Pain Pharmacology to Treat Chronic Pain in a Clinical Approach

Learn about the pain pharmacology in a clinical approach to improve your knowledge of medications used in pain management.

Abstract

In this educational post, I present an integrated, evidence-based journey through modern pain management from my perspective as a clinician practicing both chiropractic medicine and advanced practice nursing. I explain why pain is a complex physiological and functional experience, how it is generated in the body, and how we can intervene at multiple levels using safe, thoughtful pharmacology and conservative care. I cover foundational analgesics (acetaminophen and NSAIDs); topical agents (topical diclofenac, lidocaine patches, capsaicin including Qutenza); neuropathic modulators (gabapentin, pregabalin); antidepressants used as true pain medicines (duloxetine, milnacipran, venlafaxine, tricyclics); muscle relaxants and their limitations; low-dose naltrexone; modern non-opioid sodium channel modulators; opioids and their careful, patient-centered role; cytochrome P450 metabolism; pharmacogenomics; and opioid-induced constipation solutions. I show how integrative chiropractic care fits into each treatment domain by reducing mechanical nociception, improving biomechanics, and restoring functional movement capacity. I share clinical observations and practice insights from Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, where I collaborate with Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933), our Medical Director and Collaborative Physician, who has over 40 years of experience. In this multidisciplinary model, a physician provides medical direction alongside a chiropractor, enabling safety, precision, and individualized plans for acute and chronic pain, personal injury, and complex conditions. Throughout, I use modern, research-informed methods and provide APA-style in-text citations and linked references.

About Me, Our Team, and Our Integrative Model

I am Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. My clinical path blends chiropractic medicine, advanced practice nursing, functional medicine, and rehabilitation. I treat acute injuries, chronic musculoskeletal pain, neuropathic conditions, spine disorders, and complex cases that benefit from both conservative care and medical oversight.

At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas, I work in a multidisciplinary structure with Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is Board Certified in Internal Medicine, has over 40 years of experience as an internist, and serves as our Medical Director and Collaborative Physician. Her professional identifiers include NPI #1164426749 and Texas MD License #J2933. Our model is common in integrative and injury clinics, where an MD provides medical direction alongside a chiropractor. This supports medication safety, diagnostic precision, and personalized rehabilitation within a unified plan.

How we integrate care:

• I lead chiropractic evaluation and treatment, neuromusculoskeletal diagnosis, functional medicine assessment, and structured rehabilitation.
• Cardenas provides internal medicine oversight, risk stratification, medication safety review, diagnostics, and coordination across comorbid medical conditions.
• Together we integrate functional medicine strategies, personal injury care, advanced topical agents, neuropathic modulators, appropriate antidepressants for pain, activity-based rehabilitation, and education into cohesive, patient-centered plans.

My clinical observations and articles are available at:

• https://pushasrx.com/
• https://www.linkedin.com/in/dralexjimenez/

Pain Is a Process, Not a Pill: How I Frame Care

Pain is not just a number. Pain is a complex physiological and lived experience shaped by tissue injury, inflammatory signaling, nerve excitability, central sensitization, sleep quality, biomechanics, metabolic health, and expectations. Medications are tools, not solutions. The best outcomes arise when medications are used thoughtfully in a multimodal plan that restores movement, function, and resilience.

When I meet a patient in pain, I ask:

• What caused the pain and what tissues or nerves are involved?
• Is inflammation, nerve irritation, instability, or mechanical dysfunction present?
• Is the pain acute, subacute, or chronic, and how does it affect sleep and daily tasks?
• Are metabolic factors (obesity, insulin resistance, systemic inflammation, nutrient status) amplifying sensitivity?
• Are medications helping or creating risk?
• What functional goals matter most?

I focus on functional outcomes:

• Sleeping through the night
• Sitting through a meal without repeatedly standing
• Walking for 15, 30, or 60 minutes
• Returning to work tasks safely
• Driving without severe pain
• Lifting groceries and household items
• Playing with children or grandchildren
• Reengaging in exercise
• Participating in therapy and chiropractic rehabilitation
• Reducing reliance on rescue medications

Modern pain studies consider a 30% to 60% improvement clinically meaningful, especially in chronic pain (Dworkin et al., 2008). In practice, layered improvements from multiple interventions—conservative care, movement retraining, sleep support, anti-inflammatory nutrition, and medication when necessary—combine to produce significant changes in real life.

Measuring Pain Beyond a Scale: Functional Questions and Impact

The zero-to-ten pain scale is useful but incomplete. I pair it with functional questions:

• How long can you sit before pain increases?
• How far can you walk, and can you sleep through the night?
• Can you bend, lift, twist, reach, work a full shift, or drive comfortably?
• Are you avoiding movement due to fear?
• What activity do you most want to return to?

