Spinal cord and meninges
Spinal cord, spinal meninges and blood supply of the cord
MRI shows the cord, its coverings and the spaces around them, and every spinal mass is first placed in one of three compartments. CPSP asks where the cord ends, where each tract lies, the classic cord syndromes and the cord's arteries.
Levels: cord, sac and segments
| Structure | Level |
|---|---|
| Conus medullaris (adult) | L1–L2 (lower border of L1) |
| Conus at birth | About L2–L3; lower than this in a term baby suggests tethering |
| Dural sac | S2 |
| Filum terminale | Internum (pia) inside the sac; externum (dural sheath) to the coccyx |
| Lumbosacral enlargement | Behind the T10–T12 vertebrae |
- Cord segments lie higher than their vertebrae, more so lower down, so a T11–T12 fracture damages lumbar and sacral segments.
- Lumbar puncture is done at L3–L4 or L4–L5 (infants L4–L5 or lower), with the spine flexed.
- In young infants the cord is seen by ultrasound through unossified posterior arches; a normal conus moves with each heartbeat.
- Tethered cord: conus below L2 with a thick (over about 2 mm) or fatty filum, often with a hairy patch or dimple; symptoms worsen during growth spurts from stretching and ischaemia. Diastematomyelia: two hemicords split by a bony or fibrous spur.
Spinal meninges and spaces
- The spinal dura is a single layer, separate from the periosteum, so there is a real epidural space containing fat (bright on T1) and the internal vertebral venous plexus. This is why a spinal epidural abscess or haematoma spreads over many levels, unlike a cranial extradural collection.
- Epidural lipomatosis (long-term steroids) squeezes the sac into a Y shape. A spinal epidural haematoma on anticoagulants is venous and biconvex.
- Needle path: supraspinous and interspinous ligaments, ligamentum flavum (loss of resistance), epidural space, dura, arachnoid, CSF.
- Pia forms the denticulate ligaments (anchoring the cord laterally to the dura) and the filum.
- Dorsal root ganglia enhance normally (no blood–nerve barrier); the roots inside the sac do not.
| Finding | Meaning |
|---|---|
| CSF cysts on sacral roots at the ganglion, scalloping the canal | Perineural (Tarlov) cysts |
| Roots stuck to the sac wall, "empty" central sac | Adhesive arachnoiditis |
| Diffuse smooth dural enhancement, engorged sinuses, epidural fluid | CSF leak (intracranial hypotension): veins swell to replace lost CSF |
Where is the mass?
| Compartment | Imaging | Typical lesions |
|---|---|---|
| Extradural | Epidural fat lost, thecal sac and cord pushed away | Disc, metastasis (commonest in the thoracic spine; image the whole spine), abscess, haematoma |
| Intradural extramedullary | Cord displaced, not expanded; CSF space widened above and below the mass (CSF cap) | Schwannoma (dumbbell through a widened foramen), meningioma (thoracic, women, broad dural base, dural tail, calcification), myxopapillary ependymoma of the filum |
| Intramedullary | Cord expanded | Ependymoma (adult, central, haemosiderin cap), astrocytoma (child, eccentric, ill-defined), haemangioblastoma (pial nodule, syrinx, flow voids; VHL) |
Tracts on an axial slice
| Tract | Position and lamination | Carries |
|---|---|---|
| Dorsal columns | Gracile medial (legs), cuneate lateral (arms) | Vibration, position, fine touch, same side |
| Lateral corticospinal | Arm fibres medial, leg fibres lateral | Voluntary movement, same side below the decussation |
| Lateral spinothalamic | Sacral fibres outermost | Pain and temperature, crossed |
| Anterior spinothalamic | Anterolateral | Crude touch and pressure |
| Posterior spinocerebellar | From Clarke nucleus (T1–L2) | Unconscious proprioception |
- Pain fibres ascend 1–2 segments before crossing, so the sensory level may lie below the lesion; a cordotomy is made in the opposite anterolateral quadrant a few segments above the pain.
