Management of chronic / persistent pain in the elderly; classification and pathophysiology of pain; role of palliative care

Chronic (persistent) pain is pain that persists or recurs for more than 3 months, beyond the expected period of tissue healing. It is regarded as a disease in its own right, not merely a symptom.

Prevalence rises steeply with age — roughly 25–50% of community-dwelling older adults and up to 80% of long-term care residents. Commonest causes: osteoarthritis, degenerative spine disease, osteoporotic vertebral fracture, diabetic neuropathy, post-herpetic neuralgia, peripheral arterial disease and cancer.

Pain in older people is under-reported, under-diagnosed and under-treated. Barriers include the belief that pain is a normal part of ageing, fear of being labelled "difficult", fear of what the pain signifies, fear of addiction, cognitive and sensory impairment, and the clinician assumption that older patients feel less pain — for which there is very little evidence.

Mechanistic (IASP) classification — three types:

Nociceptive — nociceptor activation by actual or threatened tissue damage.

Somatic (skin, bone, joint, muscle, connective tissue) → well localised, constant; aching, throbbing, gnawing, stabbing. Examples: arthritis, fracture, bone metastases.

Visceral (internal organs) → diffuse, poorly localised, referred, intermittent; colicky, cramping, squeezing, often with nausea, vomiting and sweating. Examples: renal colic, bowel obstruction.

Neuropathic — lesion or disease of the somatosensory nervous system, with abnormal processing of sensory input → burning, tingling, shooting, electric-shock-like, with paraesthesia, dysaesthesia, allodynia, hyperalgesia, sensory loss, weakness or altered reflexes. Examples: diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, radiculopathy, post-stroke central pain.

Nociplastic — pain from altered nociception without demonstrable tissue damage or somatosensory lesion. Examples: fibromyalgia, myofascial pain syndrome, complex regional pain syndrome.

Other axes of classification — by duration (acute <1 month, subacute, chronic >3 months); by aetiology (cancer versus non-cancer); by ICD-11 (chronic primary pain versus chronic secondary pain). Most persistent pain in older people is mixed.

Special categories to recognise: breakthrough (incident) pain, procedural pain, and "total pain" — physical + psychological + social + spiritual suffering.

Four processes of nociception:

Transduction — noxious stimulus converted into an electrical impulse at peripheral nociceptors. A-delta fibres carry fast, sharp, localised pain; C fibres carry slow, dull, burning pain. Mediators: prostaglandins, bradykinin, substance P, histamine, serotonin, hydrogen ions and ATP (the "inflammatory soup").

Transmission — impulse passes via the dorsal root ganglion → dorsal horn (laminae I, II, V) → spinothalamic tract → thalamus → somatosensory cortex. Key dorsal-horn transmitters are glutamate (NMDA receptor) and substance P (NK1 receptor).

Perception — conscious awareness in cortex and limbic system; explains the affective and emotional dimension of pain.

Modulation — descending inhibitory pathways from the periaqueductal grey and rostral ventromedial medulla, using endogenous opioids, noradrenaline, serotonin and GABA. The gate control theory (Melzack and Wall) explains how large A-beta fibre input inhibits nociceptive transmission at the dorsal horn — the basis of TENS, rubbing and massage.

Transition from acute to chronic pain:

Peripheral sensitisation — inflammatory mediators lower the nociceptor threshold → primary hyperalgesia.

Central sensitisation — repetitive C-fibre input produces "wind-up" via NMDA receptor activation, increasing dorsal-horn excitability and expanding receptive fields → secondary hyperalgesia and allodynia.

Loss of descending inhibition, glial activation, and maladaptive cortical reorganisation then maintain pain independently of the original injury.

Age-related changes in the nociceptive system: reduced density of myelinated and unmyelinated peripheral fibres, slowed conduction, reduced substance P and CGRP, and impaired descending inhibitory modulation with reduced endogenous opioid function. The net effect is that pain threshold may be marginally raised but tolerance is reduced, sensitisation occurs more readily, and established pain resolves more slowly. Older people are therefore more vulnerable to persistent pain, not less sensitive to it.

