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
| Tract | Carries | Crosses | Position in cord |
|---|---|---|---|
| Lateral corticospinal | Voluntary skilled movement | Medullary pyramids (about 85%) | Lateral column |
| Anterior corticospinal | Axial muscles | At the segment where it ends | Anterior column |
| Dorsal columns (gracile medial = legs; cuneate lateral = arms, above T6) | Fine touch, vibration, proprioception | Medulla (internal arcuate fibres to medial lemniscus) | Posterior column |
| Lateral spinothalamic | Pain and temperature | Within 1–2 segments (anterior white commissure) | Anterolateral |
| Anterior spinothalamic | Crude touch, pressure | Same as above | Anterolateral |
| Dorsal spinocerebellar | Unconscious proprioception from leg | Uncrossed; inferior cerebellar peduncle | Lateral edge |
| Ventral spinocerebellar | Same, whole limb movement | Crosses twice; superior peduncle | Lateral 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
| Sign | UMN lesion | LMN lesion |
|---|---|---|
| Tone | Spasticity, clasp-knife; velocity dependent (greater with faster stretch) | Flaccid |
| Reflexes | Brisk, clonus, Hoffmann sign | Reduced or absent |
| Plantar | Extensor (Babinski) | Flexor |
| Bulk | Little 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
| Syndrome | Cause | Features |
|---|---|---|
| Brown-Séquard (hemisection) | Stab wound, tumour | Ipsilateral 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 cord | Anterior spinal artery occlusion, aortic surgery | Paraplegia, loss of pain and temperature; dorsal columns spared |
| Central cord | Neck hyperextension in spondylosis; syringomyelia | Arms worse than legs; cape-like loss of pain and temperature with preserved touch |
| Posterior cord | Tabes dorsalis, B12 deficiency | Loss of vibration and proprioception, sensory ataxia, positive Romberg |
| Subacute combined degeneration | B12 deficiency | Dorsal columns plus lateral corticospinal tracts plus neuropathy: absent ankle jerks with extensor plantars |
| Complete transection | Trauma | All 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
| Lesion | Bladder |
|---|---|
| Above S2–S4 (suprasacral, after spinal shock) | Spastic reflex bladder: small capacity, involuntary emptying, detrusor–sphincter dyssynergia |
| S2–S4 segments or cauda equina | Atonic 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.
After a knife wound to the right side of the thoracic spinal cord, which pattern of deficit is expected below the level of injury?
Answer: Right weakness/JPS; left pain loss
Brown-Séquard syndrome (hemisection of the cord): the corticospinal tract has already crossed in the medulla, so weakness (UMN) is ipsilateral; the dorsal columns (fine touch, vibration, proprioception) ascend ipsilaterally and cross in the medulla, so these are lost ipsilaterally; the spinothalamic tract crosses within one or two segments of entry, so pain and temperature are lost contralaterally a level or two below the lesion. Anterior cord syndrome (anterior spinal artery) spares dorsal columns; central cord syndrome (hyperextension in cervical spondylosis) affects arms more than legs.
Brown-Séquard
- Ipsilateral: weakness, dorsal column loss
- Contralateral: pain and temperature loss
- Spinothalamic crosses near entry; dorsal columns cross in medulla
Remember Same side can't move or feel position; other side can't feel pain.
Why the other options are wrong
- Left weakness; right pain loss Reversed.
- Bilateral weakness; JPS intact Anterior cord pattern spares dorsal columns but power is bilateral.
- Right-sided loss of all sensation Not correct.
- Bilateral pain loss; normal power Central or anterior cord patterns.
During thoracoabdominal aneurysm repair, the surgeon reimplants intercostal arteries from T9 to T12. Which artery is he trying to preserve?
Answer: Artery of Adamkiewicz
The anterior spinal artery arises from the vertebral arteries but cannot supply the whole cord alone; it is reinforced by segmental radiculomedullary arteries. The largest, the great anterior radiculomedullary artery of Adamkiewicz, usually arises on the left from a lower intercostal or upper lumbar artery (T9–L2) and supplies the lower two-thirds of the cord. Losing it causes an anterior cord syndrome with paraplegia and loss of pain and temperature, while posterior column sensation is preserved.
