Image MCQ: MRI Spine Common Findings for NEET PG (Disc Prolapse, Cord Compression, MS Plaques, Syringomyelia, Transverse Myelitis) | NEETPGAI
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NEET PG 2026
Image MCQ: MRI Spine Common Findings for NEET PG (Disc Prolapse, Cord Compression, MS Plaques, Syringomyelia, Transverse Myelitis)
5 high-yield MRI spine image MCQs for NEET PG: disc prolapse with nerve root impingement, cauda equina, MS plaques, syringomyelia, transverse myelitis — with teaching pearls.
Dr. NEETPGAI Editorial TeamPublished 1 May 2026Updated 2 May 202624 min read
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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.
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MRI spine image MCQs contribute 3-5 questions per NEET PG paper across radiology, neurology, orthopaedics, and emergency medicine. Five MRI spine patterns recur reliably:
Disc prolapse with nerve root impingement — focal posterolateral T2-bright disc material indenting the thecal sac and effacing the foramen
Cord compression by extradural mass — central or saddle cauda-equina compression from a vertebral metastasis, abscess, hematoma, or massive central disc prolapse
Syringomyelia — longitudinal CSF-isointense tubular cavity within the cord, often cervicothoracic with associated Chiari I
Transverse myelitis — segmental cord T2 hyperintensity with cord swelling and no compressing mass
The location-shape-signal triad plus 'cord pushed vs cord expanded vs canal pinched' anatomy rule covers nearly every MRI spine NEET PG question.
Why MRI spine image MCQs are high-yield for NEET PG
MRI spine sits at the intersection of radiology, neurology, orthopaedics and emergency medicine. NEET PG and FMGE consistently feature MRI spine images in 3-5 questions per paper, often as the final discriminator between two diagnoses with similar symptoms. The patterns are highly stereotyped — pattern recognition pays off enormously.
Five patterns recur in nearly every paper: lumbar disc prolapse with radiculopathy, cord compression with cauda equina or conus syndrome, demyelinating cord plaque (MS or NMOSD), syringomyelia, and transverse myelitis. Drill these five patterns plus 5-10 PYQ MRI spine images daily for 2 weeks, and your accuracy will move from 40 to 80 percent on spine image MCQs.
Foundational concepts before the MCQs
The 'cord pushed vs cord expanded vs canal pinched' rule
Tumor enhancement, abscess wall, active demyelinating plaque, leptomeningeal disease
Lumbar nerve root anatomy and disc-prolapse rules
Disc level
Exiting root
Traversing root
Posterolateral prolapse classically affects
L3-L4
L3 (lateral)
L4 (passing inferiorly)
L4 root (the traversing root)
L4-L5
L4 (lateral)
L5 (passing inferiorly)
L5 root (the traversing root)
L5-S1
L5 (lateral)
S1 (passing inferiorly)
S1 root (the traversing root)
The exception is the far-lateral / foraminal disc prolapse — this affects the EXITING root (e.g., far-lateral L4-L5 disc affects the L4 root). The exam loves this trap: ankle jerk lost (S1) plus L5-S1 disc prolapse — the traversing S1 root is impinged, not L5.
MCQ 1: 38-year-old labourer with low-back pain and right-leg radiation
Image description:[Sagittal T2-weighted MRI of the lumbar spine. At the L4-L5 level, there is a focal posterior protrusion of T2-hyperintense disc material indenting the anterior thecal sac. Axial T2 image at the same level shows the disc material in the right paracentral location, narrowing the right lateral recess and displacing the traversing right L5 nerve root. The disc material does not extend behind the adjacent vertebral bodies (no migration). The disc heights at other levels are preserved. The conus medullaris ends at L1. There is no marrow signal abnormality. The cauda equina nerve roots are otherwise normal in distribution and signal.]
Clinical vignette: A 38-year-old construction worker presents with 4 weeks of low-back pain radiating down the back of the right thigh and the lateral aspect of the right leg into the dorsum of the foot. Pain worsens with bending forward and coughing. Examination: positive straight-leg raise at 40 degrees on the right with pain in the L5 dermatome, weakness of right ankle dorsiflexion (3/5), reduced sensation over the dorsum of the right foot, normal ankle and knee jerks.