Consequences of untreated pain — depression, anxiety, sleep disturbance, anorexia and weight loss, deconditioning, immobility, falls and fractures, functional decline, social isolation, delirium, increased healthcare use and caregiver burden. Pain is a key reversible cause of agitation in dementia.

AGS recommends that every older person be screened for persistent pain on initial presentation or admission to any healthcare service; anyone whose pain affects physical function, psychosocial function or quality of life needs a comprehensive pain assessment. Pain is treated as the "fifth vital sign".

History — site and radiation, character, timing, aggravating and relieving factors; relationship of pain to physical and social function and sleep; complete analgesic history (prescribed, over-the-counter, alternative remedies, alcohol, side effects); patient's attitudes and beliefs about pain and its treatment; effectiveness of and satisfaction with current management; social support and access to healthcare. Examination — the painful site and common referral zones; focused musculoskeletal and neurological examination; observation of physical function; psychological and cognitive assessment.

Measurement tools:

Cognitively intact — self-report is the gold standard. The numerical rating scale (0–10) is the most suitable in older people; verbal descriptor scales, pain thermometer and faces scales are also validated. Visual analogue scales are the least reliable. Always use the same scale on follow-up.

Cognitively impaired or non-verbal — use observational tools: Abbey Pain Scale, PAINAD, DOLOPLUS-2, plus caregiver report. Assess during movement, assess frequently (poor recall), and treat any unexplained behavioural change in advanced dementia as possible pain until proved otherwise.

Set realistic, function-based goals (better sleep, mobility and participation — not zero pain). Use a multimodal, multidisciplinary, biopsychosocial approach. Treat the underlying cause where possible. Follow the geriatric rule of the fewest agents, by the least invasive route, at the lowest effective dose — start low, go slow, but go. Give analgesia regularly ("by the clock") for constant pain, with breakthrough doses. Review, titrate, and deprescribe what does not work.

Non-pharmacological measures are first-line and are always combined with drugs: patient and caregiver education; structured exercise and physiotherapy (strengthening muscles around the joint, aerobic and balance training); weight reduction; occupational therapy — walking aids, appropriate footwear, joint protection, environmental modification; heat and cold; massage, TENS, acupuncture; relaxation, guided imagery, distraction, music; and psychological therapy — cognitive behavioural therapy (CBT), mindfulness and support groups.

Non-opioids:

Paracetamol — first-line for mild-to-moderate musculoskeletal pain. Maximum 4 g/24 h; reduce to 2–3 g/day in frailty, low body weight, hepatic impairment or regular alcohol use.

NSAIDs — effective for inflammatory, bone and visceral pain, but hazardous in the elderly: GI bleeding and peptic ulcer, acute kidney injury, fluid retention, heart failure, hypertension, and multiple drug interactions. Use the lowest dose for the shortest time, prefer topical formulations, co-prescribe a PPI if systemic use is unavoidable.

Topical agents — capsaicin, lidocaine 5% patch, diclofenac gel, ketamine or combination gels; minimal systemic absorption makes these particularly valuable in old age. Intra-articular corticosteroid injection for localised joint pain.

Opioids — reserved for moderate-to-severe pain limiting function and quality of life after non-opioid measures have failed.

Start low and titrate slowly; prefer short-acting immediate-release morphine, oxycodone or hydromorphone; convert to a long-acting preparation with breakthrough cover once requirements are stable.

In older adults expect a higher peak effect (fewer receptor sites) and a longer duration of action (slower elimination).

Avoid meperidine (pethidine) and propoxyphene (ineffective, neurotoxic); use caution with fentanyl patches and methadone, and never initiate a patch in an opioid-naive patient.

