Quick Answer
Spine disorders are a 3 to 5 question topic across NEET PG orthopedics, medicine, and neurology. Lock these:
- Nerve root anatomy — spinal cord ends at L1-L2 in adults; below L1 is cauda equina.
- Cervical roots exit above the same-numbered pedicle — C5-C6 disc compresses C6 root.
- Lumbar roots exit below the same-numbered pedicle — L4-L5 posterolateral disc compresses L5 root (traversing).
- L5 root — foot drop, big toe extension weakness, dorsum foot sensory, NO reflex.
- S1 root — plantar flexion weakness, lateral foot sensory, absent ankle jerk.
- Cauda equina syndrome — saddle anaesthesia + bilateral leg weakness + urinary retention with overflow + reduced anal tone; urgent MRI + decompression within 24-48 hours.
- Cervical myelopathy — UMN signs, hand clumsiness, wide-based gait, Hoffmann + Lhermitte + Babinski; MRI, ACDF or laminectomy.
- Spondylolisthesis Meyerding I-V — forward slip graded by percentage.
- Spinal stenosis — neurogenic claudication relieved by forward flexion (shopping-cart sign).
- Ankylosing spondylitis — HLA-B27, young male, inflammatory back pain, sacroiliitis, uveitis, bamboo spine; NSAIDs then TNFi.
- Pott spine — India-relevant; thoracic most common; kyphotic gibbus; cold abscess; ATT 12 months + surgery for neuro deficit.
- Spinal cord tumours — extradural (metastasis most common), intradural extramedullary (meningioma, schwannoma), intramedullary (ependymoma, astrocytoma).
Spine anatomy, radiculopathy patterns, and cauda equina are permanent NEET PG favourites because they demand precise knowledge of dermatomes, myotomes, reflexes, and red flags. This deep dive walks through the anatomy first, then the disc pathology, then cauda equina and myelopathy, then the inflammatory and infective causes with an India lens on Pott spine.
Spinal cord and nerve root anatomy
- 31 pairs of spinal nerves — 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal
- Cervical roots — C1 exits above the C1 vertebra; each subsequent cervical root exits above its same-numbered vertebra (C6 exits at the C5-C6 foramen). The mismatch resets at C8, which exits between C7 and T1.
- Thoracic and lumbar roots — exit below their same-numbered vertebra (L4 exits at the L4-L5 foramen).
- Spinal cord ends at L1-L2 in adults (higher at birth — L3, ascends with growth).
- Below L1-L2 the lumbar cistern contains the cauda equina nerve roots — targets for spinal anaesthesia and lumbar puncture without cord injury.
Dermatome and myotome pearls
| Root | Sensory | Motor | Reflex |
|---|
| C5 | Lateral upper arm | Deltoid, biceps | Biceps |
| C6 | Thumb, index finger, lateral forearm | Biceps, brachioradialis, wrist extensors | Brachioradialis |
| C7 | Middle finger | Triceps, wrist flexors, finger extensors | Triceps |
| C8 | Ring, little finger, medial forearm | Finger flexors, hand intrinsics | — |
| T1 | Medial upper arm | Hand intrinsics | — |
| L2-L3 | Anterior thigh | Hip flexion, knee extension | — |
| L4 | Medial leg and medial malleolus | Knee extension, ankle dorsiflexion | Knee jerk |
| L5 | Dorsum of foot, big toe | Ankle dorsiflexion, big toe extension | — (no reflex) |
| S1 | Lateral foot, sole | Ankle plantar flexion | Ankle jerk |
| S2-S4 | Perineum, saddle | Bladder, anal sphincter | Anal wink, bulbocavernosus |
Disc herniation
Cervical disc herniation
Cervical roots exit above their same-numbered pedicle, so:
| Level | Root affected | Clinical |
|---|
| C4-C5 | C5 | Deltoid + biceps weakness; lateral arm sensory; biceps reflex |
| C5-C6 | C6 | Biceps + brachioradialis + wrist extensor weakness; thumb + index sensory; brachioradialis reflex (also most common cervical level) |
| C6-C7 | C7 | Triceps + wrist flexor weakness; middle finger sensory; triceps reflex (most commonly herniated cervical disc overall) |
| C7-T1 | C8 | Finger flexor + intrinsic weakness; medial hand sensory |
Lumbar disc herniation
Lumbar roots exit below their same-numbered pedicle, but a posterolateral (paramedian) herniation compresses the traversing (descending) root, not the exiting root — the traversing root is the one going to the foramen one level below.
