): Research has consistently shown a correlation between the use of NSAIDs and COX-2 inhibitors and a higher incidence of heart attacks. This risk is not trivial; it is a statistically significant danger that we must factor into our clinical decision-making.
• Peripheral Vascular Disease: The systemic effects of these drugs on blood vessels can contribute to the progression of vascular disease throughout the body.

The data are startling:

• In patients who have already had a heart attack (post-MI), adding an NSAID to their regimen can double the risk of a new cardiovascular event, and this increased risk can be seen in as little as three days of use.
• Even more shockingly, in patients with no prior history of heart disease, taking an oral NSAID during an acute respiratory infection (like the flu or a bad cold) was associated with a threefold increased risk of having a heart attack (Shao et al., 2023). This is a common scenario: someone feels sick, aches all over, and reaches for an anti-inflammatory, unknowingly elevating their cardiac risk.

The widespread availability of drugs like ibuprofen and naproxen can create a false sense of security. As such, monitoring becomes a non-negotiable part of our practice when these medications are part of a treatment plan. We need to be aware of changes in blood pressure, signs of fluid retention like ankle swelling, and any new cardiac symptoms.

This brings me to a core principle of integrative and functional medicine: the concept of polypharmacy with a purpose. The risks associated with high doses of a single medication are often greater than the risks of using lower doses of several different medications that work through different mechanisms. This is why our approach is often to use “a little of this and a little of that,” rather than pushing the dose of one drug to its maximum limit.

As an integrative practitioner, this is where our comprehensive approach becomes vital. When a patient presents with musculoskeletal pain and has significant cardiovascular risk factors, we heavily favor non-pharmacological options. Chiropractic adjustments, for example, can modulate pain signaling pathways and improve joint mechanics without any systemic chemical exposure. Targeted physical rehabilitation can strengthen supporting musculature and improve biomechanics, reducing the inflammatory load on a joint. These interventions become first-line therapy, reserving NSAIDs for only the most severe, short-term flare-ups after a thorough risk-benefit discussion.

Here is a list of some common NSAIDs, grouped by their chemical class. This can be helpful when a patient fails a drug in one class; trying an agent from a different class may yield a better response. You don’t need to memorize this, but it’s a useful reference.

• Propionic Acids:

• • Ibuprofen (Advil, Motrin)
  • Naproxen (Aleve, Naprosyn)
  • Oxaprozin (Daypro)

• Acetic Acids:

• • Diclofenac (Voltaren, Cambia)
  • Indomethacin (Indocin)
  • Ketorolac (Toradol)

• Enolic Acids (Oxicams):

• • Meloxicam (Mobic)
  • Piroxicam (Feldene)

• Fenamates:

• • Meclofenamate

• COX-2 Selective Inhibitors:

• • Celecoxib (Celebrex)

In my practice, I often start with meloxicam for its once-daily dosing and relatively balanced COX-1/COX-2 inhibition profile. If that isn’t effective or causes side effects, I might trial naproxen or celecoxib, depending on the patient’s specific risk profile.

Targeting Pain at its Source: The Power of Topical Agents

Given the significant systemic risks of oral NSAIDs, it’s natural to look for alternatives that can deliver medication directly to the site of pain. I feel that topical agents are often overlooked or underestimated in mainstream pain management, but they are an excellent option in our therapeutic arsenal. They are a cornerstone of our integrative approach at Injury Medical Clinic because they align perfectly with the principle of treating the root cause with minimal systemic impact.

The most common topical agents used in pain management are topical NSAIDs (most notably, diclofenac), topical lidocaine, and capsaicin.

Topical NSAIDs: Diclofenac (Voltaren)

One of the most widely used and studied topical agents is diclofenac gel, commonly known by the brand name Voltaren. It is also available in other formulations, such as an ointment and a patch (brand name Flector).