I use validated instruments like the Brief Pain Inventory to assesspain’ss impact on mood, walking, sleep, work, relationships, and enjoyment of life (Cleeland & Ryan, 1994). This moves us from pain intensity to pain impact and ties improvement to meaningful life changes.

Pain Physiology: From Peripheral Signals to Central Experience

Understanding the physiology of pain allows us to intervene intelligently, at the right level, for the right patient.

Key stages:

• Transduction: Tissue injury triggers chemical mediators—prostaglandins, bradykinin, histamine, substance P, cytokines—sensitizing nociceptors.
• Transmission: Signals travel via A-delta and C fibers to the dorsal root ganglia and dorsal horn, ascend via spinothalamic tracts.
• Modulation: Spinal interneurons, descending inhibitory systems (serotonergic, noradrenergic), glial cells, and local circuitry adjust signal intensity.
• Perception: The brain integrates sensory input with context, emotion, and cognition; this shapes the subjective experience.

Two key phenomena:

• Peripheral sensitization: Nociceptors become hyperresponsive at the injury site.
• Central sensitization: Spinal cord and brain amplify pain signaling, producing widespread sensitivity and persistent pain even after local tissues heal (Woolf, 2011).

Clinical relevance:

• Early intervention in the periphery reduces downstream amplification.
• Reducing abnormal mechanical inputs via chiropractic care lowers nociceptor drive and segmental facilitation.
• Targeted pharmacology can adjust inflammatory chemistry and nerve excitability.
• Sleep, stress regulation, and metabolic health influence central sensitization.

Where Integrative Chiropractic Care Fits

My integrative chiropractic approach targets structural biomechanics, neurological function, inflammatory physiology, movement quality, and functional capacity. It is not anti-medication. It aligns conservative care with appropriate pharmacology and medical oversight.

Chiropractic may help by addressing:

• Joint restriction and segmental dysfunction
• Muscle guarding and trigger points
• Postural strain and altered movement patterns
• Nerve irritation from mechanical stress
• Reduced range of motion and compensatory overload
• Functional instability and fear-driven avoidance

Common conservative strategies:

• Spinal and extremity adjustments
• Joint mobilization and flexion-distraction techniques
• Myofascial release and instrument-assisted soft tissue therapies
• Neuromuscular re-education and corrective exercise
• Core stabilization and motor control training
• Gait retraining and postural correction
• Functional movement reintegration

Evidence supports spinal manipulation as an option for certain types of low back pain within multimodal care (Qaseem et al., 2017). For many, chiropractic reduces mechanical pain drivers, improves movement tolerance, and lowers the need for higher-risk medications.

Our Multidisciplinary Model: Internal Medicine Oversight and Safety

At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), our integrated model pairs chiropractic and functional medicine with internal medicine oversight.

Dr. Maria Guadalupe Cardenas, MD:

• Board Certified in Internal Medicine
• NPI #1164426749
• Texas MD License #J2933
• Medical Director and Collaborative Physician
• Over 40 years of experience

Why oversight matters:

Patients often have hypertension, diabetes, kidney disease, liver disease, cardiovascular risk, GI disorders, autoimmune disease, polypharmacy, anticoagulant use, respiratory issues, and age-related factors that influence medication decisions and diagnostics. Our collaboration ensures:

• Medication safety review
• Diagnostic coordination and imaging decisions
• Risk stratification for GI, cardiac, renal concerns
• Referral and specialist coordination
• Integration of conservative care with safe pharmacology

When Medications Cannot Be Avoided: Principles for Use

Medication should not be viewed as “good” or “bad.” The central question is: What is the safest and most effective use of medication while we correct underlying pain drivers?

Use medication when:

• Pain prevents sleep or movement
• Inflammation limits rehabilitation
• Acute injury symptoms are severe
• Daily activities are intolerable
• Conservative care alone is insufficient
• Pharmacologic treatment is medically required

Use medication with a plan:

• Clear goals, risk screening, contraindication checks, interaction review
• Functional outcome tracking
• Time limits when appropriate
• Reassessment and integration with rehabilitation
• Patient education on safety and expectations

Acetaminophen: Benefits, Risks, and Clinical Reasoning

Acetaminophen (paracetamol) is widely used for pain and fever. It appears to work centrally and may involve cyclooxygenase modulation, serotonergic descending pathways, endocannabinoid signaling, and other mechanisms (Graham et al., 2013).

Why I use acetaminophen:

• Mild to moderate pain, headache, musculoskeletal discomfort
• Osteoarthritis symptoms in selected patients
• Fever
• Patients who cannot tolerate NSAIDs or are at higher GI bleeding risk with NSAIDs

Cautions:

• Liver toxicity at excessive doses; adult max commonly cited as 4,000 mg/day
• Risks increase with liver disease, heavy alcohol use, fasting/malnutrition, older age, drug interactions, and accidental overdose.
• Hidden acetaminophen in combination products (cold meds, sleep aids, opioid combos)
• FDA warnings emphasize awareness (U.S. Food and Drug Administration, 2018)

Clinical observation:

Some patients with significant degenerative changes experience meaningful relief from modest doses; others do not. Pain is individualized,d and imaging does not perfectly predict severity or response.