| Level | Root affected (posterolateral herniation) | Clinical |
|---|
| L3-L4 | L4 (traversing) | Quadriceps weakness; medial leg sensory; reduced knee jerk |
| L4-L5 | L5 (traversing) | Ankle dorsiflexion + big toe extension weakness; dorsum foot sensory; no reflex change |
| L5-S1 | S1 (traversing) | Plantar flexion weakness; lateral foot sensory; absent ankle jerk |
A rare far-lateral (foraminal) herniation compresses the exiting root instead (L4-L5 far-lateral compresses L4).
Clinical assessment
- Straight-leg-raise (Lasegue) test — supine, lift straight leg; positive if radicular pain reproduced between 30 and 70 degrees; sensitive for L5 and S1 roots
- Crossed straight-leg-raise — pain on the affected side when the opposite leg is lifted; highly specific for disc herniation
- Femoral stretch test — prone, extend the hip with the knee flexed; positive reproduces L2-L4 radicular pain
- Neurological examination — motor, sensory, reflex screen at every level
Imaging
- MRI — gold standard for disc herniation, spinal stenosis, tumour, infection, cord compression
- X-ray — for suspected fracture, spondylolisthesis, gross deformity, instability; not for uncomplicated back pain
- CT — when MRI contraindicated; better for bony detail
- Nerve conduction studies + EMG — differentiate radiculopathy from peripheral neuropathy in ambiguous cases
Management of radiculopathy without red flags
- Conservative (6-8 weeks) — activity modification (avoid bed rest), NSAIDs, short course oral steroids in severe pain, gabapentin or pregabalin for neuropathic pain, physiotherapy
- Epidural steroid injection — for persistent pain not responding to conservative therapy at 4-6 weeks
- Surgery indications — persistent severe pain despite 6-plus weeks of conservative care, progressive motor weakness, cauda equina syndrome (emergency), foot drop, severe unremitting pain interfering with function
Cauda equina syndrome — surgical emergency
Red flag features
- Saddle anaesthesia — perineal, buttock, and posterior thigh sensory loss (S2-S5)
- Bilateral lower limb weakness — often asymmetric and multi-radicular
- Painless urinary retention with overflow incontinence — the most sensitive early sign; post-void residual over 200 mL is red flag
- Faecal incontinence, reduced anal tone on PR examination
- Sexual dysfunction
Investigations
- MRI lumbosacral spine within hours — CT-myelogram if MRI unavailable
- Post-void residual bladder scan — mandatory in acute low back pain with any red flag
Causes
- Large central lumbar disc herniation (commonest)
- Epidural abscess (fever, IVDU, immunosuppression)
- Epidural haematoma (post-spinal anaesthesia, anticoagulation)
- Tumour (metastasis to spine, primary spinal tumour)
- Trauma (burst fracture)
- Iatrogenic (post-surgical haematoma)
Management
- Urgent surgical decompression within 24-48 hours — wide laminectomy and discectomy for disc; debulk tumour; drain abscess
- Time-to-decompression is the strongest predictor of bladder recovery — delay yields permanent deficit
- Post-op — bladder training, physiotherapy, sexual function counselling
Cervical spondylotic myelopathy
Clinical picture
- Compression of cervical cord by degenerative changes — osteophytes, disc bulge, ligamentum flavum hypertrophy, ossification of the posterior longitudinal ligament (OPLL — especially in East Asian populations)
- Presenting symptoms — hand clumsiness (buttons, coins, chopsticks), wide-based unsteady gait, neck stiffness with or without radicular arm pain, urinary urgency and frequency
- Signs — hyperreflexia below the level, spasticity, positive Hoffmann sign (flick distal middle finger down; thumb and index flex), inverted supinator jerk, Lhermitte sign, Babinski, clonus
Investigation and management
- MRI cervical spine — cord compression + T2 hyperintensity (myelomalacia — worse prognosis)
- Anterior cervical discectomy and fusion (ACDF) — 1-2 level anterior compression
- Cervical laminectomy or laminoplasty — multilevel or predominantly posterior compression; often with posterior fusion
- Combined anterior-posterior approach — severe multilevel disease