What’s truly compelling is that research has demonstrated that the efficacy of topical non-steroidal anti-inflammatory drugs (NSAIDs) is comparable to that of oral NSAIDs when used consistently for localized pain, such as in osteoarthritis of the knee or hand (Derry et al., 2015). A key study found that when applied daily for a week, topical diclofenac was just as effective as taking an oral NSAID for pain relief. The crucial difference? It achieved this without the significant gastrointestinal (GI) side effects, like stomach ulcers or bleeding, and with a markedly reduced risk of cardiovascular side effects. The risk profile is vastly better because systemic absorption is only about 6% of what would be absorbed from an equivalent oral dose. This dramatically reduces, but does not eliminate, the risk of systemic side effects.

How does it work?

Topical diclofenac works by blocking the cyclooxygenase (COX) enzymes, which are responsible for producing prostaglandins. By applying diclofenac directly to the painful area, we inhibit prostaglandin synthesis right at the source, preventing this sensitization and effectively raising the pain threshold. This stops that initial link in the chain of pain transmission.

The American College of Rheumatology now strongly recommends topical NSAIDs for patients over 75 with osteoarthritis, particularly because this population is at higher risk for the side effects of oral medications (Hochberg et al., 2012). These are often my patients who either cannot undergo or do not want a joint replacement. I have countless patients, especially my avid knitters who suffer from hand arthritis, who find tremendous relief using diclofenac gel on their hands, allowing them to continue their hobbies with less pain.

Different Formulations and Application:

• Diclofenac Gel (1%): This is now available over the counter. I often advise patients to apply a measured dose (e.g., 2 grams for a smaller joint like the hand or wrist, 4 grams for a larger joint like the knee) up to four times a day.
• Diclofenac Topical Solution (1.5% or 2%) (Pennsaid): This formulation is interesting because it contains dimethyl sulfoxide (DMSO), a solvent that enhances the penetration of the active ingredient through the skin.
• Diclofenac Patch (1.3%) (Flector): These patches are specifically indicated for acute pain due to minor strains, sprains, and contusions. In my clinical experience, this is an excellent option for patients who come in with acute low back pain after “throwing out their back.”

Integrating these topical agents with chiropractic care is a perfect example of our multimodal approach. A patient with acute lumbar strain will receive chiropractic adjustments to restore proper spinal mechanics and reduce nerve irritation, while simultaneously using a diclofenac patch to control the local inflammation and muscle pain. This combination addresses both the structural and biochemical components of the injury, accelerating recovery.

Topical Anesthetics: The Role of Lidocaine

Another powerful class of topical agents is local anesthetics, with lidocaine being the most common. Topical lidocaine is available as a 5% patch by prescription (Lidoderm) and in lower concentrations (4%) over the counter. A landmark study on postherpetic neuralgia (the persistent, severe nerve pain that can follow a shingles outbreak) found that using 5% lidocaine patches led to a 65% improvement in pain scores and a 77% improvement in quality of life within the first week of treatment.

These are not trivial numbers. Anyone who has treated a patient with postherpetic neuralgia understands the profound impact it has on their life. Providing this level of relief with a topical patch is a massive victory.

How does it work?

While diclofenac targets inflammatory chemicals, lidocaine works on a completely different mechanism: the ion channels of the nerve itself. Nociceptors transmit their electrical signals by rapidly allowing sodium ions to flow into the nerve cell through specialized sodium channels. Lidocaine is a sodium channel blocker. It physically obstructs these channels, preventing the influx of sodium and thereby stopping the nerve from firing and transmitting the pain signal. I might say, “The diclofenac gel helps with the inflammatory chemicals causing the irritation, while this lidocaine patch works by numbing the nerve endings so they can’t send the pain message.”

Safety and Application:

The standard regimen for lidocaine patches is 12 hours on, followed by 12 hours off. This “off” period is designed to prevent skin desensitization. A key benefit of the lidocaine patch is its exceptionally low systemic absorption. Very little of the drug enters the bloodstream, making it a very safe option with virtually no systemic side effects or drug-drug interactions.