Patient education:

• Read labels for acetaminophen/APAP
• Avoid exceeding daily limits
• Avoid alcohol when dosing
• Report liver disease and all medications to providers
• Never assume OTC means risk-free

Acetaminophen in low back pain:

An RCT found no significant improvement over placebo in acute low back pain (Williams et al., 2014). I consider acetaminophen an adjunct, not stand-alone therapy, and pair it with movement-based care.

NSAIDs: Mechanisms, Trials, Risks, and Individualization

Nonsteroidal anti-inflammatory drugs reduce pain and inflammation by inhibiting cyclooxygenase (COX-1/COX-2), lowering prostaglandin production.

Common NSAIDs:

• Ibuprofen, naproxen, diclofenac, meloxicam, celecoxib, indomethacin, ketorolac, etodolac, nabumetone, piroxicam

Why NSAIDs help:

• Reduce prostaglandin-mediated sensitization
• Lower swelling and improve movement tolerance
• Support rehab participation during flares

Trial duration:

Patients often try one or two doses and stop; a consistent short trial (e.g., around four days) can be reasonable when safe. But not every patient should take NSAIDs even briefly; safety screening is required.

Safety screening:

• Kidney function and hydration
• GI history (ulcer, bleeding)
• Cardiovascular risk, blood pressure
• Anticoagulant/antiplatelet use, steroids
• Age, comorbidities, interactions
• Liver function, pregnancy, allergies, asthma sensitivity

No single best NSAID:

Responses vary due to absorption, half-life, COX selectivity, metabolism, genetic differences, dosing, tissue distribution, and comorbidities.

Gastrointestinal risk:

NSAIDs reduce protective GI prostaglandins (mucus production, bicarbonate, blood flow, mucosal repair), increasing risks of gastritis, ulcers, bleeding, perforation, anemia, and small bowel injury. GI bleeding risk can rise within days in susceptible patients (Lanas & Chan, 2017).

Low-dose aspirin and NSAIDs:

Combining antiplatelet aspirin with NSAIDs increases GI bleeding risk. Certain NSAIDs may interfere with aspirin’s antiplatelet effect depending on timing and choice (U.S. Food and Drug Administration, 2006). We coordinate timing and choices under medical oversight when aspirin is required.

Celecoxib:

A COX-2 selective inhibitor with reduced (not eliminated) GI ulcer risk compared to nonselective NSAIDs (Nissen et al., 2016). Caution in cardiovascular disease, kidney disease, hypertension, sulfonamide allergy, fluid retention, interactions.

Cardiovascular risk:

Non-aspirin NSAIDs can increase blood pressure, fluid retention, heart failure exacerbation, myocardial infarction, and stroke risk; effects may occur early (U.S. Food and Drug Administration, 2015).

Respiratory illness:

NSAID use during acute respiratory infections has been associated with increased cardiovascular risk in certain populations (Wen et al., 2017). We educate patients not to assume they are risk-free.

Kidney function:

NSAIDs can reduce renal perfusion via prostaglandin inhibition, especially in dehydration, CKD, heart failure, liver disease, older age, diuretic use, ACEi/ARB use, or low blood volume states. We review cumulative risks carefully in our multidisciplinary model.

Chiropractic and rehab to reduce NSAID reliance:

Pain driven by mechanical overload often recurs if biomechanics remain uncorrected. Chiropractic and rehabilitation improve joint motion, reduce abnormal loading, activate muscles properly, restore movement confidence, reduce guarding, and improve posture and tissue tolerance—thus reducing recurrence and repeated medication reliance.

Balancing Body and Metabolism- Video

Topical Agents: Local Relief with Lower Systemic Exposure

Topical therapies target peripheral nociception early in the cascade, often with better safety profiles for older adults or those with GI/cardiac risks.

Topical diclofenac:

• Gel and patches inhibit COX, reducing local prostaglandin synthesis
• Comparable efficacy to oral NSAIDs for certain localized musculoskeletal pain with lower systemic absorption (Derry et al., 2015; Moore et al., 2012)
• Ideal for hand and knee osteoarthritis, soft-tissue injuries; consistent application matters
• Practical tip: apply gel and allow about 20 minutes before washing hands
• Patches useful for acute strains, sprains, contusions, and low back flare-ups while we correct mechanics

Lidocaine patches:

• 5% patches modulate voltage-gated sodium channels in hyperexcitable peripheral nerves
• Effective in postherpetic neuralgia and focal neuropathic pain, improving comfort and sleep (Galer & Jensen, 1997)
• Typical use: 12 hours on, 12 hours off; monitor skin integrity and rotate sites