Artery of Adamkiewicz
- Largest radiculomedullary artery
- Usually left, T9–L2
- Feeds the anterior spinal artery
- Loss: anterior cord syndrome
Remember Aortic surgery paraplegia: think Adamkiewicz.
Exam trap The mid-thoracic cord is a watershed zone with a poor segmental supply.
Why the other options are wrong
- Posterior spinal artery Paired, supplies the posterior third; not the main risk.
- Vertebral artery Supplies the cervical cord via the anterior spinal artery.
- Superior mesenteric artery A visceral branch; does not supply the cord.
- Inferior phrenic artery Supplies the diaphragm, not the cord.
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?
Answer: Anterior horn motor neurons
Poliovirus spreads from the gut to the bloodstream and enters the central nervous system, where it selectively infects and kills lower motor neurons in the anterior horn of the spinal cord and motor nuclei of the brainstem. This causes acute, asymmetric flaccid paralysis with lost reflexes and later wasting, while sensation is spared because sensory neurons are not affected. Every case of acute flaccid paralysis in a child under 15 in Pakistan is reported and stool tested for poliovirus.
Paralytic polio
- Virus kills anterior horn cells
- Asymmetric flaccid paralysis, areflexia
- Sensation normal
- Report every AFP case; test stool
Remember Floppy leg, normal feeling, unvaccinated child: polio.
Exam trap Asymmetry and preserved sensation separate polio from Guillain–Barré syndrome.
Why the other options are wrong
- Dorsal root ganglion cells Damage here would cause sensory loss.
- Schwann cells of peripheral nerves Demyelination (as in Guillain–Barré) gives symmetrical weakness and often sensory symptoms.
- Motor end-plate receptors The neuromuscular junction is spared; botulism acts here.
- Lateral corticospinal tract axons A UMN lesion gives spasticity and brisk reflexes.
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?
Answer: Pain fibres ascend 1–2 segments before crossing
Pain and temperature fibres enter the dorsal horn and travel up one or two segments in the dorsolateral (Lissauer) tract before synapsing and crossing in the anterior white commissure. A hemisection therefore cuts the crossed spinothalamic fibres only from segments a little below the lesion, so contralateral pain loss starts one or two segments lower. Ipsilaterally there is a narrow band of total sensory loss at the level, with weakness and loss of dorsal column sensation below.
Hemisection: the level gap
- Pain fibres climb in Lissauer tract
- Cross in the anterior white commissure
- Contralateral pain loss starts 1–2 segments below
- Ipsilateral band of total loss at the level
Remember Pain fibres climb before they cross.
Exam trap The sensory level found on examination may be lower than the real lesion level.
Why the other options are wrong
- Dorsal column fibres cross in the medulla True, but explains the ipsilateral position-sense loss, not the level of pain loss.
- Dermatomes of the trunk do not overlap Trunk dermatomes overlap, which would make the level less sharp, not lower.
- Sacral fibres lie laterally in the tract Lamination explains sacral sparing, not the two-segment gap.
- The left lateral horn has been spared The lateral horn carries sympathetic outflow, not pain.
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?
Answer: Demyelinated cervical dorsal columns
This is Lhermitte sign, common in multiple sclerosis. Demyelinated axons in the dorsal columns of the cervical cord become mechanosensitive and fire ectopic impulses when the cord is stretched by neck flexion, giving a shock-like sensation along the spine and limbs. It can also occur with cervical cord compression, B12 deficiency or radiation myelopathy. Root compression gives pain in a dermatomal band with neck extension or rotation, not a spinal electric shock.
Lhermitte sign
- Neck flexion gives electric shock down spine
- Demyelinated dorsal columns fire when stretched
- Classic in multiple sclerosis
- Also B12 deficiency, cord compression
Remember Bend the neck, feel the shock: think MS.
Exam trap Lhermitte sign is not specific to MS; it reflects any cervical dorsal column lesion.
Why the other options are wrong
- Compressed lower cervical nerve roots Root pain is dermatomal and usually worse with extension.
- Anterior horn cells of the cervical cord Damage here causes weakness and wasting, not sensory shocks.
- Thoracic spinothalamic tracts Neck flexion stretches the cervical cord, and the sensation is a dorsal column one.
- Cerebellar vermis Causes ataxia, not shock-like sensations.
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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