Capsaicin: Harnessing the Heat of Chili Peppers

Capsaicin, the compound that gives chili peppers their heat, is another unique topical agent that works on yet another distinct receptor in the periphery. It targets the Transient Receptor Potential Vanilloid 1 (TRPV1) receptor. This receptor is a heat-activated calcium channel.

When applied topically to a painful area, capsaicin initially causes a burning or stinging sensation because it activates these TRPV1 receptors on the nociceptors. With repeated application, however, this prolonged activation overwhelms the nerve ending. It essentially exhausts the nerve’s supply of Substance P, the neuropeptide that helps transmit pain signals. By depleting Substance P from the presynaptic terminal, capsaicin effectively desensitizes the nerve fiber to painful stimuli. It’s a process of “defunctionalization”—the nerve ending is still there, but it can no longer effectively transmit pain signals.

Formulations and Use:

• Over-the-Counter (OTC) Creams and Gels: These come in low concentrations (e.g., 0.025% to 0.1%) and need to be applied three to four times a day, every day. Consistency is key, and it can take several weeks of regular use to achieve significant pain relief.
• Qutenza (8% Capsaicin Patch): This is a high-concentration, prescription-only patch that must be applied in a clinical setting for conditions like diabetic peripheral neuropathy and postherpetic neuralgia. The intense activation leads to profound, long-lasting desensitization of the nerve endings. A single application can provide pain relief for up to three months.

Off-Label and Compounded Topical Agents

In complex cases, especially for patients who haven’t responded to standard therapies, we sometimes turn to compounded topical agents.

• Clonidine Gel: Clonidine is an alpha-2 adrenergic agonist. Alpha-2 receptors are part of the sympathetic nervous system (“fight or flight” system) and are involved in modulating pain signals. When applied topically, clonidine can help reduce sympathetically mediated pain, which we sometimes use for our patients with Complex Regional Pain Syndrome (CRPS).
• “Magic Mouthwash”: This is a general term for a variety of compounded oral rinses used to treat painful mouth sores (oral mucositis), often seen in patients undergoing chemotherapy or radiation. It’s also something I use for patients with a perplexing condition called Burning Mouth Syndrome. The formulations vary but typically include a local anesthetic (like lidocaine), an antacid (to help it coat the mouth), and an antihistamine.

Modulating the Central Nervous System: Neuropathic Agents

While topical agents are fantastic for localized, peripheral pain, many pain conditions involve the central nervous system. This is where we see changes in how the spinal cord and brain process pain signals, a phenomenon known as central sensitization. For this, we turn to medications that work centrally, which I refer to as neuropathic agents.

“Neuropathic agent” refers to the medication’s mechanism of action, not necessarily the type of pain it’s treating. While these medications are the go-to choice for classic nerve pain—that burning, zinging, shooting pain—they can also be effective for other chronic pain states like fibromyalgia, where central sensitization is a key driver.

Anticonvulsants as “Membrane Stabilizers”

The primary class of neuropathic agents we use is anticonvulsants, specifically gabapentin and pregabalin. If you take one thing away from this section, let it be the concept of these drugs as “membrane stabilizers.” This is a concept that patients can readily grasp.

I often tell my patients: “When a nerve has been irritated for a long time, it becomes hyper-excitable. Its cell membrane is almost ‘quivering,’ ready to fire off a pain signal at the slightest provocation. A membrane stabilizer is like a therapeutic blanket for the nerve. It doesn’t just numb the pain; it calms the nerve, making its membrane more stable and less likely to fire erratically. This allows the nerve to heal and return to a more normal, less painful state.”

This explanation helps patients understand why these medications are not a “quick fix” like an opioid. They are therapeutically altering the nerve’s function over time. This helps foster patience and adherence, which are critical for success with these drugs.

It’s equally important to know which medications don’t have the evidence to support their use for general chronic pain. Two common examples are Lamotrigine (Lamictal), which has no evidence for efficacy in chronic pain, and Topiramate (Topamax), whose only well-established indication in pain management is for migraine prophylaxis.