Capsaicin:

• Targets TRPV1, produces initial burning followed by desensitization and reduced substance P signaling
• OTC formulations help localized neuropathic pain, peripheral joint discomfort, scar hypersensitivity
• In-office Qutenza (8%) for postherpetic neuralgia and diabetic neuropathy; applied every ~3 months, often 30–60 minutes per session (Baron et al., 2010; Ziegler et al., 2017)
• We coordinate authorization and medical necessity; pair with desensitization and graded movement to consolidate gains

Selective compounded topicals:

• Clonidine gel (alpha-2 agonist) for complex regional pain syndrome in selected cases, under careful oversight
• Magic mouthwash for mucositis or burning mouth presentations, tailored formulations coordinated with medical review and functional medicine to support mucosal integrity

Integration with chiropractic:

• Topicals provide immediate local symptom relief while I correct joint mechanics, reduce myofascial drivers, and normalize movement patterns—combining chemical and mechanical relief.

Neuropathic Modulators: Membrane Stabilizers and Pain Signaling

Neuropathic pain arises from nerve injury or dysfunction and presents as burning, electric shocks, tingling, numbness with pain, radiating, dermatomal distributions, and hypersensitivity. Membrane stabilizers reduce excitatory neurotransmitter release and dampen abnormal signaling.

Gabapentin:

• Binds alpha-2-delta subunit of voltage-gated calcium channels; reduces presynaptic excitatory neurotransmitters (Finnerup et al., 2015)
• Indicated for postherpetic neuralgia; widely used off-label in neuropathic and mixed pain
• Start low, go slow; renal dosing adjustments; extended-release options (Gralise, Horizant) can smooth pharmacokinetics
• Bioavailability decreases at higher doses; more is not linearly better
• Rare hypersensitivity (DRESS); educate about fever, rash, systemic symptoms; screening for sleep apnea or respiratory compromise if indicated
• Patient explanation: gabapentin slows the excitatory “tag” between nerve segments, allowing quivering nerves to normalize

Pregabalin:

• Similar alpha-2-delta mechanism; steadier kinetics with faster steady-state (48–72 hours), titrate no sooner than every 48 hours
• BID or TID schedules; max 600 mg/day, with benefits often plateauing above 450 mg/day
• Screen cardiovascular risk and comorbidities; monitor edema, weight, dizziness
• Integrate with chiropractic adjustments, nerve gliding, graded movement, sleep hygiene, stress regulation, anti-inflammatory nutrition.

Lamotrigine and topiramate:

• Lamotrigine lacks meaningful evidence in chronic pain; topiramate is primarily for migraine prevention, not general chronic pain. Match the mechanism to the condition rather than generalize.

Integration with chiropractic:

• Neuropathic modulators calm excitability; chiropractic reduces mechanical nociception, improves kinematics, resolves trigger points, and removes peripheral drivers—dual targeting of chemical and mechanical pain.

Antidepressants as Pain Medications: Descending Inhibition and Central Sensitization

Some antidepressants are real pain medications because they enhance descending inhibitory pathways (serotonin-norepinephrine) that dampen incoming pain signals.

Duloxetine:

• SNRI with evidence for chronic musculoskeletal pain, fibromyalgia, painful diabetic neuropathy, chronic low back pain, and osteoarthritis knee pain (Finnerup et al., 2015; Chappell et al., 2009; Skljarevski et al., 2010)
• Strengthens descending inhibition; particularly valuable for patients who cannot use NSAIDs long-term due to GI, cardiovascular, renal, or anticoagulation risks
• Dosing strategy: start 30 mg daily for about a week, then increase to 60 mg daily if tolerated

Milnacipran:

• SNRI primarily indicated for fibromyalgia; stronger norepinephrine activity may feel activating
• Monitor for agitation, tremor, tachycardia, insomnia, sweating, blood pressure changes
• Even 30% pain reduction can meaningfully improve function and quality of life

Venlafaxine:

• Limited evidence for painful diabetic neuropathy; not typically first choice for pain

Tricyclic antidepressants (TCAs):

• Amitriptyline, nortriptyline, desipramine, imipramine
• Low-dose pain strategy (e.g., 10 mg qHS) due to anticholinergic side effects and cardiac risk at higher doses; watch for QT prolongation and interactions via cytochrome P450
• Trial requires 6–8 weeks; educate patients on realistic timelines

Burning mouth syndrome:

• Persistent burning without visible lesions; peripheral nerve dysfunction and central processing changes implicated
• Low-dose TCAs (e.g., nortriptyline) may reduce neuropathic signaling; gradual titration up to around 50 mg when appropriate

Safety conversations:

• Antidepressant black box warning about suicidality risk—especially ages 18–25—requires clear, calm education and close monitoring (U.S. Food and Drug Administration, 2004)
• Serotonin syndrome: rare but serious; timing often within hours of dose changes or interactions. Use Hunter criteria—clonus and hyperreflexia are more specific than vague symptoms (Dunkley et al., 2003)

Integration with chiropractic and rehab:

• Medication reduces pain intensity and central amplification; chiropractic and rehabilitation restore joint motion, muscle activation, gait, posture, load tolerance, daily function, and sleep—comprehensive recovery requires both.