- Mild myelopathy can be observed with serial exam; overt myelopathy is not managed conservatively long-term because natural history is stepwise decline
Spondylolysis and spondylolisthesis
Definitions
- Spondylolysis — defect (usually stress fracture) in the pars interarticularis; classically seen in young athletes (gymnastics, cricket fast bowlers, weightlifters); L5 most common
- Spondylolisthesis — forward slip of one vertebra on the one below
Types (Wiltse)
- Isthmic — from spondylolysis (pars defect); adolescent athletes
- Degenerative — facet joint arthritis; older adults; L4-L5 most common
- Traumatic — high-energy fracture
- Pathological — tumour, infection
- Congenital (dysplastic) — congenital dysplasia of the L5-S1 facets
- Post-surgical (iatrogenic) — after laminectomy without fusion
Meyerding grading (percentage slip)
- Grade I — 0-25 percent
- Grade II — 25-50 percent
- Grade III — 50-75 percent
- Grade IV — 75-100 percent
- Grade V (spondyloptosis) — over 100 percent
Imaging and management
- Oblique X-ray — Scotty dog appearance; a collar (defect) around the neck indicates spondylolysis
- MRI — nerve root compression, stenosis, disc pathology
- Conservative — activity modification, bracing (young athletes), physiotherapy
- Surgery — persistent symptoms, progressive slip (over grade II), neurological deficit; posterolateral fusion, sometimes with reduction
Spinal stenosis
Clinical picture
- Degenerative narrowing of the central canal, lateral recess, or foramen; older adults (over 60 years)
- Neurogenic claudication — bilateral leg pain, paraesthesiae, or weakness on walking; relieved by sitting or forward flexion (shopping-cart sign)
- Differentiate from vascular claudication — vascular pain relieved by standing still (not requiring flexion), cold peripheries, absent peripheral pulses, positional test different
Imaging and management
- MRI lumbar spine — trefoil canal, ligamentum flavum hypertrophy, facet hypertrophy
- Conservative — physiotherapy, NSAIDs, epidural steroid injection
- Surgery — decompressive laminectomy for refractory symptoms; add fusion for instability or spondylolisthesis
Ankylosing spondylitis (AS)
Clinical picture
- HLA-B27 associated seronegative spondyloarthropathy; young male 3:1; onset 15-30 years
- Inflammatory back pain — insidious onset, morning stiffness over 30 minutes, improves with exercise, worse with rest, night pain that wakes the patient
- Reduced lumbar spine mobility (modified Schober), reduced chest expansion, sacroiliac tenderness (FABER/Patrick), enthesitis (Achilles, plantar fascia)
Extraskeletal manifestations
- Anterior uveitis — commonest extra-articular manifestation; unilateral painful red eye + photophobia
- Aortic regurgitation, apical pulmonary fibrosis, cauda equina late
- Inflammatory bowel disease, psoriasis
- Osteoporotic vertebral fracture in fused spine (fatal chalk-stick fracture from minor trauma)
Investigations
- HLA-B27 — positive in 90 percent of AS but 8 percent of general population; supportive not diagnostic
- Raised ESR, CRP — variable
- X-ray SI joints — erosions, sclerosis, ankylosis (radiographic axial spondyloarthritis)
- MRI STIR SI joints — bone marrow oedema before X-ray changes (non-radiographic axial spondyloarthritis — earlier diagnosis)
- Syndesmophytes and bamboo spine — late
Management
- NSAIDs first-line — both symptomatic and disease-modifying (regular over on-demand for structural progression)
- Physical therapy — posture, spinal mobility, chest expansion
- TNF inhibitors — adalimumab, etanercept, infliximab, golimumab, certolizumab; for NSAID-refractory active disease (BASDAI over 4)
- IL-17 inhibitors — secukinumab, ixekizumab; alternative or TNF failure
- JAK inhibitors — upadacitinib, tofacitinib; emerging
- Sulfasalazine and methotrexate — for peripheral arthritis; NOT for axial disease
Tuberculosis of the spine (Pott disease)
Epidemiology
- India-relevant; 1-2 percent of all TB and 50 percent of skeletal TB
- Thoracic spine most common site; then thoracolumbar junction
Clinical picture
- Chronic (weeks to months) back pain, low-grade fever, night sweats, weight loss, anorexia