Gabapentin (Neurontin)

Gabapentin is one of the most prescribed medications for nerve pain. Despite its name, it does not directly act on GABA receptors. Instead, its primary mechanism of action is on voltage-gated calcium channels in the central nervous system.

How does it work?

When a pain signal arrives at the end of a nerve terminal, calcium channels open, allowing calcium to flood into the cell. This influx of calcium triggers the nerve to release excitatory neurotransmitters (like glutamate and Substance P). Gabapentin binds to a specific subunit of these calcium channels (the alpha-2-delta subunit) and partially blocks them. By reducing calcium influx, it decreases the release of those excitatory neurotransmitters. I explain it to patients like this: “Gabapentin slows down the ‘tag,’ reducing how fast and how often the nerve can excite the next one. This gives the whole system a chance to calm down and reset.”

Dosing and Administration:

The most critical principle for prescribing gabapentin is “start low, go slow.” The primary reason for this is to manage side effects, most commonly sedation, dizziness, and brain fog. Starting with a low dose, perhaps 100 mg or 300 mg at bedtime, and gradually titrating up every few days allows the body to acclimate.

Important Considerations for Gabapentin:

• Renal Dosing: Gabapentin is cleared by the kidneys, so the dose must be adjusted in patients with renal impairment.
• Bioavailability: The absorption of gabapentin from the gut relies on a specific transporter system that can become saturated. As the dose increases, the percentage of the drug that is actually absorbed (bioavailability) decreases. It’s a case of diminishing returns.
• Central Sleep Apnea: Gabapentin has been associated with medication-induced central sleep apnea, where the brain fails to send proper signals to the muscles that control breathing during sleep.
• DRESS Syndrome: A rare but very serious adverse reaction is Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS). This is a severe hypersensitivity reaction that typically appears 2-8 weeks after starting the drug.

Pregabalin (Lyrica)

Pregabalin is a close relative of gabapentin with a similar mechanism of action. It also works as a “membrane stabilizer” by binding to the alpha-2-delta subunit of voltage-gated calcium channels.

Key Differences and Dosing:

Pregabalin has a more predictable, linear absorption profile compared to gabapentin; its bioavailability remains high (around 90%) regardless of the dose. This allows for a slightly faster titration schedule. The maximum daily dose is 600 mg, but for many patients, doses above 450 mg per day lead to a disproportionate increase in side effects (like sedation, dizziness, and peripheral edema/swelling) relative to the additional pain relief.

New and Concerning Research:

A very important study published in 2023 has raised new safety concerns. The study looked at patients with diabetic neuropathy and found a significantly increased risk of major adverse cardiovascular events (MACE) over five years in those taking pregabalin (Yoon & Lee, 2023). This finding was then replicated in a second study with fibromyalgia patients. This is a serious consideration, especially since these are the exact patient populations for whom we frequently prescribe this medication.

At Injury Medical Clinic, this new evidence reinforces our commitment not to rely solely on one medication. For a patient with diabetic neuropathy, we would combine a carefully monitored, low-to-moderate dose of a neuropathic agent with chiropractic care to address any spinal misalignments that could be contributing to nerve compression (a “double crush” phenomenon), nutritional counseling and functional medicine interventions to improve blood sugar control and reduce systemic inflammation, and physical rehabilitation. This integrative approach allows us to use lower medication doses, thereby minimizing the risk of long-term side effects.

Repurposing Antidepressants for Pain Relief: A Central Mechanism

One of the most powerful, and often misunderstood, tools in our pain management toolkit is the use of certain types of antidepressants. When I bring this up with a patient, the conversation requires care. “Doc, are you saying this pain is all in my head?” It is our job to reframe the conversation and explain the neurobiology behind why these medications work for pain, entirely independent of their effects on mood.