Options:
(a) L4-L5 right paracentral disc prolapse with L5 nerve root impingement
(b) L4-L5 far-lateral disc prolapse with L4 nerve root impingement
(c) L5-S1 right paracentral disc prolapse with S1 nerve root impingement
(d) Cauda equina syndrome from massive central disc prolapse
Correct answer: (a) L4-L5 right paracentral disc prolapse with L5 nerve root impingement
Reasoning:Right paracentral disc prolapse at L4-L5 indents the thecal sac and impinges the traversing L5 root, producing the classic L5 radiculopathy: pain radiating to the dorsum of the foot, weakness of ankle dorsiflexion (extensor hallucis longus, tibialis anterior), reduced sensation in the L5 dermatome, and normal ankle jerk (an L5-S1 disc with S1 root impingement would lose the ankle jerk). The MRI image pattern of focal posterior disc protrusion at L4-L5 with the disc displacing the right L5 root in the lateral recess is textbook.
A far-lateral L4-L5 disc would impinge the EXITING L4 root (knee jerk loss, quadriceps weakness, anterior thigh sensory loss). L5-S1 paracentral disc impinges the traversing S1 root (loss of ankle jerk, weakness of plantar flexion, lateral foot sensory loss). Cauda equina syndrome requires bilateral leg weakness, saddle anesthesia, and bowel-bladder dysfunction — none of which are present here.
Teaching pearl: Memorise the disc-root rule: paracentral disc prolapse impinges the traversing root (root that exits at the next lower level). Far-lateral / foraminal disc prolapse impinges the exiting root (root that exits at that level). The traversing root is the same number as the lower vertebra of the disc level — L4-L5 paracentral disc → L5 root.
Conservative management for first 6-8 weeks: NSAIDs, physiotherapy, gabapentinoids for neuropathic pain. Surgery (microdiscectomy) is indicated for: persistent severe pain despite 6 weeks of conservative therapy, progressive motor deficit, or cauda equina syndrome (emergency).
MCQ 2: 64-year-old man with progressive lower-limb weakness, urinary retention and back pain
Image description:[Sagittal T1 and T2-weighted MRI of the thoracolumbar spine. At T11-T12 there is replacement of the normal T1-bright fatty marrow signal of the T11 vertebral body by T1-hypointense signal, with corresponding T2 hyperintensity (better seen on STIR). The T11 vertebra shows mild compression with a soft-tissue extradural mass extending into the canal posteriorly, severely compressing the conus and proximal cauda equina. There is loss of CSF signal around the cord at this level. There are similar smaller lesions at T8 and L2 vertebral bodies. The pedicles of T11 are absent on the T1 image (pedicle sign — winking owl).]
Clinical vignette: A 64-year-old man with a known history of prostate cancer (diagnosed 2 years ago, on hormonal therapy) presents with 2 weeks of progressive bilateral lower-limb weakness, mid-back pain that worsens at night and is non-positional, urinary retention requiring catheterization, and reduced sensation below the umbilicus.
Options:
(a) Vertebral metastasis with extradural cord compression
(b) Tuberculosis of spine (Pott's disease) with cold abscess
(c) Osteoporotic vertebral compression fracture
(d) Multiple myeloma with extradural soft-tissue extension
Correct answer: (a) Vertebral metastasis with extradural cord compression
Reasoning:Multiple T1-hypointense vertebral bodies (replacement of fatty marrow by tumor), the 'winking owl' pedicle sign at T11 (pedicle destruction by lytic metastasis on AP X-ray, paralleled by absent pedicle marrow on MRI), an extradural soft-tissue mass compressing the conus, and a known primary cancer (prostate) are textbook for vertebral metastasis with malignant cord compression. Prostate cancer typically produces sclerotic (osteoblastic) metastases — these can still produce cord compression via direct extradural extension.
Pott's disease typically affects two contiguous vertebrae with intervening disc destruction (uncommon in metastasis, where the disc is preserved), produces a paraspinal cold abscess, and shows raised ESR with constitutional symptoms. Osteoporotic compression fracture preserves marrow signal between fractures (no marrow replacement), shows acute marrow edema only in the fractured vertebra, and lacks soft-tissue extension. Multiple myeloma can mimic metastasis but typically shows multiple punched-out lytic lesions, raised serum protein with M-band, hypercalcemia, and renal failure (CRAB criteria).