- Progressive kyphotic deformity — gibbus
- Cold abscess in paraspinal soft tissues; may track along fascial planes to distant sites (psoas abscess in the groin)
- Neurological deficit — early spastic paraparesis; late paraplegia (Pott paraplegia)
Pathology and imaging
- Infection lodges in anterior vertebral body → spreads under the anterior longitudinal ligament → involves adjacent vertebra → destroys the disc late (contrast with pyogenic which destroys the disc early)
- MRI (investigation of choice) — contiguous vertebral body destruction, preserved disc height early, large paraspinal abscess disproportionate to bone destruction, epidural extension with cord compression
- CT-guided biopsy — AFB smear, Xpert MTB/RIF (rapid PCR with rifampicin resistance), MGIT culture (gold standard, 4-6 weeks), histopathology (caseating granulomas)
Management
- ATT for 12 months minimum — RIPE (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 months intensive + RIF-INH for 10 months continuation; extended to 18 months for severe or MDR cases
- Nikshay notification — mandatory under NTEP
- Nikshay Poshan Yojana — Rs 500 per month DBT nutritional support
- Surgery indications — progressive neurological deficit despite ATT, spinal instability, kyphosis over 40 degrees or progressive kyphosis, cold abscess causing cord compression, failed medical response, diagnostic uncertainty
Distinction from pyogenic vertebral osteomyelitis
| Feature | Pott spine (TB) | Pyogenic (Staph aureus) |
|---|
| Onset | Chronic (weeks to months) | Acute (days to weeks) |
| Fever | Low-grade | Often high-grade |
| Disc | Preserved early | Destroyed early |
| Spread | To adjacent vertebra | Single level |
| Paraspinal abscess | Large, disproportionate | Smaller |
| ESR/CRP | Moderately raised | Markedly raised |
| Blood culture | Rarely positive | Often positive |
| Treatment | ATT 12-18 months + surgery | IV antibiotics 6 weeks + surgery |
Spinal cord tumours
Anatomic classification
- Extradural (55 percent) — outside the dura
- Metastasis most common (lung, breast, prostate, kidney, thyroid, myeloma, lymphoma)
- Primary bone tumours (chordoma at sacrum, aneurysmal bone cyst)
- Intradural extramedullary (40 percent) — inside dura, outside cord
- Meningioma (thoracic, female, well-defined)
- Schwannoma (nerve sheath, dumbbell shape through foramen)
- Neurofibroma (NF1)
- Intradural intramedullary (5 percent) — within cord
- Ependymoma (commonest adult intramedullary; central; filum terminale — myxopapillary variant)
- Astrocytoma (commonest paediatric intramedullary)
- Haemangioblastoma (VHL)
Clinical picture
- Extradural — rapid onset back pain, radicular pain, then cord compression signs (MSCC — Metastatic Spinal Cord Compression is oncological emergency)
- Intradural extramedullary — slower onset; sensory then motor
- Intradural intramedullary — dissociated sensory loss (syringomyelia pattern for ependymoma), long tract signs
Management
- MSCC — high-dose steroids (dexamethasone), urgent surgical decompression + radiotherapy for radiosensitive tumours; direct systemic therapy for chemosensitive
- Meningioma, schwannoma — surgical resection curative
- Ependymoma, astrocytoma — maximal safe resection + adjuvant radiotherapy
India-specific context
- NTEP (National TB Elimination Programme) — replaces RNTCP; free ATT; MDR-TB screening with Xpert; Nikshay portal notification mandatory
- Nikshay Poshan Yojana — Rs 500 per month DBT nutritional support during TB treatment
- RBSK — screens 0-18 year-olds for congenital and acquired spinal deformity
- Ayushman Bharat PM-JAY — covers spine surgery packages (discectomy, laminectomy, fusion, deformity correction) in empanelled hospitals
- Pradhan Mantri Divyang Kalyan and district disability schemes provide surgical and orthotic support for cauda equina survivors and CP-associated spinal deformity
- Occupational spine injury — high burden in India in rickshaw pullers, agricultural workers, construction; disability certification via UDID card enables benefits
NEET PG MCQ traps
- Spinal cord ends at L1-L2 in adults; below is cauda equina.