The Descending Pain Pathway: How Antidepressants Act as True Analgesics

To understand the mechanism, we need to understand the descending pain modulation pathway. Think of it as a set of controls in the brainstem that can turn down the volume of incoming pain signals. When this pathway is activated, it sends signals down the spinal cord, releasing neurotransmitters that inhibit the transmission of the pain signal.

One of the most important neurotransmitters in this descending inhibitory pathway is norepinephrine. Serotonin also plays a role. The antidepressants that are most effective for pain, the Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) and the Tricyclic Antidepressants (TCAs), work precisely by increasing the levels of norepinephrine and serotonin in the central nervous system. By boosting these neurotransmitters, they enhance the function of this natural, descending, pain-dampening system. They are, in effect, amplifying the body’s own ability to control pain.

This is a profound concept to share with patients. We are not telling them the pain is in their head; we are explaining that we are using a medication to leverage a powerful pain-control center already located in their brain and spinal cord.

It is vital to communicate that these drugs have been rigorously studied for pain in patient populations that explicitly excluded individuals with mood disorders (Finnerup et al., 2015). This is the single most important fact to convey to our patients to separate the analgesic effect from the psychiatric one.

The Black Box Warning: An Important Conversation

Before discussing benefits, we must address the Black Box Warning for increased risk of suicidal thoughts and behaviors. This was mandated in response to data in children and adolescents. It’s crucial to provide context to adult patients:

1. Age-Related Risk: The increased risk was observed primarily in children and adolescents. Crucially, in clinical trials involving patients above the age of 24, there was no statistically significant increased risk of suicidality.
2. The “Activation” Effect: The highest risk was in young people, where the theory is that these medications can sometimes increase motivation and energy levels before they improve mood.
3. A Protective Effect in Older Adults: In adults aged 65 and over, antidepressants have been found to have a protective effect against suicidality.

Having this quick, direct, and honest conversation empowers our patients with knowledge and builds trust.

Serotonin Syndrome: Separating Fact from Fear

Another topic that frequently comes up is serotonin syndrome. While real and potentially life-threatening, it is not as common as the fear surrounding it might suggest. It is an acute condition, with symptoms appearing within six hours in 60% of cases.

The diagnosis is standardized using the Hunter Criteria (Dunkley et al., 2003). For a diagnosis, a patient must be taking a serotonergic agent and exhibit specific signs. What you’ll notice is the central role of a very specific neurological sign: clonus (involuntary, rhythmic, muscular contractions). Three of the five diagnostic pathways in the Hunter Criteria require the presence of clonus. We can all test for clonus in about 32 seconds by quickly dorsiflexing the patient’s foot. This allows us to confirm or rule out the condition confidently.

Spotlight on SNRIs: Duloxetine (Cymbalta) for Musculoskeletal Pain

Among the SNRIs, duloxetine (Cymbalta) stands out due to its broad FDA-approved indications for pain:

• Fibromyalgia
• Painful Diabetic Neuropathy
• Chronic Musculoskeletal Pain

That last indication, chronic musculoskeletal pain, is where duloxetine’s role becomes particularly impressive. Duloxetine was shown to significantly improve both pain and function in patients with osteoarthritis (OA) of the knee, with benefits seen as early as four weeks (Argoff & Pauer, 2021). This provides a powerful alternative to NSAIDs for older patients with comorbidities that make long-term NSAID use hazardous. Duloxetine works through a completely different, central mechanism.

The typical target dose for pain is 60 mg once daily. To minimize side effects, particularly nausea, the best practice is to start with a 30 mg dose for the first week. Other SNRIs include Milnacipran (Savella), which is only approved for fibromyalgia, and Venlafaxine (Effexor), which has less robust evidence for pain.

Old School but Relevant: Tricyclic Antidepressants (TCAs)

While largely replaced for mood disorders, tricyclic antidepressants (TCAs) remain an incredibly effective option for certain types of chronic pain, particularly at low doses. Doses for pain are dramatically lower than for depression (e.g., 10-50 mg for pain vs. 75-150 mg for depression), which minimizes side effects like dry mouth, constipation, and cardiac risks.

