Anatomy chapters

Spinal cord lesions

How to localise a spinal cord lesion from its pattern: complete transection, hemisection (Brown-Séquard), central cord and syringomyelia, anterior cord, posterior column disease, and conus and cauda equina lesions.

UHS PGET syllabus: Neuroanatomy, Spinal cord lesionsUpdated October 2026
In 30 seconds
  • Localise by asking which tracts are lost on which side and at what level.
  • Brown-Séquard (hemisection): same-side weakness and loss of vibration and position, opposite-side loss of pain and temperature.
  • Syringomyelia: a central cavity damages crossing pain fibres first, giving cape-like loss of pain and temperature with touch preserved.
On this page

Overview

A spinal cord lesion produces a pattern of loss that depends on which tracts are damaged, on which side and at what level.

You need three facts from spinal cord and its tracts:

  • Corticospinal tract (movement): has already crossed in the medulla, so a cord lesion causes same-side weakness.
  • Dorsal columns (vibration, position, fine touch): cross in the medulla, so a cord lesion causes same-side loss.
  • Spinothalamic tract (pain, temperature): crosses in the cord near entry, so a cord lesion causes opposite-side loss.

Complete transection

How it happens: major trauma (fracture-dislocation of the spine), tumour or transverse myelitis.

What you see: loss of all movement and sensation below the lesion on both sides, and loss of bladder and bowel control.

  • At first there is spinal shock: flaccid paralysis with no reflexes, lasting days to weeks.
  • Later, upper motor neuron signs appear below the level: spasticity, brisk reflexes and Babinski signs.
  • At the level of the lesion, the damaged anterior horn cells give lower motor neuron signs in a band.
High-yield

Lesions above C5 affect the diaphragm (phrenic nerve, C3–C5) and threaten breathing. Lesions above T1 cause weakness of all four limbs (tetraplegia); lower lesions cause paraplegia.

Hemisection (Brown-Séquard syndrome)

How it happens: damage to one half of the cord, often a stab wound or a tumour pressing from one side.

What you see below the lesion:

Same side as the lesionOpposite side
Weakness with UMN signs (lateral corticospinal)Loss of pain and temperature, starting 1–2 segments below (lateral spinothalamic)
Loss of vibration, position and fine touch (dorsal columns)

At the level of the lesion, there may be a band of complete sensory loss and LMN weakness on the same side.

High-yield

In Brown-Séquard syndrome, pain and temperature are lost on the opposite side; everything else is lost on the same side.

Exam trap

The pain and temperature loss starts one or two segments below the lesion, because spinothalamic fibres climb a little before they cross.

Syringomyelia (central cord lesion)

How it happens: a fluid-filled cavity (syrinx) forms in the centre of the cord, usually in the cervical region. It is often linked with a Chiari malformation.

What you see:

  • First, the cavity damages the crossing spinothalamic fibres in the anterior white commissure. This causes loss of pain and temperature on both sides over the levels involved, in a cape-like distribution over the shoulders and arms.
  • Touch, vibration and position sense are preserved (dissociated sensory loss).
  • Patients get painless burns and cuts on the hands.
  • As it grows, it damages the anterior horns (wasting of the small hand muscles, LMN signs) and then the corticospinal tracts (UMN signs in the legs).
High-yield

Dissociated sensory loss in a cape distribution, with painless burns on the hands, points to syringomyelia.

Central cord syndrome

A similar pattern after hyperextension injury of an arthritic neck in older people. The arms are weaker than the legs, because arm fibres lie closer to the centre in the lateral corticospinal tract.

Anterior cord syndrome

How it happens: blockage of the anterior spinal artery (for example after aortic surgery) or a disc or bone fragment pressing on the front of the cord.

What you see: paralysis and loss of pain and temperature below the lesion, on both sides. Vibration and position sense are preserved because the dorsal columns are spared.

Posterior column disease

Tabes dorsalis

How it happens: late syphilis damaging the dorsal roots and dorsal columns, mainly in the lower cord.

What you see: loss of position and vibration sense, unsteady stamping walk, positive Romberg test, sharp shooting pains, loss of reflexes, and pupils that react to focusing but not to light (Argyll Robertson pupils).

Subacute combined degeneration

How it happens: vitamin B12 deficiency.

What you see: damage to the dorsal columns (loss of vibration and position sense) and the lateral corticospinal tracts (UMN weakness, Babinski sign), often with peripheral neuropathy so the ankle reflexes may be lost.

High-yield

B12 deficiency = dorsal columns + lateral corticospinal tracts ("combined").

Anterior horn cell disease

  • Poliomyelitis: a virus destroys anterior horn cells, causing pure LMN weakness with no sensory loss.
  • Motor neuron disease: affects both upper and lower motor neurons, so UMN and LMN signs are mixed, with no sensory loss.

Conus medullaris and cauda equina lesions

FeatureConus medullarisCauda equina
LevelAround L1–L2 vertebraeBelow L2 (nerve roots)
OnsetOften sudden, symmetricalOften gradual, asymmetrical
PainLess markedSevere radicular (root) pain
Saddle anaesthesiaSymmetricalAsymmetrical
Bladder and bowelEarly dysfunctionLater dysfunction
Motor signsMixed UMN and LMNLMN only (flaccid, areflexic)
High-yield

Cauda equina syndrome (often from a large central disc prolapse) causes saddle anaesthesia, urinary retention and leg weakness. It is a surgical emergency.

A quick way to localise

  1. Is there a sensory level? It points to the cord.
  2. Which modalities are lost? All, or only pain and temperature, or only vibration and position?
  3. Which side? Same side vs opposite side tells you about hemisection.
  4. UMN or LMN? UMN signs below a cord lesion; LMN signs at the level or in cauda equina lesions.
Exam focus

Almost all questions are clinical vignettes. Know the pattern of Brown-Séquard syndrome, syringomyelia, anterior cord syndrome, subacute combined degeneration and tabes dorsalis, and the difference between conus and cauda equina lesions.

Quick revision

  • Transection: all lost below; spinal shock first, then UMN signs.
  • Hemisection: same-side weakness and dorsal column loss; opposite-side pain and temperature loss.
  • Syringomyelia: cape-like loss of pain and temperature, touch preserved; hand wasting later.
  • Anterior cord: dorsal columns spared.
  • B12: dorsal columns + lateral corticospinal. Tabes: dorsal columns and roots.
  • Cauda equina: LMN, radicular pain, saddle anaesthesia; emergency.

Written by The House Job from standard neuroanatomy references (Snell's Clinical Neuroanatomy).

FAQ

What are the features of Brown-Séquard syndrome?

Weakness and loss of vibration and position sense on the same side below the lesion, with loss of pain and temperature on the opposite side.

Why is touch preserved in syringomyelia?

The cavity first damages the crossing pain and temperature fibres in the centre of the cord; the dorsal columns carrying touch are spared.

Which tracts are affected in subacute combined degeneration?

The dorsal columns and the lateral corticospinal tracts.

Is cauda equina syndrome an upper or lower motor neuron lesion?

A lower motor neuron lesion, because it affects the nerve roots.