Teaching pearl: Differentiate metastasis vs Pott's vs osteoporosis vs myeloma on MRI:
Feature
Metastasis
Pott's disease
Osteoporotic fracture
Myeloma
Marrow signal
Replacement (T1 dark)
Variable
Preserved between fractures
Replacement
Disc
Preserved
Destroyed
Preserved
Preserved
Pedicle
Often destroyed
Spared
Spared
Lytic punched-out
Paraspinal mass
Soft tissue extension
Cold abscess (often subligamentous)
None
Soft tissue extension
Number of levels
Multiple
Often contiguous 2-3
Single or scattered
Multiple
Management of malignant cord compression is an oncological emergency:
High-dose IV dexamethasone 16 mg stat then 8 mg every 6 hours
Urgent MRI whole spine to define the extent
Decompressive surgery within 24-48 hours if life expectancy >3 months, single level, paraplegia <48 hours; surgery + radiotherapy is superior to radiotherapy alone (Patchell trial)
Radiotherapy if unsuitable for surgery, multiple levels, or radiosensitive tumor
Catheter drainage for retention; bowel programme; thromboprophylaxis; rehabilitation early
MCQ 3: 28-year-old woman with limb-girdle weakness, blurred vision, and urinary urgency
Image description:[Sagittal T2-weighted MRI of the cervical spine shows multiple short-segment T2-hyperintense lesions in the dorsal aspect of the cervical cord at C2-C3 and C5 levels, each spanning under one vertebral body height. Axial T2 images show the lesions occupy the dorsal columns and lateral columns asymmetrically, less than half the cord cross-section. The cord caliber is normal (no swelling). Brain MRI inset shows multiple ovoid T2/FLAIR hyperintensities arranged perpendicular to the lateral ventricles (Dawson's fingers), several juxtacortical lesions, and one infratentorial lesion in the brainstem. One lesion enhances with gadolinium. The optic nerves appear normal on this study.]
Clinical vignette: A 28-year-old IT professional presents with 1 week of bilateral lower-limb weakness, urinary urgency, a tight 'band' sensation around the trunk, and blurred vision in the right eye 6 months ago that resolved spontaneously over 4 weeks. Examination: brisk lower-limb reflexes, bilateral extensor plantars, reduced vibration sense in the lower limbs, mild ataxia, no internuclear ophthalmoplegia at present. Visual evoked potentials show prolonged P100 latency on the right.
Reasoning:Short-segment dorsal cervical cord T2 hyperintensities (under one vertebral body height each), multiple lesions in cord, classical Dawson's fingers periventricular brain lesions arranged perpendicular to the corpus callosum, juxtacortical and infratentorial brain lesions, with one gadolinium-enhancing lesion (active disease) and one prior optic neuritis episode fulfil the 2017 McDonald criteria for relapsing-remitting MS — dissemination in space (multiple cord and brain locations) and time (a prior optic neuritis with VEP evidence plus current cord disease).
NMOSD typically shows longitudinally extensive transverse myelitis spanning more than 3 vertebral bodies, often with cord swelling, central cord involvement, and severe optic neuritis (often bilateral, severe visual loss); anti-AQP4 IgG positive; brain lesions are typical of NMOSD-specific locations (area postrema, hypothalamus, periependymal). Idiopathic acute transverse myelitis also typically spans more than 2 vertebral bodies and is monophasic; multiple cord plaques with classical brain features are not idiopathic ATM. Spinal tuberculosis with intramedullary tuberculoma is rare; usually shows discrete ring-enhancing lesions, raised ESR, often with vertebral involvement.
