Spinal Cord Pathology
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Direct answer
Cord pathology is tract anatomy made clinical: a lesion's level and cross-sectional extent predict the deficits before any scan, because the corticospinal tracts cross in the medulla (upper-lesion ipsilateral weakness below), the spinothalamic fibres cross within two segments at entry (pain and temperature lost contralaterally below), and the posterior columns carry ipsilateral vibration and proprioception. Compressive disease — in India, tuberculous extradural pus and granulation tissue (Pott's disease) still competing with metastases and disc prolapse — threatens the cord with vascular compromise, while intrinsic diseases such as syringomyelia, demyelination and subacute combined degeneration of vitamin B12 deficiency produce signature dissociated patterns the exam tests relentlessly.
What you must remember
- Brown-Séquard syndrome: hemisection of the cord — ipsilateral spastic weakness with loss of vibration and proprioception, ipsilateral segmental lower-motor-neuron signs at the level, and contralateral loss of pain and temperature starting one or two segments below; pure hemisections are rare.
- Anterior spinal artery syndrome: infarction of the anterior two-thirds — bilateral spastic weakness with loss of pain and temperature, posterior columns spared, often after aortic surgery, hypotension or fibrocartilaginous embolism.
- Central cord pattern: a central lesion (syrinx, tumour) first interrupts the decussating spinothalamic fibres, giving bilateral segmental "cape-like" dissociated sensory loss (pain and temperature gone, touch and position preserved) with spastic weakness developing as the lesion enlarges.
- Subacute combined degeneration: vitamin B12 deficiency damages the posterior columns and lateral corticospinal tracts (also spinocerebellar) — loss of vibration and joint position in the legs with extensor plantars and absent ankle jerks from an accompanying peripheral neuropathy; the megaloblastic anaemia picture may be masked by folate intake, a classical Indian pitfall.
- Compression mechanics: extradural (metastasis, epidural abscess, Pott's gibbus), intradural extramedullary (meningioma, schwannoma — well-localised pain, ipsilateral Brown-Séquard evolution) and intramedullary (glioma, ependymoma — dissociated segmental signs) compartments localise before histology does.
- Tuberculosis of the cord, Indian reality: tuberculous meningitis leaves basal arachnoiditis and spinal block; arachnoiditis plus cold abscess produce compressive myelopathy; in some series tuberculosis accounts for a striking share of Indian compressive myelopathy — the exam expects it high on the differential alongside trauma and tumour.
- Syringomyelia mechanics: cavitation dilates from CSF flow obstruction at the foramen magnum, classically with a Chiari I malformation; suspends within it the segmental reflex arc (areflexic atrophy at the level) as it widens.
Working a deficit pattern back to a lesion
A 50-year-old man develops two years of clumsiness of both hands, burning himself painlessly while cooking, with small-muscle wasting. Reason backwards: bilateral segmental pain-temperature loss at C8-T1 with hand muscle wasting (anterior horn involvement) but preserved touch, plus later spastic legs and bladder urgency, maps to a central cervical cord lesion expanding outward — the syrinx. Magnetic resonance imaging confirms the dilated central canal of a Chiari I malformation. Contrast the neighbour case: a woman with diabetes and tingling feet, extensor plantars, absent vibration at the knees and megaloblastic hypersegmented neutrophils — subacute combined degeneration of B12 deficiency, where the treatable lesion is nutritional, and parenteral B12 reverses the tracts early and incompletely late. A third: bed-ridden fever with sudden paraplegia and a tender spine — spinal epidural abscess, decompress now. Each vignette begins as sensory anatomy and ends as a different disease; that is exactly how the professional examination frames the cord.
Where students slip
The recurring slip is quoting "ipsilateral proprioception, contralateral pain" without knowing the crossing levels that generate it — the examiner then asks why the spinothalamic loss starts two segments below the lesion, and only the decussation-within-two-segments answer survives. Second, students forget that Lhermitte's sign (electric sensations down the spine on neck flexion) signals posterior-column demyelination of any cause — radiation, multiple sclerosis, B12 — not one disease. Third, in Indian medicine, the index of suspicion: a gradually progressive paraplegia with a gibbus, evening fever and a soft paravertebral swelling is tuberculosis until imaging and biopsy prove otherwise — delayed therapy converts a walking Pott's paraplegia into a permanent one.
Frequently asked questions
Why does Brown-Séquard give contralateral pain loss two segments below?
Spinothalamic fibres ascend one or two segments in the posterolateral tract of Lissauer before decussating, so the sensory level sits just below the lesion on the opposite side.
What distinguishes anterior spinal artery syndrome?
Bilateral loss of motor power and pain-temperature with sparing of posterior-column modalities, because the anterior two-thirds of the cord supplied by the single anterior spinal artery is infarcted.
What causes dissociated sensory loss in syringomyelia?
Crossing spinothalamic fibres are interrupted segmentally within the central cord, abolishing pain and temperature while touch pathways in posterior columns and anterior commissure pathways are preserved.
Which tracts fail in subacute combined degeneration?
Posterior columns and lateral corticospinal tracts chiefly, with spinocerebellar involvement and a coexisting peripheral neuropathy — from vitamin B12 deficiency.
Why keep tuberculosis high on the Indian compressive myelopathy list?
Cold abscess, epidural granulation tissue and basal arachnoiditis from tuberculosis compress the cord as effectively as any tumour and respond to chemotherapy when identified early — a leading Indian cause.