FCPS Part 1 AnatomyMedicine Paper 2Surgery Paper 2

Spinal cord tracts

Spinal cord: tracts, blood supply, cord syndromes and Brown-Séquard

Spinal cord for FCPS Part 1: ascending and descending tracts, where each crosses, blood supply, dorsal horn laminae and the classic cord syndromes. Explains Brown-Séquard, anterior and central cord, B12, Friedreich ataxia, bladder lesions and pain gating.

One of the most tested topics in past papers

Gross anatomy and coverings

  • The cord runs from the foramen magnum to L1/L2 in adults, ending as the conus medullaris. At birth it reaches about L3, because the vertebral column grows faster than the cord. A neonatal lumbar puncture is therefore done at L4/5 or lower; Tuffier's line also sits lower in infants.
  • Below the conus, lumbar and sacral roots form the cauda equina. The filum terminale (pia) anchors the cord to the coccyx; a short, thick filum can tether the cord.
  • Denticulate ligaments: about 21 pairs of serrated pial bands that pass laterally between the dorsal and ventral roots to attach to the dura, holding the cord in the centre of the dural sac.
  • Enlargements at C5–T1 (brachial plexus) and L2–S3 (lumbosacral plexus).

Grey matter and dorsal horn laminae

  • Dorsal horn: sensory. Ventral horn: alpha and gamma motor neurones. Lateral horn: T1–L2 sympathetic preganglionic neurones; S2–S4 parasympathetic neurones for bladder, rectum and erection.
  • Rexed laminae: lamina I (marginal zone) and lamina V receive fast, well-localised Aδ pain fibres. Lamina II (substantia gelatinosa) receives slow, burning C-fibre pain and contains enkephalin interneurones. Lamina IX holds motor neurones.

Main tracts and where they cross

TractCarriesCrossesPosition in cord
Lateral corticospinalVoluntary skilled movementMedullary pyramids (about 85%)Lateral column
Anterior corticospinalAxial musclesAt the segment where it endsAnterior column
Dorsal columns (gracile medial = legs; cuneate lateral = arms, above T6)Fine touch, vibration, proprioceptionMedulla (internal arcuate fibres to medial lemniscus)Posterior column
Lateral spinothalamicPain and temperatureWithin 1–2 segments (anterior white commissure)Anterolateral
Anterior spinothalamicCrude touch, pressureSame as aboveAnterolateral
Dorsal spinocerebellarUnconscious proprioception from legUncrossed; inferior cerebellar peduncleLateral edge
Ventral spinocerebellarSame, whole limb movementCrosses twice; superior peduncleLateral edge
  • Lamination: in the spinothalamic and corticospinal tracts sacral fibres are outermost; in the dorsal columns sacral fibres are most medial. An expanding central lesion therefore spares sacral pain sensation (sacral sparing).
  • Spinocerebellar tracts carry unconscious proprioception to the ipsilateral cerebellum for coordinating posture and movement.

Pain gating and descending analgesia

  • Large Aβ touch fibres excite enkephalin interneurones in the substantia gelatinosa, which inhibit substance P release from C-fibre terminals (the gate control theory: rubbing an injury eases pain).
  • The periaqueductal grey (midbrain) activates the nucleus raphe magnus (medulla), which sends serotonin fibres down to the dorsal horn; these excite enkephalin interneurones. The locus coeruleus adds a noradrenergic descending pathway.
  • So the transmitter released by inhibitory interneurones onto incoming pain fibres is enkephalin; the transmitter from raphe magnus is serotonin.

Blood supply

  • Anterior spinal artery (one, formed from both vertebrals): anterior two-thirds of the cord, including corticospinal and spinothalamic tracts.
  • Posterior spinal arteries (two, from vertebral or PICA): dorsal columns and dorsal horns.
  • Artery of Adamkiewicz (great anterior radicular), usually left, T9–T12: main supply to the lower cord. Injury during aortic aneurysm repair or dissection gives anterior cord syndrome.
  • The upper thoracic cord (about T4) is a watershed zone.

Upper versus lower motor neurone

SignUMN lesionLMN lesion
ToneSpasticity, clasp-knife; velocity dependent (greater with faster stretch)Flaccid
ReflexesBrisk, clonus, Hoffmann signReduced or absent
PlantarExtensor (Babinski)Flexor
BulkLittle wasting (disuse only)Wasting, fasciculation
  • Spinal shock: after acute cord injury, tone and reflexes below the lesion are absent for days to weeks; spasticity and hyperreflexia appear later. Return of the bulbocavernosus reflex marks its end.
  • Spasticity arises from loss of descending inhibition of gamma motor neurones and stretch reflexes, so the faster the passive stretch, the stronger the resistance.