Teaching pearl: Differentiating MS, NMOSD, ADEM, and idiopathic ATM on cord MRI:
Feature
MS
NMOSD
ADEM
Idiopathic ATM
Cord segment length
Short (under 2 VBs)
Long (over 3 VBs)
Short or long
Often over 2 VBs
Cord cross-section
Less than half (asymmetric, dorsal)
More than half (often central)
Variable
Variable
Brain MRI
Dawson's fingers, juxtacortical, infratentorial
Specific NMOSD locations or normal
Multiple ill-defined large lesions
Often normal
Optic neuritis
Unilateral, mild-moderate, often resolves
Severe, often bilateral, may be sequential
May co-exist
Absent
Antibody
None specific
Anti-AQP4 IgG (or anti-MOG)
Anti-MOG in some children
None
Course
Relapsing-remitting or progressive
Relapsing
Monophasic, post-infectious
Monophasic in most
Treatment of acute MS relapse: IV methylprednisolone 1 g/day for 3-5 days. Disease-modifying therapy: interferon-beta, glatiramer acetate, fingolimod, dimethyl fumarate, natalizumab, ocrelizumab, cladribine — choice depends on disease activity and comorbidity. NMOSD requires immunosuppression with rituximab, eculizumab, satralizumab or inebilizumab — interferon-beta is HARMFUL in NMOSD.
MCQ 4: 36-year-old man with bilateral arm weakness and dissociated sensory loss
Image description:[Sagittal T2-weighted MRI of the cervical and upper thoracic spine. There is a longitudinal CSF-isointense tubular cavity within the cord, extending from C2 down to T2 (approximately 7 vertebral body heights), occupying the central cord. The cord is mildly expanded around the cavity. Axial T2 images show the cavity as a central rounded/oval CSF-bright fluid collection within the cord. Brain MRI inset shows the cerebellar tonsils descending below the foramen magnum by approximately 8 mm into the upper cervical canal, with effacement of the cisterna magna — consistent with Chiari I malformation.]
Clinical vignette: A 36-year-old man presents with 18 months of progressive weakness and wasting of the small muscles of both hands, fasciculations in the deltoids, and burning pain in the upper limbs. He reports painless burns of the fingertips while cooking. Examination: bilateral hand and forearm wasting, brisk lower-limb reflexes with extensor plantars, dissociated sensory loss with reduced pain and temperature sensation over the upper limbs and shoulders in a 'cape' distribution, but preserved light touch and joint position sense.
Options:
(a) Syringomyelia secondary to Chiari I malformation
(b) Intramedullary ependymoma with reactive cyst
(c) Cervical spondylotic myelopathy
(d) Amyotrophic lateral sclerosis
Correct answer: (a) Syringomyelia secondary to Chiari I malformation
Reasoning:A longitudinal CSF-isointense tubular cavity within the central cord, mildly expanding the cord, plus cerebellar tonsillar descent below the foramen magnum by 8 mm is textbook syringomyelia secondary to Chiari I malformation. The clinical features confirm the localisation: dissociated sensory loss in a 'cape' distribution (anterior decussating spinothalamic fibres are interrupted at the syrinx as they cross in the central cord, while dorsal column fibres are spared), bilateral lower motor neuron signs in the upper limbs (anterior horn cell involvement at the cervical syrinx levels), upper motor neuron signs in the lower limbs (lateral corticospinal tract compression by the expanding syrinx), and painless burns from analgesia.
Intramedullary ependymoma can produce a tumor cyst, but the tumor itself is solid and enhances; pure CSF-isointense cavity without enhancement and with Chiari I is syringomyelia. Cervical spondylotic myelopathy produces extradural compression from osteophytes and disc bulges, with cord T2 hyperintensity at the compression level — no central cavity. Amyotrophic lateral sclerosis (ALS) presents with combined UMN and LMN signs but has no cavity, no sensory loss, and no Chiari malformation.
Teaching pearl:Cape distribution dissociated sensory loss + bilateral hand wasting + Chiari I tonsillar descent on brain MRI = syringomyelia from Chiari I. The pathophysiology: tonsillar descent disrupts CSF flow at the foramen magnum; pulsatile CSF pressure forces fluid into the central canal, creating a syrinx that progressively expands.
Treatment of symptomatic Chiari I-related syrinx: foramen magnum decompression with duraplasty is the operation of choice — restores CSF flow and the syrinx typically collapses. Persistent or recurrent syrinx may need syringosubarachnoid or syringoperitoneal shunting. Tumor-associated syrinx (e.g., associated ependymoma) requires resection of the tumor; the syrinx then resolves. Post-traumatic syrinx (a late complication of spinal cord injury) is more challenging and may need shunting.
