Ask four linked questions:

1. What is the diagnosis? Characterise onset, site, radiation, severity, and aggravating or relieving factors.
2. How severe is it? Establish neurological compromise, structural pathology, and functional limitation.
3. Is surgery urgent and is the patient ready? Consider CES, progressive weakness, comorbidities, and operative risk.
4. What is the functional context? Walking distance, work, sleep, aids, home support, and rehabilitation potential.

Pain confined to the lower back, buttock, or posterior thigh is often referred pain. True sciatica usually extends below the knee in a dermatomal distribution.

Screen every patient for:

• new back pain at age <20 or > 55;
• significant trauma or minor trauma with osteoporosis;
• fever, immunosuppression, diabetes, steroid exposure, or IV drug use;
• known malignancy, unexplained weight loss, or constitutional symptoms;
• night pain or pain unrelieved by rest;
• deformity or focal percussion tenderness;
• progressive motor or sensory deficit;
• bilateral sciatica or weakness;
• saddle anaesthesia; and
• new urinary retention/overflow, bowel dysfunction, reduced anal tone, or sexual dysfunction.

• Observe from front, side, and behind for scoliosis, kyphosis, loss of lordosis, gibbus, scars, sinuses, and muscle wasting.
• Note an antalgic or forward-flexed gait, foot-drop/steppage gait, Trendelenburg gait, or a sciatic list.
• Look for quadriceps wasting (L3/4) or calf wasting (S1).
• A broad-based or spastic gait with hyperreflexia suggests a cord lesion above the lumbar region.

• Palpate and percuss each spinous process: focal tenderness raises concern for fracture, infection, or tumour.
• Assess paraspinal tenderness and spasm.
• Palpate the sacroiliac joints.
• Examine the hip because hip OA, avascular necrosis, and other hip disease can mimic lumbar pain.

What the disc / SLR slides show: sagittal and axial drawings of nucleus pulposus protruding into the canal; clinical photos of lumbar palpation and the supine straight-leg raise — flexion/bending loads the disc; SLR stretches the irritated root. ^[1] | Femoral stretch | Anterior-thigh pain with prone knee flexion/hip extension | Upper lumbar L2–L4 root irritation |

Hamstring tightness above 70°, back pain alone, or posterior-thigh discomfort without the patient’s usual below-knee symptoms is not a positive SLR.

• Test lower-limb tone, power by myotome, sensation by dermatome, knee and ankle jerks, plantar responses, and clonus.
• UMN signs in the legs imply cervical/thoracic cord or conus involvement, not an isolated lower lumbar root lesion.
• When CES is suspected, assess perianal sensation, anal tone, and voluntary contraction.
• Palpate femoral, popliteal, posterior tibial, and dorsalis pedis pulses; use ABPI if vascular claudication is possible.

Imaging should confirm a clinical hypothesis. Degenerative discs and bulges are common in asymptomatic adults, so an abnormal MRI is not automatically the pain generator.

Order according to the suspected pathology:

CRP rises and falls relatively quickly. ESR responds more slowly and is affected by anaemia, immunoglobulins, and fibrinogen; a markedly elevated ESR with a relatively normal CRP should raise the possibility of paraproteinaemia.

X-rays are useful for alignment, deformity, fracture, spondylolisthesis, and established degeneration, but a normal film does not exclude early infection, tumour, disc herniation, or neural compression.

On T2 MRI, a desiccated “black disc” indicates loss of water content. Review sagittal alignment and disc height, then axial central canal, lateral recesses, foramina, facets, ligamentum flavum, thecal sac, and nerve roots.

• Uncomplicated acute mechanical pain: no immediate imaging; review if it fails to improve.
• Trauma or suspected instability: X-ray, then CT when fracture definition is needed.
• Progressive neurological deficit or CES: emergency MRI.
• Fever, immunosuppression, night pain, or focal percussion tenderness: inflammatory markers, cultures, and urgent MRI.
• Known cancer or suspected malignancy: MRI, appropriate blood tests, and tissue diagnosis where needed.
• Inflammatory back pain: SI-joint radiographs may be normal early; MRI SI joints can detect active sacroiliitis.

Disc-height loss transfers load posteriorly to the facets. The annulus bulges, facets hypertrophy, and ligamentum flavum buckles inward, producing circumferential canal narrowing.

Posterolateral herniation is most common. Lower levels, especially L4/5 and L5/S1, are most often affected. Extruded and sequestered fragments may resorb through inflammation and macrophage activity, supporting an initial conservative approach when there is no emergency deficit.

Both can weaken ankle/toe dorsiflexion. Hip abduction and ankle inversion weakness favour L5 radiculopathy because these functions are supplied outside the common peroneal nerve. A common peroneal lesion more selectively affects dorsiflexion and eversion.

• central stenosis: bilateral neurogenic claudication and diffuse leg symptoms;
• lateral recess stenosis: traversing-root radiculopathy;
• foraminal stenosis: exiting-root radiculopathy; and
• severe central narrowing: possible CES.

Extension narrows the canal and foramina; flexion enlarges them. This explains the shopping-cart sign, easier cycling, and often better tolerance of uphill than downhill walking.

Quantitatively, extension decreases spinal canal size by ~11% and foraminal size by ~15%, while flexion increases canal size by ~11% and foraminal size by ~12% (Inufusa et al., Spine 1996). ^[6]

A pars interarticularis stress injury is commonest at L5 and is associated with repetitive extension/rotation in young athletes. It causes insidious activity-related back pain; radicular symptoms usually imply associated slip or another compressive lesion.