Anticipate every side effect: constipation (never tolerated — always co-prescribe a stimulant plus osmotic laxative), nausea, sedation, delirium, falls and fractures, respiratory depression, myoclonus, urinary retention. Methylnaltrexone and other PAMORAs for refractory opioid-induced constipation.

Assess misuse risk (Opioid Risk Tool) — risk factors are personal or family history of substance abuse, PTSD or past abuse, and psychiatric comorbidity.

Adjuvants:

Neuropathic pain — gabapentin and pregabalin (dose-reduce in renal impairment; cause sedation, dizziness, oedema, falls); duloxetine and venlafaxine (SNRIs); topical lidocaine and capsaicin; carbamazepine for trigeminal neuralgia. Tricyclic antidepressants should generally be avoided in older adults because of anticholinergic effects — dry mouth, urinary retention, constipation, delirium, tachycardia, blurred vision and falls; if unavoidable, use low-dose nortriptyline (least anticholinergic).

Corticosteroids — useful for inflammatory, bone and nerve-compression pain; watch for delirium, hyperglycaemia, fluid retention and immunosuppression.

Bisphosphonates or denosumab for metastatic bone pain.

Always review anticholinergic burden, Beers and STOPP-START criteria, and drug–drug and drug–disease interactions.

Procedural and interventional modalities when drugs and rehabilitation fail — trigger-point and intra-articular injections, epidural steroid injection, medial branch block and radiofrequency ablation, sympathetic and coeliac plexus block, intrathecal drug delivery, spinal cord stimulation, vertebroplasty and kyphoplasty, and palliative radiotherapy for bone metastases. Refer to a specialist pain clinic if pain remains uncontrolled.

Palliative care is not restricted to cancer or to the last days of life. It can be delivered alongside disease-modifying treatment from the time of diagnosis, in any life-limiting illness — cancer, heart failure, COPD, end-stage renal disease, dementia and frailty — and the best outcomes occur when it is started early.

It addresses "total pain" — physical, psychological, social and spiritual — through an interdisciplinary team (physician, clinical nurse specialist, physiotherapist, occupational therapist, social worker, pharmacist, chaplain, counsellor). It reduces unnecessary treatment and polypharmacy, improves quality of life, smooths care transitions and averts avoidable admissions.

What palliative care specifically adds to persistent pain management in old age:

Application of the WHO analgesic ladder with adjuvants and interventional techniques

Expertise in opioid titration, opioid rotation and alternative routes (sublingual, transdermal, rectal, subcutaneous) when the oral route fails

Systematic prevention and management of predictable opioid side effects

Correction of patient and family misconceptions about addiction, somnolence and hastened death

Goals-of-care discussion and advance care planning

Caregiver support and bereavement follow-up

The guiding principle: a clinician should never say "there is nothing more that can be done" — that is the point at which specialist palliative care should be involved INDIAN CONTEXT LASI wave-1 documented a heavy burden of arthritis and musculoskeletal disease in Indians aged 45 and above. Persistent pain in Indian elders is compounded by limited access to physiotherapy and rehabilitation, low awareness of pain services, and restricted opioid availability despite the 2014 NDPS amendment, with fewer than 4% of those needing palliative care actually receiving it.

WHO guideline on non-surgical management of chronic primary low back pain (December 2023) The first WHO guideline in this field, developed explicitly for adults including older people in primary and community care. 37 interventions were assessed, yielding 24 recommendations.

May be offered: structured education and advice; structured exercise therapy; needling therapies such as acupuncture; spinal manipulative therapy; massage (warn about short-term increase in pain); CBT and operant therapy; NSAIDs; topical capsaicin; multicomponent biopsychosocial care by a multidisciplinary team; and quality, affordable mobility assistive products based on person-centred assessment.

Should NOT be used as routine care: opioid analgesics, SNRI antidepressants, tricyclic antidepressants, anticonvulsants, skeletal muscle relaxants, glucocorticoids, injectable local anaesthetics, traction, therapeutic ultrasound, TENS, lumbar braces, belts and supports, and pharmacological weight loss.