MCQ 5: 24-year-old woman with sudden bilateral leg weakness, numbness, and bladder dysfunction
Image description:[Sagittal T2-weighted MRI of the thoracic spine shows a segmental T2-hyperintense lesion in the cord extending from T6 to T9 (approximately 4 vertebral body heights), with expansion of the cord at this level. Axial T2 images show the hyperintensity occupying the central two-thirds of the cord cross-section. Post-contrast T1 sagittal shows patchy enhancement within the lesion. There is no extradural mass, no disc prolapse, no marrow signal abnormality, and no extramedullary mass. Brain MRI inset shows no lesions. Optic nerves appear normal.]
Clinical vignette: A 24-year-old woman presents with 5 days of progressive bilateral lower-limb weakness, a sensory level at the umbilicus, urinary retention requiring catheterization, and constipation. She had a viral illness with fever and diarrhea 2 weeks ago. There is no prior neurological history. Examination: spastic paraparesis with brisk reflexes, bilateral extensor plantars, sensory level at T10, and reduced anal tone. CSF analysis shows 32 lymphocytes per mm³, protein 65 mg/dL, normal glucose, no oligoclonal bands.
Reasoning:A segmental T2-hyperintense cord lesion spanning 4 vertebral body heights with cord swelling, central involvement of more than half the cord cross-section, patchy enhancement, no extradural mass, in a young woman with subacute progression of motor, sensory, and autonomic dysfunction following a viral illness, with CSF lymphocytic pleocytosis is textbook acute transverse myelitis (ATM), post-infectious.
Multiple sclerosis would typically show short-segment dorsal cervical cord lesions (under 2 vertebral body heights), with brain Dawson's fingers and oligoclonal bands in CSF. NMOSD would also span more than 3 vertebral bodies (longitudinally extensive transverse myelitis) but typically presents in older patients with severe optic neuritis and has anti-AQP4 IgG positive. Spinal cord infarction (anterior spinal artery syndrome) presents with sudden onset (minutes), preserves dorsal column function (vibration, position sense), and shows axial T2 hyperintensity in the anterior 2/3 of the cord with a 'snake-eye' or 'owl's-eye' pattern; a longitudinal swelling pattern is less typical. Spinal epidural abscess produces an extradural collection with rim enhancement, marrow edema in adjacent vertebrae, and clinical features of fever and severe back pain.
High-dose IV methylprednisolone 1 g/day for 5 days
Plasmapheresis if no response after 5-7 days of steroids — 5-7 sessions
Etiology-directed therapy if specific cause identified (rituximab for NMOSD, antimicrobials for infection, immunosuppression for autoimmune)
Catheter, bowel care, thromboprophylaxis, rehabilitation
Long-term follow-up with MRI; some idiopathic ATM cases later evolve into MS, NMOSD, or MOG-AD
Common pitfalls and how to avoid them
Pitfall 1: Calling every cord T2 hyperintensity 'transverse myelitis'. Compression-induced cord edema looks similar — always check for an extradural or extramedullary mass before labelling a cord T2 hyperintensity as ATM.
Pitfall 2: Misapplying the disc-root rule. Paracentral disc impinges the traversing root; far-lateral disc impinges the exiting root. NEET PG loves the trap of "L4-L5 disc with L4 radiculopathy = far-lateral L4-L5 disc, NOT paracentral".
Pitfall 3: Missing the conus level. Always note where the conus medullaris ends (typically L1-L2 in adults). A lesion at L1-L2 affecting the conus produces conus medullaris syndrome (early bowel-bladder dysfunction, mixed UMN-LMN). A lesion below L2 affects only cauda equina (LMN, asymmetric, severe pain, late bowel-bladder).
Pitfall 4: Misclassifying short-segment vs longitudinally extensive cord lesions. MS plaques are short (under 2 VBs), dorsal, asymmetric, less than half cross-section. NMOSD and idiopathic ATM are typically longer than 3 VBs, central, and more than half the cross-section. Match the lesion length to the differential.