Possible findings include hamstring tightness, short stride, flattened lordosis, and pain on extension. Use radiographs first, CT for bony definition, MRI for marrow oedema/neural structures, and SPECT/CT selectively to identify an active stress reaction.

Meyerding grades: I 0–25%, II 25–50%, III 50–75%, IV 75–100%, and V > 100% (spondyloptosis).

Slippage can kink the central canal and narrow the foramen through disc-height loss and superior articular-process encroachment. If surgery requires decompression in an unstable segment, fusion is added to prevent worsening translation.

SI-joint pain can refer to the buttock, posterior thigh, or groin and overlap with disc, facet, and hip pain. No single provocation test is definitive; use a cluster such as FABER, thigh thrust, compression, distraction, and Gaenslen tests. A substantial response to image-guided diagnostic injection supports the SI joint as the pain source.

Key features are:

• onset before 40 and insidious course;
• symptoms for at least three months;
• prolonged morning stiffness;
• improvement with exercise but not rest;
• night pain, especially in the second half of the night;
• alternating buttock pain;
• enthesitis (blue-highlighted skeletal sites of enthesopathy are characteristic), uveitis, psoriasis, inflammatory bowel disease, or family history.

AS affects both sexes; the male-to-female ratio is approximately 6:1 in patients < 16 years and 2:1 in those ≥30 years. It is a spondyloarthropathy (axial and/or peripheral) that is rheumatoid-factor negative. ^[5]

HLA-B27 supports but does not establish the diagnosis. Plain SI-joint films may be normal early; MRI can show active bone-marrow oedema. ESR and CRP can also be normal.

Management includes exercise/physiotherapy and NSAIDs first. Persistent active axial disease may require biologic therapy such as TNF or IL-17 inhibition under specialist care. Conventional DMARDs have little efficacy for purely axial disease, though some may help peripheral arthritis.

Consider pyogenic spondylodiscitis, vertebral osteomyelitis, epidural abscess, or TB in a patient with fever, immunosuppression, bacteraemia risk, night pain, focal percussion tenderness, or raised inflammatory markers. MRI is the key imaging test. Obtain cultures and, when required, image-guided biopsy before targeted antimicrobial therapy.

Operate when there is an epidural abscess with neurological compromise, mechanical instability/deformity, failure of medical treatment, or a need for source control.

A known cancer patient with new severe back pain, weakness, sensory change, or sphincter symptoms requires urgent assessment for metastatic epidural spinal cord/conus compression. Arrange urgent MRI, start corticosteroid treatment when clinically indicated, and involve spinal surgery and oncology immediately. Staging investigations must not delay treatment of neurological compression.

Think of traumatic, osteoporotic, steroid-related, or pathological vertebral collapse. X-ray may identify wedging or height loss; CT defines the fracture pattern, while MRI identifies marrow oedema, posterior-element/neural involvement, and malignant features.

Keep aortic aneurysm, nephrolithiasis, pyelonephritis, pelvic inflammatory disease, endometriosis, hip disease, pancreatobiliary disease, and other visceral sources in the differential when the history or examination is not mechanically concordant.

• Explain the diagnosis and favourable natural history when appropriate.
• Encourage continued tolerable activity; avoid prolonged bed rest.
• Use physiotherapy, graded conditioning, core strengthening, and ergonomic/activity modification.
• Choose analgesia following the WHO analgesic ladder ^[7]:
  • Step 1 — Non-opioids (paracetamol, NSAIDs) ± adjuvants.
  • Step 2 — Weak opioids (codeine, tramadol) ± adjuvants, if pain persists.
  • Step 3 — Strong opioids (morphine, oxycodone, fentanyl) + non-opioid ± adjuvants, if pain persists.
• Long-term opioids are generally undesirable; steroids may be used in selected situations.
• Consider targeted injections (epidural, facet/medial branch block, SI-joint injection) for selected radicular, facet, or SI-joint pain; they may be diagnostic and temporarily therapeutic but are not a cure.

1. Pain: a confirmed, concordant pain generator with disabling symptoms despite adequate conservative care.
2. Neurology: progressive deficit or neural compression requiring decompression.
3. Instability: painful/pathological motion requiring stabilisation and fusion.
4. Deformity: fixed or progressive malalignment requiring correction and fusion.

Removing a large portion of a facet can itself create instability and may necessitate fusion.

Endoscopic techniques: Endoscopic flavectomy (ipsilateral and contralateral decompression) is an emerging minimally invasive option for lumbar stenosis, allowing bilateral decompression through a unilateral approach. ^[7]

During posterior lumbar surgery, prone positioning with the abdomen free reduces intra-abdominal pressure and epidural venous engorgement. Lumbar flexion also opens the interlaminar space for access.

• Posterolateral L4/5 disc → L5 traversing root.
• Far-lateral/foraminal L4/5 disc → L4 exiting root.
• Positive SLR → the patient’s radicular pain below the knee at 30–70°.
• Flexion-provoked axial pain → think disc; extension-provoked pain → think facet/stenosis.
• Neurogenic claudication needs flexion/sitting for relief; vascular claudication improves by simply stopping.
• Hyperreflexia and upgoing plantars are not explained by a routine lower lumbar root lesion.
• Spondylolysis is a pars defect; spondylolisthesis is a slip; spondylosis is degeneration.
• Stable stenosis → decompression; stenosis with instability → consider decompression plus fusion.