A clinical tidbit I feel is my personal duty to disseminate is their use for burning mouth syndrome (BMS). This is a chronic, debilitating burning sensation in the mouth, with no visible abnormalities, that typically affects peri-menopausal and older women. The tricyclic antidepressants, above all other medication classes, are what seem to work for it (Patatanian & Divasta, 2011). My typical protocol is to start with 10 mg of nortriptyline at bedtime, titrating up weekly as needed. This simple intervention can be life-changing for these suffering patients.

Re-evaluating Common Prescriptions: Benzodiazepines and Muscle Relaxants

Let’s shift our focus now to other commonly prescribed classes of drugs for pain. When we look closely at the scientific evidence, the rationale for some common practices begins to crumble.

The Misuse of Benzodiazepines in Pain Care

I want to make a clear, direct, and unequivocal statement: Benzodiazepines are not pain medications. While effective for acute anxiety, their role in chronic pain is not only unsupported by evidence but is potentially harmful.

1. Lack of Efficacy for Back Pain: For acute low back pain, benzodiazepines showed a failure to improve pain outcomes. We see diazepam (Valium) prescribed frequently as a “muscle relaxer,” but the evidence does not support this practice for pain relief.
2. Antagonism of Opioid Analgesia: This is a critically important finding. Studies have shown that benzodiazepines can act as antagonists to opioid analgesia (Gudin et al., 2021). They can prevent opioids from working effectively, leading to a dangerous cycle of dose escalation.

The Dangerous Intersection of Benzodiazepines and Opioids

The concurrent use of benzodiazepines and opioids can create a perfect storm of adverse effects. The data on overdose risk is alarming. For patients on high-dose opioids, the overdose rate is ten times higher if they are also taking benzodiazepines (Jones et al., 2012). Over a recent ten-year period, the number of individuals entering substance abuse treatment programs for the concurrent use of these drugs increased by a staggering 570%.

However, we must have a balanced approach. Anxiety is a real and debilitating condition, and we must not avoid its appropriate medical treatment. It’s not about choosing to treat pain or anxiety; it’s about finding safe and effective ways to treat both. This is where an integrative approach shines, utilizing non-pharmacological options like mind-body therapies, chiropractic care to modulate the autonomic nervous system, functional medicine to address biochemical imbalances, and movement therapies.

The Limited Role of Muscle Relaxants in Pain Management

As a drug class, muscle relaxants are not that great for sciatica. Studies have consistently shown that for pain radiating down the leg, they offer no significant benefit over a placebo (van Hees et al., 2019). For acute low back pain without sciatica, they might provide a modest 30% improvement in symptoms for the first week, but the benefit disappears after that.

The prevailing theory for why these drugs seem to help, even modestly, is that they depress the central nervous system (CNS). The perceived benefit is likely due to this generalized sedation.

A Detailed Look at Common Muscle Relaxants

• Diazepam (Valium): A benzodiazepine, not superior to other muscle relaxants, with the significant added risk of dependence and dangerous interactions.
• Cyclobenzaprine (Flexeril): Chemically similar to tricyclic antidepressants (TCAs). Caution is needed in patients with mood disorders (especially bipolar disorder). It has a long half-life and accumulates in the body, leading to a constant state of sedation after just a few days of regular use.
• Tizanidine (Zanaflex): A central alpha-2 adrenergic agonist, similar to clonidine. It has a very short duration of therapeutic effect, which is beneficial as it gives the patient control. They can take it when needed (e.g., at bedtime) and have it wear off by morning, allowing them to function safely during the day.
• Carisoprodol (Soma): Its active metabolite has significant abuse potential, and it was reclassified as a Schedule IV controlled substance. It is generally not a first-line choice.
• Baclofen (Lioresal): Indicated for muscle spasticity, not simple spasms. It works on the GABA-B receptor. Abruptly stopping it long-term can lead to fatal adverse reactions, including seizures and hallucinations. It can also lower the seizure threshold, so I would not recommend it for a patient with a known history of epilepsy.