Pitfall 5: Confusing syringomyelia with hydromyelia. Both are CSF-isointense central cord cavities. Syringomyelia is a discrete cavity within the cord parenchyma, often associated with Chiari I or post-traumatic; hydromyelia is dilatation of the central canal communicating with the fourth ventricle, often congenital, less symptomatic. The distinction is technical; both can be managed similarly when symptomatic.
Pitfall 6: Not checking the brain when reviewing spine MRI. Many spinal cord lesions have brain co-conspirators that clinch the diagnosis: Dawson's fingers in MS, area postrema lesion in NMOSD, Chiari I tonsillar descent in syringomyelia, leptomeningeal enhancement in sarcoidosis. Always pair spine MRI with brain MRI when an inflammatory or infiltrative cord lesion is suspected.
Pitfall 7: Forgetting marrow signal in vertebral metastasis. T1 marrow signal that is darker than disc signal is abnormal — it suggests marrow replacement by tumor, infection, or infiltrative process. Compare T1 vertebral body signal to disc and to muscle: vertebral body should be brighter than disc and similar to or brighter than muscle in adults under 50. Replacement by metastasis flips this rule.
How NEET PG tests MRI spine
Six recurring patterns. Recognise the pattern and the question collapses.
Pattern 1 — The disc-root question: Vignette gives a patient with L5 radiculopathy and asks the level of disc prolapse. L5 radiculopathy = L4-L5 paracentral disc (traversing L5 root) OR L5-S1 far-lateral disc (exiting L5 root). NEET PG often uses paracentral.
Pattern 2 — The cord compression question: Patient with progressive paraparesis and bladder dysfunction; MRI shows extradural mass. Best next step? High-dose dexamethasone 16 mg IV stat then 8 mg q6h, urgent MRI whole spine, urgent neurosurgery/oncology referral, decompression within 24-48 hours.
Pattern 3 — The MS-vs-NMOSD question: Young patient with cord lesion. Short-segment dorsal cord plus brain Dawson's fingers = MS. Longitudinally extensive (over 3 VBs) plus severe optic neuritis = NMOSD (anti-AQP4 IgG positive). Treatment: MS — IFN-beta, fingolimod, ocrelizumab; NMOSD — rituximab, eculizumab. Interferon-beta is HARMFUL in NMOSD.
Pattern 4 — The syringomyelia question: Cape distribution dissociated sensory loss + bilateral hand wasting + Chiari I = syringomyelia from Chiari I. Treatment: foramen magnum decompression with duraplasty.
Pattern 5 — The transverse myelitis question: Subacute paraparesis + sensory level + bowel-bladder dysfunction + cord T2 hyperintensity over 2-4 VBs without compression. Treatment: IV methylprednisolone 1 g/day for 5 days, plasmapheresis if no response.
Pattern 6 — The cauda-equina question: Massive central disc prolapse with bilateral leg weakness, saddle anesthesia, bowel-bladder dysfunction. Surgical emergency — decompression within 24-48 hours preserves bowel-bladder function.
Pott's: contiguous vertebrae with disc destruction and cold abscess
Malignant cord compression: dexamethasone + decompressive surgery within 24-48 hours
Frequently Asked Questions
How do you differentiate intramedullary, intradural-extramedullary, and extradural spinal lesions on MRI?
Intramedullary lesions arise within the cord substance — they expand the cord, displace CSF symmetrically away from the lesion, and produce a fusiform widening of the cord shadow. Examples: ependymoma (central, often hemorrhagic), astrocytoma (eccentric, longer segment), syringomyelia (CSF-density tubular cavity), demyelinating plaque (short segment). Intradural-extramedullary lesions sit inside the dura but outside the cord — they widen the ipsilateral subarachnoid space and displace the cord to the contralateral side. Examples: meningioma (thoracic, female, dural-based broad attachment), schwannoma (dumbbell shape extending through neural foramen), neurofibroma. Extradural lesions sit outside the dura — they compress the dura and cord/cauda equina from outside, narrowing the canal. Examples: disc prolapse, vertebral metastasis, epidural abscess, hematoma. The visual rule: cord pushed = extramedullary; cord expanded = intramedullary; canal pinched from outside = extradural.