Muscle Relaxants: Evidence, Mechanisms, and Clinical Caution

Muscle relaxants often provide short-term symptom relief via global CNS depression rather than targeted peripheral spasm relief. They are not effective for radicular leg pain and only modestly helpful for localized acute low back pain in the first week (van Tulder et al., 2003).

Diazepam:

• Benzodiazepine with dependence risk and additive CNS depression; not superior for muscle spasms compared to alternatives. We rarely use it except for specific short-term indications.

Cyclobenzaprine:

• Structurally similar to TCAs; screen for mood disorders (e.g., bipolar). Accumulates with TID dosing and reaches steady-state CNS depression in days, increasing fall and cognitive risk in older adults.

Tizanidine:

• Central alpha-2 adrenergic agonist; indicated for spasticity rather than simple strains. Short therapeutic duration can be useful for strategic nighttime dosing.

Carisoprodol:

• Schedule IV; high abuse potential via meprobamate metabolite. Rarely a first-line choice.

Baclofen:

• GABA-B agonist; indicated for spasticity. Abrupt discontinuation can trigger severe withdrawal (including seizures), especially in intrathecal pump patients—medical emergency if malfunction occurs. Use caution in diabetes (hyperglycemia), psychiatric comorbidity, and seizure risk.

Integration with chiropractic:

• We prioritize spinal adjustments, mobilization, neuromuscular re-education, myofascial therapies, breathing mechanics, and graded movement to address the underlying mechanical drivers of muscle guarding.

Low-Dose Naltrexone: Glial Modulation and Neuroinflammation

Low-dose naltrexone (LDN) at 1.5–4.5 mg acts differently than standard-dose naltrexone (50 mg). LDN appears to modulate glial cell activity, reducing neuroinflammation and central sensitization,n while transient receptor blockade may upregulate endogenous endorphins and receptor sensitivity (Patten et al., 2018).

Clinical applications:

• Fibromyalgia: pain, fatigue, sleep disturbances respond in select patients
• Long COVID: neuroinflammatory features make LDN logical
• Autoimmune conditions (e.g.Crohn’s’s disease): promising data includes objective endoscopic improvement in some cases

Dosing:

• Start ~1.5 mg at bedtime, titrate to ~4.5 mg over weeks; requires compounding pharmacy

Surgical or emergency analgesia:

• Due to low dose and brief receptor occupancy, standard opioid dosing in emergencies remains effective—receptor blockade is surmountable.

Integration with chiropractic and functional medicine:

• We pair LDN with conservative care, anti-inflammatory nutrition, sleep retraining, stress regulation, and graded exercise to target both neuroinflammation and mechanical contributors.

Modern Non-Opioid Sodium Channel Modulators: Nav1.8 Selectivity

A newer non-opioid analgesic class targets peripheral sodium channels, notably Nav1.8, aiming to block pain signal transmission at the source without CNS opioid effects (Park & Ho, 2022).

Key points about suzotregine (VX-548):

• Indication: short-term management of acute pain; typical treatment course is two weeks
• Dosing: a 100 mg loading dose, followed by 50 mg twice daily
• Efficacy: comparable to hydrocodone 5 mg BID; not superior but aligns with a non-scheduled profile
• Access: some insurers require prior hydrocodone trial, which is counterintuitive; we advocate for rational approvals
• Interaction: may reduce effectiveness of oral contraceptives; counsel patients to use alternative reliable contraception during therapy and at least one month after

Integration:

• We use this option strategically in acute scenarios while prioritizing biomechanical correction, movement-based care, and medical oversight for comprehensive safety.

Opioids: Patient-Centered, Guardrailed, and Integrated Use

Opioids remain necessary for some patients who have exhausted other options or have contraindications to alternatives. My approach is measured, careful, and function-focused.

Mechanisms:

• Mu, delta, kappa receptors modulate ascending and descending pathways; primary analgesia and respiratory/euphoric effects via mu; GI motility slows via GI mu receptors.