Cord syndromes

SyndromeCauseFeatures
Brown-Séquard (hemisection)Stab wound, tumourIpsilateral UMN weakness and loss of vibration and proprioception below; contralateral loss of pain and temperature from 1–2 segments below; at the level, ipsilateral band of total sensory loss and LMN signs
Anterior cordAnterior spinal artery occlusion, aortic surgeryParaplegia, loss of pain and temperature; dorsal columns spared
Central cordNeck hyperextension in spondylosis; syringomyeliaArms worse than legs; cape-like loss of pain and temperature with preserved touch
Posterior cordTabes dorsalis, B12 deficiencyLoss of vibration and proprioception, sensory ataxia, positive Romberg
Subacute combined degenerationB12 deficiencyDorsal columns plus lateral corticospinal tracts plus neuropathy: absent ankle jerks with extensor plantars
Complete transectionTraumaAll modalities lost below; spinal shock, then spasticity
  • The band of total loss at the level of a hemisection comes from destruction of the entering dorsal root fibres of all modalities on that side.
  • Syringomyelia: a fluid cavity in the central cord, often with a Chiari I malformation. It cuts crossing spinothalamic fibres first (dissociated sensory loss, painless burns), then the ventral horns (wasted small hand muscles).
  • Friedreich ataxia: autosomal recessive GAA trinucleotide repeat in the frataxin gene. Degeneration of dorsal columns, spinocerebellar and corticospinal tracts plus peripheral nerves gives ataxia, dysarthria, absent ankle jerks with extensor plantars, pes cavus, scoliosis, hypertrophic cardiomyopathy and diabetes. Onset is in childhood or adolescence.
  • Degenerative cervical myelopathy: spondylotic narrowing of the cervical canal in older adults. Clumsy hands, difficulty with buttons, unsteady gait, brisk reflexes in all four limbs, positive Hoffmann sign and upgoing plantars. Often mistaken for carpal tunnel syndrome.
  • Neuromyelitis optica: severe optic neuritis plus a longitudinally extensive cord lesion (three or more vertebral segments) with a normal brain MRI. Caused by aquaporin-4 IgG against astrocyte water channels; some MS drugs worsen it.
  • Metastatic cord compression (breast, lung, prostate): back pain, then weakness, sensory level and sphincter loss; urgent MRI, dexamethasone and radiotherapy or surgery.

Bladder after cord injury

LesionBladder
Above S2–S4 (suprasacral, after spinal shock)Spastic reflex bladder: small capacity, involuntary emptying, detrusor–sphincter dyssynergia
S2–S4 segments or cauda equinaAtonic bladder, retention with overflow dribbling
Afferent loss (tabes dorsalis, diabetic neuropathy)Large insensate atonic bladder because the sensory limb is cut

Remember Pain crosses early in the cord; touch, proprioception and movement cross late in the medulla.

Exam trap In Brown-Séquard, pain and temperature are lost on the opposite side, but the band of total loss at the level is on the same side.

Exam trap Absent ankle jerks with upgoing plantars mean combined dorsal column, pyramidal and peripheral nerve disease: B12 deficiency or Friedreich ataxia.

How FCPS asks about this

  • Hemisection by stab wound: ipsilateral weakness and proprioception loss, contralateral pain loss, ipsilateral band of total loss at the level.
  • Anterior spinal artery occlusion: paraplegia and pain loss with dorsal columns spared.
  • Slow burning C-fibre pain terminates in: lamina II, substantia gelatinosa.
  • Teenager with ataxia, pes cavus and hypertrophic cardiomyopathy: Friedreich ataxia, GAA repeat in frataxin.
  • Sacral cord S2–S4 crushed: atonic bladder with overflow incontinence.
  • Optic neuritis with a long cord lesion and normal brain: aquaporin-4 antibody, neuromyelitis optica.
  • Sympathetic preganglionic neurones lie in: lateral horn T1–L2.

Test yourself on this topic

5 of the 67 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.

Question 1Medium

After a knife wound to the right side of the thoracic spinal cord, which pattern of deficit is expected below the level of injury?

Question 2Medium

During thoracoabdominal aneurysm repair, the surgeon reimplants intercostal arteries from T9 to T12. Which artery is he trying to preserve?

Question 3Easy

An unvaccinated 3-year-old boy in Bannu has fever and muscle pain, then sudden floppy weakness of his left leg. The knee and ankle jerks on that side are absent but sensation is normal. Which of the following cells has the virus destroyed?

Question 4Medium

A stab wound hemisects the right side of the spinal cord at T6, but pain loss on the left begins only at T8. What explains this gap?

Question 5Medium

A 27-year-old woman with previous optic neuritis feels an electric shock down her spine whenever she flexes her neck. Which of the following is the site of the lesion?

Practise all 67 questions on this topic

Where this sits in the CPSP syllabus

  • Paper 1: Neuroanatomy, Spinal cord: tracts, blood supply and lesions (Brown-Sequard, cord syndromes)
  • Surgery & Allied, Paper 2: Cranium and brain, Spinal cord: tracts, blood supply and lesions (Brown-Sequard, cord syndromes)
  • Medicine & Allied, Paper 2: Central nervous system, Spinal cord: tracts, blood supply and lesions (Brown-Sequard, cord syndromes)

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