What is the difference between cauda equina syndrome and conus medullaris syndrome?
The conus medullaris is the tapered terminal end of the spinal cord, typically at L1-L2 in adults. Conus syndrome (lesion at L1-L2) produces early bilateral symmetric perineal sensory loss, prominent and early bowel-bladder dysfunction, mixed upper and lower motor neuron features (UMN signs from corticospinal tracts plus LMN signs from sacral roots), and relatively preserved leg strength. Cauda equina syndrome (lesion BELOW L1-L2 affecting nerve roots) produces asymmetric leg weakness, asymmetric saddle anesthesia, late bowel-bladder dysfunction, severe radicular pain, and pure LMN signs (areflexia, atrophy). Both are surgical emergencies — early decompression (within 24-48 hours of acute presentation) preserves bowel-bladder function. Common causes: massive central disc prolapse (commonest), epidural abscess, vertebral metastasis, hematoma, lumbar stenosis, infiltrative tumor. MRI lumbosacral spine is the imaging gold standard.
What MRI features identify a multiple sclerosis plaque in the spinal cord?
MS plaques in the cord are classically: short-segment (under 2 vertebral body heights), peripheral or dorsal, asymmetric (less than half the cord cross-section), in the cervical cord (most common location), T2 hyperintense, T1 iso or hypointense, with mild or no cord swelling, and may enhance acutely with gadolinium (active plaque). The brain MRI is critical — Dawson's fingers (ovoid periventricular T2 hyperintensities perpendicular to the corpus callosum), juxtacortical lesions, infratentorial lesions, and gadolinium-enhancing lesions support dissemination in space. McDonald 2017 criteria require dissemination in space and time, supported by clinical attacks plus MRI features. Spinal cord MS plaques are distinguished from neuromyelitis optica spectrum disorder (NMOSD) lesions, which are typically longitudinally extensive transverse myelitis (LETM) spanning more than three vertebral bodies, and from acute transverse myelitis, which is also typically longer than three segments and often more central.
What is the differential for a longitudinal T2 hyperintense cavity in the spinal cord?
A tubular CSF-isointense cavity within the cord on MRI is syringomyelia until proven otherwise. The differential of cord cavitation includes: (1) classic syringomyelia secondary to Chiari I malformation (commonest cause; cervicothoracic location; descended cerebellar tonsils through foramen magnum on brain MRI); (2) post-traumatic syrinx (months to years after spinal cord injury); (3) tumor-associated syrinx (associated cord tumor, especially intramedullary ependymoma or hemangioblastoma); (4) hydromyelia (dilatation of central canal — typically wider, communicates with fourth ventricle); (5) myelomalacia (post-traumatic or post-ischemic cord softening, usually irregular not tubular). Treatment of symptomatic syringomyelia from Chiari I is foramen magnum decompression; idiopathic or progressive syrinx may need syringosubarachnoid or syringoperitoneal shunt; tumor-associated syrinx requires resection of the tumor.
What is acute transverse myelitis and how is it differentiated from cord compression on MRI?
Acute transverse myelitis (ATM) is a non-compressive inflammatory disorder of the spinal cord with onset of motor, sensory and autonomic dysfunction over hours to weeks. MRI features: segmental cord T2 hyperintensity (typically more than 2 vertebral segments — longitudinally extensive in NMOSD; shorter in MS), cord swelling without external compression, gadolinium enhancement, and absence of an extradural or extramedullary mass. Causes include MS, neuromyelitis optica spectrum disorder (anti-AQP4 IgG), MOG antibody-associated disease, post-infectious (post-viral, post-vaccine), systemic autoimmune (lupus, Sjogren), spinal cord ischemia (anterior spinal artery syndrome — typically anterior 2/3 of cord and disc-shaped on axial T2), and idiopathic. Differentiation from cord compression: ATM has cord swelling without an external compressing mass; cord compression has visible extradural or intradural-extramedullary lesion narrowing the canal. ATM is treated with high-dose IV methylprednisolone 1 g/day for 5 days, with plasmapheresis as second-line; etiology-directed therapy follows.
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: April 2026