Buprenorphine:

• Partial mu agonist, kappa antagonist; ceiling effect on respiratory depression; useful in pain formulations like Butrans patch and Belbuca films (Argoff, 2020)
• Weekly Butrans patch dosing can be ideal for elderly or cognitively vulnerable patients
• Current guidance supports continuing buprenorphine through surgery with post-op pain managed on top

Methadone:

• Mu opioid and NMDA receptor modulation; potent, inexpensive, but dangerous without experience due to long, variable half-life vs short analgesic duration—risk of accumulation and delayed overdose
• Outpatient titration must be slow; monitor QT prolongation
• Unique conversion ratios demand expertise; sometimes beneficial at low doses in carefully selected chronic pain

Cytochrome P450 and pharmacogenomics:

• CYP450 variability (inhibitors/inducers) drastically affects opioid metabolism; slow metabolism increases drug effect; rapid metabolism reduces effect (Crews et al., 2021)
• Clinical observation can substitute for pharmacogenetic testing in many cases: a patient who poorly tolerates oxycodone (CYP3A4/2D6) but responds to morphine or hydromorphone (glucuronidation pathways) provides metabolic clues
• Equianalgesic charts are guides, not absolutes—apply judgment based on metabolism and patient history

Benzodiazepines are not pain medications:

• They reduce anxiety and perception of spasm via global CNS depression but do not treat pain mechanisms; co-prescription with opioids increases overdose risk and may diminish opioid analgesia (Jones et al., 2012; National Institute on Drug Abuse, 2024)

Pre-prescribing safety checklist:

• Comprehensive exam and mechanism-focused diagnosis
• Validated risk screening (e.g., SOAP-R, ORT, CAGE-AID)
• Exhaust fixable causes and non-pharmacologic measures
• Medication agreement outlining expectations and risks
• PDMP check for controlled substance history
• Meticulous documentation of tried/failed therapies and contraindications (e.g., anticoagulated patient cannot use NSAIDs)

Patient narratives:

• “Mike,” a 56-year-old construction worker with bulging discs, facet arthropathy, prior MI, anticoagulants; hydrocodone 5 mg BID allows him to function at work and at home
• “Sheila,” 84-year-old with prior lumbar fusion, adjacent segment disease, poor bone density, respiratory issues—not a surgical candidate; stable ER oxycodone twice daily plus short-acting Percocet for breakthrough pain provides mobility and quality time

Opioid-induced constipation (OIC):

• Mu receptors in the gut decrease motility and secretions, increase water absorption—do not rely on bulk agents alone
• Assess frequency, stool form, completeness of evacuation, comfort
• Peripherally acting mu-opioid receptor antagonists (PAMORAs) like methylnaltrexone (Relistor), naloxegol (Movantik), naldemedine (Symproic) reverse GI effects without crossing the blood-brain barrier or reducing CNS analgesia (Webster, 2017)

Naloxone:

• “Naloxone is for a risky drug, not a risky patient.” Prescribing naloxone reduces overdose rates through awareness and preparedness; educate families on use, repeat dosing, and always call 911 (prescribetoprevent.org)

Integration with chiropractic and rehabilitation:

• Even when opioids are needed, they are only one part of care. My focus remains on correcting mechanics, restoring movement, strengthening capacity, and reducing systemic drivers—aiming to lower doses and improve quality of life.

Cytochrome P450, Opioids, and Personalized Pharmacology

The CYP450 enzyme system metabolizes many pain medications. Differences in genetic expression, inflammation, diet, age, comorbidities, and drug interactions modify enzyme activity. Relevant enzymes include CYP2D6, CYP3A4, CYP2C9, and CYP2C19.

Why CYP2D6 matters:

• Codeine requires CYP2D6 conversion to morphine; poor metabolizers gain little benefit, ultra-rapid metabolizers risk toxicity
• Tramadol also needs CYP2D6 for an active metabolite
• Hydrocodone and oxycodone are influenced by CYP metabolism and drug interactions

Pharmacogenomics:

• Patients may be poor, intermediate, normal, or ultra-rapid metabolizers, shaping analgesic response and risk (Crews et al., 2021)
• We combine clinical observation, medication history, and, when appropriate, pharmacogenetic testing to tailor therapy

Clinical approach:

• Consider alternative opioids metabolized via glucuronidation (morphine, hydromorphone) in suspected CYP interactions
• Use equianalgesic tables as flexible guides
• Reassess diligently after medication changes; track both pain and function

Functional Medicine: Systems Biology in Pain Recovery

Pain may be local, but recovery is systemic. Functional medicine asks: In what biological terrain is this pain and injury healing?

Metabolic inflammation and pain:

• Visceral adiposity produces inflammatory cytokines (TNF-alpha, IL-6, CRP-related signaling) and leptin-mediated immune modulation that amplifies pain sensitivity and slows tissue repair
• Insulin resistance and hyperglycemia impair healing and neuropathic recovery

Nutrition and tissue repair:

• Adequate protein, essential fatty acids, vitamin C, vitamin D, magnesium, zinc, B vitamins, hydration, and stable blood sugar support collagen synthesis, immune function, and mitochondrial energy production
• Correcting micronutrient deficits enhances resilience and rehabilitation tolerance

Sleep and pain:

• Poor sleep increases pain sensitivity, reduces repair, worsens mood, and impairs immune regulation
• Sleep support includes consistent schedules, reduced late screen exposure, caffeine timing, breathing exercises, pain-positioning strategies, magnesium assessment, apnea screening, stress reduction, and medical evaluation when insomnia persists

Gut and neuroimmune crosstalk:

• Microbiome dysbiosis can influence systemic inflammation and central pain modulation
• Dietary fiber, polyphenols, and targeted probiotics may contribute to better inflammatory tone

Integration with chiropractic and rehab:

• Systems biology supports my mechanical and neurological interventions by lowering baseline inflammatory load and improving recovery capacity.