Emerging and Advanced Pharmacological Strategies

Let’s turn our attention to some of the more exciting and newer players on the pain management scene, as well as a more nuanced look at opioids.

Low-Dose Naltrexone (LDN): An Emerging Tool for Chronic Pain

Low-dose naltrexone (LDN) is a promising development. Naltrexone is an opioid receptor antagonist used at 50mg to treat addiction. However, at a much lower dose (typically 1.5 to 4.5 mg), it appears to have a paradoxical effect.

The primary mechanism by which LDN is thought to help with chronic pain is through its effect on glial cells, the immune cells of the central nervous system. In chronic pain states, these cells become overactivated and release inflammatory chemicals. LDN has been shown to modulate these glial cells, calming their inflammatory response (Younger et al., 2014). This targets the neuro-inflammatory processes that drive chronic pain.

LDN is used for fibromyalgia, long COVID, and autoimmune conditions like Crohn’s disease. Because it is used at such low doses, it must be specially prepared by a compounding pharmacy. The dosing protocol is to start low and go slow, usually beginning at 1.5 mg at bedtime and titrating up to 4.5 mg.

Suzotrigine (VX-548): The New Kid on the Block for Acute Pain

This medication, suzotrigine, was approved by the FDA in February of 2026. It is currently only indicated for the treatment of moderate-to-severe acute pain for up to two weeks.

• Mechanism of Action: It is a selective inhibitor of the NaV 1.8 sodium channel, which is preferentially expressed in pain-sensing neurons. It dampens pain signals at their source without affecting the CNS in the same way opioids do.
• Efficacy: Clinical trial data found its efficacy to be almost equal to the effect of hydrocodone 5 mg taken twice a day (Mackey & Kao, 2022).
• Important Side Effect: Suzotrigine can affect the metabolism of some oral contraceptives, potentially rendering them less effective. It is imperative to counsel patients to use an alternative, non-hormonal form of contraception during treatment and for at least one month after.

A Humanistic View of Opioid Management

The conversation around opioids has become so charged that it’s often difficult to have a rational, patient-centered discussion. They are not stereotypes; they are human beings with complex stories.

• Case Study 1: Mike: A 56-year-old construction worker with lumbar bulging discs and facet arthropathy. He had a heart attack and is on anticoagulants, so he cannot take NSAIDs. Muscle relaxants would sedate him. He remains functional and employed by taking hydrocodone/acetaminophen 10/325mg, one tablet twice a day. For Mike, this low-dose opioid is the tool that allows him to remain functional.
• Case Study 2: Sheila: An 84-year-old woman with a history of spinal fusion and now severe adjacent segment disease. She is not a surgical candidate due to terrible bone density and respiratory issues. She is stable on a regimen of extended-release oxycodone plus a small dose for breakthrough pain. This regimen is what allows her to get out of bed and have quality time with her husband in her final years.

These are the faces of chronic pain. When we discuss opioids, we must remember that we are talking about people who have tried and failed all the other available and appropriate options.

The Science of Opioids and Responsible Prescribing

Opioids work by activating mu, delta, and kappa opioid receptors in the central nervous system. This enhances descending inhibitory pain pathways and dampens ascending signals. However, before prescribing, a systematic process is imperative:

• Did you do a thorough physical exam?
• Did you perform a risk assessment (e.g., SOAP-R tool)?
• Did you rule out “fixable” causes of pain?
• Do you have a medication agreement or “pain contract”?
• Did you check the Prescription Drug Monitoring Program (PDMP)?
• Did you document what the patient has tried and failed?

The Critical Role of Cytochrome P450 in Opioid Selection

The cytochrome P450 (CYP450) system is a family of liver enzymes that metabolize most drugs. Genetic variations can cause these enzymes to work faster (ultra-rapid metabolizers) or slower (poor metabolizers). This profoundly impacts how a patient will respond to certain opioids.

