Low Back Pain

By duration:

• Acute — under 6 weeks. Most improves substantially within a few weeks regardless of treatment.
• Subacute — 6 to 12 weeks, the window where the risk of chronicity is most modifiable.
• Chronic — beyond 12 weeks. A different problem from acute pain, with central sensitization, deconditioning and psychosocial factors carrying increasing weight.

By cause:

• Non-specific low back pain — around 90%. Pain arising from muscles, ligaments, joints and discs without a clear structural culprit.
• Radicular pain / sciatica — nerve-root compression producing leg-dominant pain in a dermatomal pattern, often with numbness or weakness.
• Spinal stenosis — narrowing of the canal, classically causing leg pain on walking that eases on sitting or leaning forward.
• Specific serious pathology — under 1–2% combined: fracture, malignancy, infection, inflammatory spondyloarthritis, cauda equina syndrome. Rare, and what the red flags screen for.

The lumbar spine is a stack of vertebrae, intervertebral discs, facet joints, ligaments and deep stabilizing muscles, richly innervated in the outer annulus, facet capsules and ligaments. Pain can arise from any of them, and in most people it is not possible to say which — the structures share innervation, and pain from deep spinal tissue refers poorly.

Imaging misleads more than it helps. A systematic review of 33 studies covering 3,110 asymptomatic people found disc degeneration in 37% of 20-year-olds rising to 96% of 80-year-olds, and disc bulges in 30% at age 20 rising to 84% at 80 ^{9Reference 9Brinjikji et al. · 2015Systematic reviewSystematic literature review of imaging features of spinal degeneration in asymptomatic populations — systematic review (33 studies, 3,110 subjects)View study →}. The authors concluded that these features are largely part of normal ageing and unassociated with pain.

Someone with back pain who is scanned will almost certainly be told something was found — and that finding is, statistically, as likely to be present in a pain-free person of the same age. Early imaging in the absence of red flags does not improve outcomes and reliably increases anxiety, further investigation and intervention.

In chronic low back pain, the driver shifts. Ongoing pain is maintained less by tissue damage than by central sensitization, fear-avoidance behaviour, deconditioning and sleep disruption — which is why psychological and exercise-based treatments outperform anything aimed at the disc, and why depression, anxiety and fibromyalgia travel with it so often.

Cauda equina syndrome is a surgical emergency, and its signs cannot wait:

• New urinary retention or incontinence, or faecal incontinence
• Numbness in the saddle area — inner thighs, buttocks, genitals
• Weakness or numbness in both legs, or rapidly progressive weakness

Any of these needs emergency assessment the same day; delayed decompression risks permanent bladder, bowel and sexual dysfunction.

Other features warranting prompt (non-emergency) assessment: a history of cancer, unexplained weight loss, fever or recent infection, injection drug use, significant trauma or osteoporosis with minor trauma, long-term corticosteroid use, age of onset under 20 or over 50, pain that is worse at night or unrelieved by rest, and morning stiffness lasting over an hour with gradual onset in a young adult (inflammatory back pain).

The guidance changed substantially, and much popular advice has not caught up. The American College of Physicians guideline recommends non-pharmacological treatment first-line for both acute and chronic low back pain: superficial heat, massage, acupuncture or spinal manipulation for acute pain; exercise, multidisciplinary rehabilitation, acupuncture, yoga, tai chi and cognitive behavioural therapy for chronic pain — all strong recommendations. Medication is for when those are insufficient, with NSAIDs first, then tramadol or duloxetine, and opioids as a last resort ^{10Reference 10Qaseem et al. · 2017Noninvasive treatments for acute, subacute, and chronic low back pain — American College of Physicians clinical practice guidelineView study →}.

Paracetamol does not work for low back pain — a meta-analysis of placebo-controlled trials found high-quality evidence that it fails to reduce pain intensity or disability, while nearly quadrupling abnormal liver function tests ^{11Reference 11Machado et al. · 2015Meta-analysisEfficacy and safety of paracetamol for spinal pain and osteoarthritis — systematic review and meta-analysis of randomised placebo-controlled trialsView study →}. Bed rest is counterproductive: staying active within the limits of pain produces better outcomes than resting.

Effect sizes across the board are modest. There is no treatment for non-specific low back pain that reliably abolishes it, and setting expectations — that most acute episodes settle, that recurrence is common, that chronic pain is manageable rather than curable — is itself part of good care.

Movement, above everything. Exercise is the best-supported intervention for chronic low back pain and for preventing recurrence. The specific type matters far less than doing it consistently; the best programme is the one someone will keep doing.

Heat has reasonable evidence for acute pain and is cheap and safe. Manual therapy and acupuncture are guideline-endorsed options with modest effects. Cognitive behavioural therapy and mindfulness-based approaches have real evidence in chronic pain, aimed at function and fear-avoidance rather than at implying the pain is imagined.

Devil’s claw and willow both carry low back pain as their leading researched indication, with randomized trial evidence rather than tradition alone. Comfrey has dedicated acute-back-pain trial data as a topical. Cayenne works through capsaicin-mediated defunctionalization of pain fibres, studied as a plaster in chronic low back pain.

Willow bark is pharmacologically aspirin-adjacent (salicin is metabolized to salicylic acid), so it shares aspirin’s bleeding, gastric and Reye’s-syndrome considerations and should not be stacked with NSAIDs casually. Comfrey is for topical use on intact skin only — the plant contains hepatotoxic pyrrolizidine alkaloids, oral use is not appropriate, and application should be time-limited.