Personal Injury Care: Mechanisms, Documentation, and Integrated Treatment

In motor vehicle collisions and occupational accidents, patients often present with whiplash-associated disorders, cervical and lumbar sprain-strain, disc irritation, radicular symptoms, headaches, shoulder/hip/knee trauma, myofascial pain, sleep disruption, and post-traumatic stress.

Our role:

• Evaluate neuromusculoskeletal injury, document functional impairment, coordinate imaging, and integrate conservative care under medical oversight
• Use topical diclofenac patches for acute pain and swelling; gentle mobilization and motor mapping to prevent chronicity
• Incorporate anti-inflammatory nutrition and sleep support to accelerate healing
• Progress to motor control training, eccentric loading for tendinopathies, and staged return-to-work plans

Documentation includes:

• Mechanism of injury, symptom onset, ROM, orthopedic and neurological findings
• Functional limitations, imaging indications, treatment response, activity modifications, rehab progression
• Care plans often require coordination with legal and insurance documentation—our focus remains patient-centered and function-tracked

Complex Pain Syndromes: CRPS, Postherpetic Neuralgia, Diabetic Neuropathy

Complex regional pain syndrome (CRPS):

• Approach sympathetic modulation via alpha-2 agonists (selected compounded topicals), nerve glides, desensitization, and careful graded exposure
• Chiropractic uses gentle, non-provocative mobilization to reduce peripheral inputs without triggering flares
• Medical oversight monitors autonomic features and medication safety; interdisciplinary referrals coordinated when needed (Deer et al., 2017)

Postherpetic neuralgia:

• Lidocaine patches for dermatomal stabilization; capsaicin/Qutenza for TRPV1 desensitization
• Thoracic mobilization and breathing mechanics reduce intercostal strain and discomfort

Diabetic neuropathy:

• Capsaicin-based therapy in refractory cases; pregabalin with cardiovascular risk evaluation
• Functional medicine focuses on glycemic control, micronutrients, and lifestyle changes to improve nerve health

Patient Education: Empowerment Through Understanding

I emphasize a clear narrative of how treatments act along the peripheral-to-central pain pathway:

• Topical agents target prostaglandins, histamine, CGRP, sodium channels (local chemistry)
• Neuropathic modulators stabilize presynaptic calcium channel activity (nerve excitability)
• Antidepressants bolster descending inhibition (central modulation)
• Chiropractic and rehabilitation correct joint mechanics, normalize proprioception, reduce mechanical nociception (peripheral driver reduction), and improve function

Expectations:

• Some benefits are immediate (topicals); others require time (gabapentin/pregabalin, duloxetine, tricyclics, LDN)
• Medication reduces barriers to movement; conservative care builds capacity
• We measure outcomes by function, sleep, activity tolerance, and quality of life—not just pain scores

Clinical Observations from My Practice

From Injury Medical Clinic PA:

• Consistent topical diclofenac gel in hand osteoarthritis, combined with finger joint mobilizations and tendon gliding, produces meaningful pain relief and dexterity improvements for craftspeople and office workers (Moore et al., 2012).
• Lidocaine patches over thoracic dermatomes after shingles reduce clothing-related allodynia; rib mobilization, diaphragmatic breathing, and gentle thoracic extension restore sleep and daily comfort (Galer & Jensen, 1997).
• Capsaicin creams help scar hypersensitivity when paired with graded tactile desensitization and gentle stretching; Qutenza yields significant relief after two sessions when carefully managed (Baron et al., 2010; Ziegler et al., 2017).
• Gabapentin with slow titration reduces nocturnal paresthesia; combining sleep hygiene and cervical adjustments for thoracic outlet-like symptoms improves overall neural function (Finnerup et al., 2015).
• Pregabalin benefits patients with fibromyalgia-like neural excitability; I pair it with low-load movement, autonomic downregulation, and anti-inflammatory nutrition to reduce flares and enhance function (Finnerup et al., 2015).
• Duloxetine in chronic musculoskeletal pain may reduce reliance on NSAIDs in patients with comorbid GI or cardiovascular risks, while chiropractic and rehabilitation restore motion and capacity (Chappell et al., 2009; Skljarevski et al., 2010).