• Opioids that USE the CYP450 system: Oxycodone, Hydrocodone, Fentanyl, Tramadol, Methadone
• Opioids that do NOT use the CYP450 system: Morphine, Hydromorphone (Dilaudid), Oxymorphone (Opana)

Simply by listening to a patient’s experience and knowing the metabolic pathways, you can make a more rational choice. If a patient tells you, “Oxycodone does nothing for me, but Dilaudid works great,” they are probably right, and the reason might be purely metabolic (Smith, 2009).

Special Considerations for Buprenorphine and Methadone

• Buprenorphine (for pain): Formulated as the Butrans patch and Belbuca buccal films. As a partial agonist, it has a “ceiling effect,” meaning less potential for life-threatening respiratory depression. The patch is a great option for older people. It is no longer recommended to stop buprenorphine before surgery.
• Methadone (for pain): A powerful and effective opioid, but it has a very long and variable half-life (8 to 59 hours) while its analgesic effect only lasts 4-8 hours. This disconnect means it can accumulate dangerously if doses are increased too quickly. It also works as an NMDA receptor antagonist, making it effective for neuropathic pain. It can cause QT prolongation, so EKG monitoring is standard practice.

Safe Storage and Disposal of Opioids

Following a typical surgical procedure, about 72% of patients have leftover opioid medications, and 71% of them keep them. These medications often fall into the wrong hands. We must educate patients to get rid of them promptly and properly. The FDA recommends using drug take-back days or, if unavailable, flushing certain high-risk medications like opioids down the toilet to prevent accidental ingestion or diversion.

Managing a Major Side Effect: Opioid-Induced Constipation (OIC)

The most common and bothersome side effect of opioids is opioid-induced constipation (OIC). Do not tell patients on opioids to take bulk-forming agents like Metamucil (psyllium husk). Opioids slow gut movement; adding bulk is like adding more dry cement mix to a bucket of concrete that’s already setting.

We now have PAMORAs (Peripherally Acting Mu-Opioid Receptor Antagonists) like methylnaltrexone (Relistor), naloxegol (Movantik), and naldemedine (Symproic). These drugs block mu-opioid receptors in the gut without interfering with pain relief in the brain. They are brilliant and can be life-changing for patients suffering from OIC.

Naloxone (Narcan): An Essential Safety Tool for Everyone

My philosophy is simple: Naloxone is for a risky drug, not a risky patient. Any patient on long-term opioid therapy should have naloxone available. Accidents happen. Having naloxone in the house is like having a fire extinguisher. The simple act of prescribing naloxone has been shown to decrease the overall overdose rate, likely by increasing patient awareness. It is critical to educate patients and their families that if someone becomes unresponsive, you are not going to hurt them by giving them naloxone.

Final Thoughts: The Art and Science of Pain Management

As we bring this extensive discussion to a close, I want to leave you with some final thoughts on the practice of pain management.

1. Limited Pharmacologic Options Require Creativity: We often need to be creative, trying new combinations of existing medications or revisiting medications a patient tried long ago. Our physiology changes, and something that didn’t work in the past may be worth retrying now.
2. Sometimes It’s About Dosing, Not a New Drug: We don’t always need a new medication. Sometimes, the solution is to look at how and when the patient is taking their current medication. Optimizing their schedule can make a huge difference.
3. Medications Are Only One Component of Care: This is the most important point. Medications are a valuable tool, but they are only one component of a comprehensive care plan. True and lasting relief comes from an integrative approach that includes chiropractic care to address structure, functional medicine to address biochemistry, physical therapy and rehabilitation to restore function, nutrition to reduce inflammation, and mind-body practices to manage the psychological aspects of pain.

Pain management is a journey. It is a process that requires patience, persistence, and partnership between the clinician and the patient. It can be challenging, but it is always worth going through the process to help someone reclaim their life from pain.

Thank you for being with me on this educational journey today.

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