- Cervical roots exit ABOVE same-numbered pedicle; C5-C6 disc = C6 root.
- Lumbar roots exit BELOW same-numbered pedicle; L4 exits at L4-L5 foramen.
- Posterolateral (paramedian) herniation compresses TRAVERSING root — L4-L5 disc = L5 root.
- Far-lateral (foraminal) herniation compresses EXITING root — L4-L5 far-lateral = L4 root.
- L5 root — foot drop + big toe extension weakness + dorsum foot sensory; NO reflex change.
- S1 root — plantar flexion weakness + lateral foot sensory + absent ankle jerk.
- Most common cervical disc herniation level — C6-C7 (affects C7 root).
- Most common lumbar disc herniation level — L4-L5 (affects L5 root).
- Cauda equina red flags — saddle anaesthesia, bilateral weakness, urinary retention, reduced anal tone.
- Cauda equina — urgent MRI + surgical decompression within 24-48 hours.
- Cervical myelopathy signs — Hoffmann, Lhermitte, Babinski, hyperreflexia, wide-based gait, hand clumsiness.
- Spondylolysis — pars interarticularis defect; Scotty dog collar on oblique X-ray.
- Meyerding grade V — spondyloptosis (over 100 percent slip).
- Spinal stenosis — neurogenic claudication relieved by forward flexion (shopping-cart sign).
- AS — HLA-B27 positive in 90 percent but not diagnostic alone.
- AS extra-articular — anterior uveitis (most common), aortic regurgitation, apical fibrosis.
- AS bamboo spine — late; treatment TNFi (adalimumab, etanercept) for NSAID failure.
- Modified Schober test — assesses lumbar flexion in AS.
- Pott spine — India relevant; thoracic most common; anterior vertebral body first; disc late.
- Cold abscess — psoas, can track distally; classic Pott sign.
- Pott treatment — ATT 12 months minimum; surgery for progressive neuro deficit, instability, kyphosis over 40.
- Pyogenic osteomyelitis — Staph aureus, acute, disc destruction early, single level.
- Metastatic spinal cord compression — oncological emergency; steroids + urgent decompression + radiotherapy.
- Intradural intramedullary — adult — ependymoma most common.
- Intradural intramedullary — paediatric — astrocytoma most common.
- Chordoma — sacrum; slow-growing; midline.
- Nikshay notification — mandatory for every TB case in India.
Recent updates and Indian context
- NTEP goal — India TB elimination by 2025 (revised from SDG 2030); major push on active case finding, drug-resistance screening
- Xpert MTB/RIF Ultra — replacing older Xpert cartridges at NTEP labs; faster and more sensitive for paucibacillary TB (including spinal)
- BPaL and BPaLM regimens for MDR/XDR-TB — shorter oral regimens (bedaquiline, pretomanid, linezolid, moxifloxacin) being rolled out through NTEP
- Non-radiographic axial spondyloarthritis — ASAS criteria now allow diagnosis on MRI-only sacroiliitis; earlier TNFi initiation
- JAK inhibitors (upadacitinib) — new option in AS after TNFi failure
- Enhanced recovery after spine surgery (ERAS) — protocols reducing hospital stay and complications
- Minimally invasive spine surgery (MISS) — expanding role in disc herniation and stenosis
- Ayushman Bharat spine packages — cover discectomy, laminectomy, fusion, deformity correction
Frequently asked questions
Which nerve root is affected by an L4-L5 posterolateral disc herniation, and why?