A Day in Our Collaborative Clinic

• Initial evaluation: I assess biomechanics, movement patterns, and pain distribution; Dr. Cardenas reviews medical history, medications, and orders labs or imaging when indicated.
• Treatment plan: We discuss topical options, neuropathic modulators, antidepressants for pain, chiropractic care, and rehab; patients leave with clear dosing and application schedules plus movement prescriptions.
• Follow-ups: We jointly review outcomes, adjust medications or topicals, progress exercises, and reinforce ergonomics. We track patient-reported outcomes, ROM, strength, endurance, and meaningful activities.

Building Layered, Mechanism-Matched Plans

We combine:

• Peripheral chemistry control (topicals)
• Neural membrane stabilization (gabapentin, pregabalin)
• Descending inhibition enhancement (duloxetine, selected SNRIs/TCAs)
• Mechanical correction (chiropractic adjustments and mobilization)
• Tissue health optimization (soft tissue therapy, graded loading)
• Movement retraining (rehabilitation and motor control)
• Systems biology support (functional medicine: sleep, nutrition, glycemic control, stress physiology)
• Internal medicine oversight (risk management, diagnostics, interactions, comorbid care)

This multimodal plan targets the full arc from pain initiation to perception.

Safety Principles I Emphasize With Pain Medications

• Use the lowest effective dose for the shortest appropriate duration
• Match medication to mechanism and patient risk profile
• Review all current medications and supplements for interactions
• Consider liver, kidney, heart, and GI risks
• Avoid duplicate therapy and be cautious with combination products
• Educate patients on OTC risks and hidden ingredients
• Track function and participation in daily life, not only pain intensity
• Pair medication with rehabilitation and chiropractic
• Reassess frequently and taper appropriately
• Refer for red flags and coordinate care beyond our clinic when needed

Red Flags: Urgent Evaluation Needed

• New bowel or bladder dysfunction, saddle anesthesia, progressive weakness
• Fever with severe spine pain, unexplained weight loss
• History of cancer with new severe pain, major trauma, suspected fracture
• Chest pain, shortness of breath, stroke signs
• Severe abdominal pain, sudden “worst headache,” infection signs after procedure or injury

Medication should never mask serious pathology.

Why Evidence-Based Integrative Care Matters

Modern guidelines for low back pain emphasize non-pharmacologic foundations—exercise, spinal manipulation, rehabilitation, patient education—with judicious pharmacology when necessary (Qaseem et al., 2017). Medication can reduce symptoms; chiropractic improves mechanics; rehabilitation restores capacity; functional medicine reduces systemic contributors; internal medicine oversight improves safety; patient education reduces fear and improves adherence.

This is how we move from symptomatic relief toward durable recovery.

Final Thoughts: A Practical, Safer Journey Through Pain Management

When medications cannot be avoided, use them thoughtfully and always in context. Acetaminophen may help some patients but requires liver safety education. NSAIDs can be effective for inflammatory pain but demand careful GI, cardiovascular, renal, and interaction risk management. Topicals, neuropathic modulators, and selected antidepressants are powerful when matched to mechanism. Low-dose naltrexone and modern sodium channel modulators expand non-opioid options. Opioids retain a role in select, carefully managed cases—with clear guardrails, naloxone availability, and peripherally acting mu-opioid receptor antagonists for constipation. Throughout, I integrate chiropractic care, functional medicine, rehabilitation, and personal injury services under internal medicine oversight.

At Injury Medical Clinic PA in El Paso, Texas, our multidisciplinary model—MD medical direction alongside chiropractic—supports safety, precision, and patient-centered outcomes. Pain management is a journey. My goal is not only to reduce pain but to restore movement, improve function, protect patient safety, and help each patient return to a more active and meaningful life.

References

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• Duloxetine for Osteoarthritis Knee Pain Chappell, A. S., Desaiah, D., Liu-Seifert, H., Zhang, S., Skljarevski, V., Belenkov, Y., Brown, J. P., & Spaeth, M. (2009). A double-blind, randomized, placebo-controlled study of the efficacy and safety of duloxetine for the treatment of chronic pain due to osteoarthritis of the knee. Pain Practice, 9(4), 285–295.
• Duloxetine in Chronic Low Back Pain Skljarevski, V., Zhang, S., Desaiah, D., Alaka, K. J., Palacios, S., Miazgowski, T., & Patrick, K. (2010). Duloxetine versus placebo in patients with chronic low back pain: A 12-week, fixed-dose, randomized, double-blind trial. The Journal of Pain, 11(12), 1282–1290.
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• Low-Dose Naltrexone in Chronic Pain Patten, D. K., Schultz, B. G., & Berlau, D. J. (2018). The safety and efficacy of low-dose naltrexone in the management of chronic pain and other co-morbid symptoms: A systematic review. Scandinavian Journal of Pain, 18(2), 9–21.
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