Tools to Reduce & Manage Pain | Dr. Sean Mackey

Nociceptors in skin, muscle, and viscera detect heat, pressure, chemical changes, etc., and send electrical signals (nociception) via A-delta and C fibers to the spinal cord and then the brain. Those signals are *not* pain by themselves; pain only emerges when those inputs are integrated with emotion, cognition, memory, and context in distributed brain networks (insula, cingulate, amygdala, thalamus, cortex). This explains why the same injury can feel very different across people and situations, and why beliefs, anxiety, and attention can dramatically change pain.

A central clinical and self-management principle is separating painful sensations (hurt) from ongoing tissue damage (harm). Many chronic pain conditions (e.g., Morton's neuroma, stable chronic back pain) are *very* painful but not structurally worsening; activity may hurt but is not damaging. Conversely, some injuries (fractures, unstable spine, heart attack) represent real harm and require protection or urgent care. Getting accurate medical evaluation, then reframing safe pain as non-dangerous, can unlock function (e.g., Mackey’s tennis patient who returned to play once he understood his foot pain was not harmful).

NSAIDs (ibuprofen, naproxen, aspirin) reduce inflammation and peripheral sensitization (anti-hyperalgesic) but are not classic analgesics; they act on COX/prostaglandin pathways in periphery, spinal cord, and brain. They can delay tissue healing (e.g., bone, post-arthroplasty) and carry GI, kidney, and cardiac risks—use lowest effective dose, with food, and consult a clinician if you have comorbidities. Acetaminophen acts centrally, is easier on the stomach but can damage the liver above ~4 g/day, especially with alcohol. Opioids can be life-changing for a subset of patients but also highly addictive and dangerous; they should generally not be first-line for chronic pain, require careful individualized prescribing, and must be clearly separated from illicit fentanyl driving the current overdose epidemic.

Melzack and Wall’s gate control theory plus descending inhibition explain why rubbing, shaking, or running water over an injury reduces pain: fast A-beta touch fibers and brainstem pathways inhibit nociceptive transmission in the spinal cord. TENS units exploit the same mechanism with electrical stimulation. Cold can reduce pain by decreasing inflammatory mediator release and slowing nerve conduction; heat increases blood flow, relaxes muscles, and often feels soothing. For acute injuries, cold is typically emphasized in the first ~48 hours and heat later, but there is individual variability—use what helps, avoid extremes (e.g., frostbite, burns), and remember that movement and sleep quality are critical for healing.

Chronic pain often leads to activity avoidance, deconditioning, and a boom-bust cycle: doing too much on good days, crashing on bad days, then developing fear of movement. Mackey emphasizes pacing: set small, consistent, progressive goals (e.g., walk 1 block daily, then 1.5, then 2), cap activity even on very good days, and resume gently after flares. Pain-trained physical and occupational therapists can guide safe progression, correct biomechanics, and help distinguish hurt from harm. Interventions like nerve blocks and meds should be used to *enable* increased functional rehab, not as stand-alone fixes.