An L4-L5 posterolateral (paramedian) disc herniation compresses the L5 nerve root, not the L4 root. This is one of the highest-yield exam traps in spine because the numbering feels counter-intuitive. In the lumbar spine the nerve root exits below its numbered pedicle through the intervertebral foramen at that level — the L4 root exits at the L4-L5 foramen. However, the traversing (descending) root at the L4-L5 level is L5 — the L5 root passes across the L4-L5 disc on its way down to exit at the L5-S1 foramen. A posterolateral disc herniation displaces the nucleus pulposus into the lateral recess where it compresses the traversing root, not the exiting root — so at L4-L5 the L5 root is hit. Only a rare far-lateral (foraminal) herniation at the same level would compress the exiting L4 root. The L5 root produces weakness of ankle dorsiflexion (foot drop) and big toe extension, sensory loss over the dorsum of the foot and big toe, and no reflex change (there is no L5 reflex — the ankle jerk is S1 and the knee jerk is L4). The equivalent trap at L5-S1 posterolateral is S1 compression — plantar flexion weakness, lateral foot sensory loss, and lost ankle jerk. In the cervical spine the anatomy is different — the C6 root exits at the C5-C6 foramen (above its numbered pedicle), so a C5-C6 posterolateral disc compresses the C6 root.
How do you recognise and manage cauda equina syndrome?
Cauda equina syndrome is a surgical emergency requiring MRI within hours and decompression within 24-48 hours to avoid permanent neurological deficit — every hour of delay after symptom onset worsens the recovery of bladder function. The classical clinical picture is a central (or large paracentral) lumbar disc herniation compressing the cauda equina nerve roots below the L1-L2 conus, producing (1) saddle anaesthesia — sensory loss over the perineum, buttocks, and posterior thighs in the S2-S5 distribution; (2) bilateral lower limb motor weakness — often asymmetric and multi-radicular rather than pure single-root; (3) urinary dysfunction — painless urinary retention with overflow incontinence is the most sensitive early sign, so a post-void residual bladder scan is mandatory in every acute low back pain with any red flag; (4) faecal incontinence and reduced anal tone on PR examination; (5) sexual dysfunction. Any of these red flags in a patient with acute low back pain mandates urgent MRI lumbosacral spine — CT if MRI unavailable, myelogram if both unavailable. Once cauda equina is confirmed, urgent surgical decompression by wide laminectomy and discectomy (or debulking of tumour, drainage of abscess) is the definitive treatment. Non-disc causes include epidural abscess, epidural haematoma, tumour (metastasis, primary), fracture, and iatrogenic (post-spinal anaesthesia haematoma). The prognostic factor most strongly linked to recovery is duration of bladder dysfunction before decompression — hence the 24-48 hour rule.
How does cervical myelopathy present and how is it managed?
Cervical spondylotic myelopathy is compression of the cervical cord by degenerative changes — osteophytes, disc bulge, ligamentum flavum hypertrophy, and ossification of the posterior longitudinal ligament (OPLL, especially in East Asian populations) — usually in patients over 55 years. The clinical hallmark is upper motor neuron signs below the level of compression and lower motor neuron signs at the level of compression. Presenting symptoms are commonly missed — hand clumsiness (loss of fine motor control — struggle to fasten buttons, hold coins, use chopsticks), a wide-based unsteady gait, neck stiffness with or without radicular arm pain, and later urinary urgency and frequency. Examination — hyperreflexia in the lower limbs, spasticity, positive Hoffmann sign (flick the distal middle finger down; positive if the thumb and index finger flex), inverted supinator jerk (tapping the brachioradialis produces finger flexion instead), Lhermitte sign (electric shock down the spine on neck flexion), Babinski, clonus. MRI cervical spine is diagnostic — cord compression with T2 hyperintensity in the cord signals myelomalacia and worse prognosis. Once significant myelopathy is established, surgical decompression is offered because natural history is progressive stepwise decline — anterior cervical discectomy and fusion (ACDF) for 1-2 level anterior compression, cervical laminectomy or laminoplasty with or without posterior instrumented fusion for multilevel or predominantly posterior compression, or a combined approach for severe multilevel disease. Mild myelopathy can be observed with serial examination but overt myelopathy is not managed conservatively long-term.
How do you differentiate ankylosing spondylitis from mechanical low back pain?