Good practice statement: initiate any new medicine at the lowest effective dose for the shortest duration, with close monitoring for benefit and harm — especially in older people.

No recommendation possible for paracetamol, benzodiazepines or cannabis-related preparations — no eligible trials were identified.

ICD-11 chronic pain classification (in force since 2022) The first systematic coding framework for chronic pain, adding a second axis to the mechanistic classification:

Chronic primary pain — pain is the disease itself (fibromyalgia, chronic primary low back pain, ICD-11 code MG30.02, chronic widespread pain).

Chronic secondary pain — six groups: cancer-related, post-surgical/post-traumatic, neuropathic, headache and orofacial, visceral, and musculoskeletal.

Cochrane network meta-analysis of antidepressants for chronic pain (2023) 176 trials, over 28,000 participants, 25 antidepressants compared.

Duloxetine was consistently the highest-ranked antidepressant, with moderate-to-high certainty evidence for both substantial pain relief and reduced pain intensity.

Standard-dose duloxetine 60 mg was as effective as higher doses for most outcomes.

Milnacipran ranked next, with lower certainty.

There was insufficient evidence to draw robust conclusions for any other antidepressant, including amitriptyline — despite its long-standing first-line status in neuropathic pain guidelines.

OPAL trial (Lancet 2023) 347 adults with acute or subacute low back and/or neck pain, randomised to modified-release oxycodone up to 20 mg/day (with naloxone) or placebo for up to 6 weeks, alongside guideline care.

No difference in pain severity at 6 weeks.

Pain and quality of life at long-term follow-up were better in the placebo group.

Significantly higher risk of opioid misuse at 12 months in the opioid arm.

Conclusion: opioids should not be recommended for acute non-specific low back or neck pain.

AGS Beers Criteria 2023 update — implications for pain prescribing

Avoid non-COX-2-selective NSAIDs for chronic use, and avoid short-term scheduled NSAIDs combined with systemic corticosteroids, anticoagulants or antiplatelets.

Avoid indomethacin (most adverse effects of all NSAIDs, including CNS effects) and ketorolac (oral and parenteral).

Avoid meperidine — ineffective at usual doses and higher neurotoxicity and delirium risk than other opioids.

Avoid all skeletal muscle relaxants — carisoprodol, chlorzoxazone, cyclobenzaprine, metaxalone, methocarbamol, orphenadrine — poorly tolerated because of anticholinergic effects, sedation and fracture risk.

Rationale for anticholinergic drugs expanded to explicitly recognise cumulative anticholinergic burden.

The accompanying "Alternative Treatments" resource (2025) states that for first-line management of chronic pain, non-pharmacological approaches should be used alone or with medication, and suggests short-course NSAIDs, topical NSAIDs or COX-2 selective agents instead of chronic NSAIDs or muscle relaxants.

NICE chronic pain guidance (NG193) remains the reference position for chronic primary pain — offer supervised group exercise, CBT or acceptance and commitment therapy, and acupuncture, and consider an antidepressant; do not initiate paracetamol, NSAIDs, opioids, gabapentinoids, benzodiazepines, corticosteroid injections or antipsychotics.

Gabapentinoid deprescribing — accumulating evidence of harm in older adults (sedation, dizziness, falls and fractures, peripheral oedema, and respiratory depression when combined with opioids, with mandatory dose reduction in renal impairment). Prescribe only for a defined neuropathic indication, with a planned review and stopping date.

Palliative care evidence — early integrated palliative care continues to show improved symptom burden and quality of life across both cancer and non-cancer illness. In parallel, the negative BETTER-B (mirtazapine, 2024) and MABEL (morphine, 2025) trials for chronic breathlessness have shifted palliative practice toward non-pharmacological measures first — the same direction of travel as in persistent pain.