Ankylosing spondylitis is an HLA-B27 associated seronegative spondyloarthropathy of young men (typical onset 15-30 years, male 3:1) that causes progressive fusion of the axial skeleton from below upward — sacroiliitis first, then lumbar, thoracic, and cervical spine. The critical mistake is to dismiss the pain as mechanical low back pain and delay diagnosis by years. Inflammatory back pain features (the ASAS criteria — 4 of 5 needed) — age at onset under 40 years, insidious onset, improvement with exercise (not with rest), no improvement with rest, and pain at night with improvement upon getting up. Mechanical low back pain does the opposite — pain worse with activity and improved by rest. Examination findings — reduced lumbar spine mobility (modified Schober test), reduced chest expansion (over 5 cm normal in young adult), sacroiliac tenderness (FABER test — Patrick sign), and enthesitis at the Achilles tendon and plantar fascia. Extraskeletal manifestations — anterior uveitis (unilateral painful red eye with photophobia — the commonest extra-articular manifestation), inflammatory bowel disease, psoriasis, aortic regurgitation, apical pulmonary fibrosis, cauda equina syndrome late in disease. Investigations — HLA-B27 positive in 90 percent of AS but 8 percent of general population so not diagnostic alone; X-ray sacroiliac joints show erosions, sclerosis, then ankylosis (radiographic axial spondyloarthritis); MRI sacroiliac STIR shows bone marrow oedema before X-ray changes (non-radiographic axial spondyloarthritis, earlier diagnosis); syndesmophytes and the bamboo spine appear late. Treatment — NSAIDs first-line (both symptomatic and disease-modifying), physical therapy central for maintaining posture, TNF inhibitors (adalimumab, etanercept, infliximab, golimumab, certolizumab) for NSAID-refractory active disease, IL-17 inhibitors (secukinumab, ixekizumab) as alternative or for TNF-failure, JAK inhibitors emerging. India considerations — AS prevalence is significant, biologics are cost-limited, and PMJAY coverage varies by state.
What is Pott spine and how does it differ from pyogenic vertebral osteomyelitis?
Pott spine (spinal tuberculosis, tuberculous spondylitis) is a major cause of adult and paediatric spinal deformity and paraplegia in India and accounts for about 1-2 percent of all TB and 50 percent of skeletal TB. The classic picture is a chronic (weeks to months) presentation — insidious back pain, low-grade fever, night sweats, weight loss, and progressive kyphotic deformity (gibbus) with or without neurological deficit. The infection lodges in the anterior vertebral body, spreads under the anterior longitudinal ligament to involve the adjacent vertebra (spread to the next vertebra above or below is characteristic of TB), destroys the intervertebral disc late (in contrast to pyogenic infection which destroys the disc early), and forms a cold abscess in the paraspinal soft tissues that can track along fascial planes to distant sites (psoas abscess presenting in the groin). Thoracic spine is the most common site. MRI is the investigation of choice — contiguous vertebral body destruction, preserved disc height early, large paraspinal abscess out of proportion to bone destruction, and epidural extension causing cord compression. CT-guided biopsy for AFB smear, Xpert MTB/RIF (rapid PCR with rifampicin resistance), MGIT culture (gold standard, 4-6 weeks), and histopathology (caseating granulomas) confirms the diagnosis. Treatment is prolonged anti-tubercular therapy — RIPE (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 months intensive plus RIF-INH for 10 months continuation (total 12 months minimum, extended to 18 months for severe or MDR cases). Surgery is indicated for progressive neurological deficit despite ATT, spinal instability, kyphosis over 40 degrees or progressive kyphosis, cold abscess causing cord compression, failed response to medical therapy, or diagnostic uncertainty (biopsy). The classical distinction from pyogenic vertebral osteomyelitis (Staph aureus predominant, acute onset, disc destruction early, single-level, elevated CRP and WBC) is that TB is insidious, spreads to adjacent vertebra, preserves the disc initially, forms disproportionate paraspinal abscess, and requires prolonged ATT. India programmatic context — every diagnosed TB spine case must be notified via Ni-kshay and enrolled in the National TB Elimination Programme (NTEP) for standardised regimen and DBT-linked nutritional support (Nikshay Poshan Yojana, Rs 500 per month).
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: July 2026