- The lateral horn (T1–L2) holds sympathetic neurones: a syrinx reaching T1 causes Horner syndrome.
Cord syndromes
| Syndrome | Findings |
|---|---|
| Hemisection | Same side: weakness, loss of vibration and position, a band of total sensory loss at the level; opposite side: pain and temperature loss from 1–2 segments below |
| Central cord | Hyperextension in a spondylotic neck: arms weaker than legs, sacral sparing |
| Anterior spinal artery | Paraplegia and pain loss with vibration and position preserved (aortic surgery, hypotension) |
| Posterior spinal artery | Isolated loss of vibration and position, positive Romberg |
| Syrinx (often with Chiari I) | Cape-like loss of pain and temperature, hand wasting |
| Subacute combined degeneration | Symmetric T2 bright dorsal columns (inverted V); B12 deficiency or nitrous oxide abuse (oxidises B12 cobalt) |
| Conus medullaris | Early sphincter loss, symmetrical saddle numbness, little root pain |
| Cauda equina | Asymmetric root pain and weakness, saddle anaesthesia, retention |
- MS cord plaque: short (under two segments), peripheral, dorsolateral, less than half the cord width. A long central swollen lesion suggests neuromyelitis optica.
- Low T2* signal in an injured cord means haemorrhage and a poor outlook.
- Breathing: phrenic neurones lie at C3–C5. A C2 transection stops breathing because descending drive is cut; a C6 injury leaves diaphragmatic breathing with paralysed intercostals.
- Dural arteriovenous fistula: older man; lower cord and conus swollen and T2 bright from venous hypertension, with serpentine flow voids on the surface.
Blood supply of the cord
- Anterior spinal artery: single, formed by a branch from each vertebral artery, in the anterior median fissure; supplies the anterior two-thirds of the cord.
- Posterior spinal arteries: paired (vertebral or PICA); supply the dorsal columns.
- Radicular (segmental) arteries reinforce them through the foramina, from vertebral, posterior intercostal and lumbar arteries. The largest, the artery of Adamkiewicz, usually arises on the left between T9 and T12 (range about T5–L2) and makes a hairpin turn on angiography.
- The mid-thoracic cord (about T4–T8) has few feeders and is a watershed, the first to infarct with hypotension or when intercostal arteries are sacrificed at aortic surgery.
Remember The cord ends at L1–L2, the sac at S2: needles go in between, at L3–L4 or L4–L5.
Exam trap An anterior spinal artery infarct spares vibration and position sense; a posterior spinal artery infarct loses only these.
Exam trap Intradural extramedullary masses widen the CSF space around them; intramedullary masses expand the cord.
Test yourself on this topic
5 of the 66 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 70-year-old man on warfarin with an INR of 5.8 develops sudden severe interscapular pain followed within hours by weakness of both legs. A haematoma lies in the epidural space behind the thecal sac from T4 to T8, compressing the cord. What is the most likely source of the bleeding?
Answer: Epidural venous plexus
Spontaneous spinal epidural haematoma is usually venous, from the thin-walled, valveless internal vertebral venous plexus, and is linked to anticoagulation, bleeding disorders and minor strain. It collects in the epidural space, most often posteriorly where this space is widest, as a biconvex mass over several levels that compresses the cord. It needs urgent reversal of anticoagulation and often decompression.
Spinal epidural haematoma
- Source: epidural venous plexus
- Anticoagulation a common cause
- Posterior, biconvex, several levels
- Emergency: reverse and decompress
Remember Anticoagulated plus sudden back pain and paraparesis: epidural bleed.
Exam trap Neurological outcome depends on speed of decompression; do not wait for weakness to progress.
Why the other options are wrong
- Anterior spinal artery Bleeding from it would be within the subarachnoid space or cord.
- Intramedullary vessels Would cause haematomyelia within the cord.
- Bridging cortical veins These cross the cranial subdural space, not the spinal canal.
- Radicular artery aneurysm Rare; would usually cause subarachnoid bleeding.
A 9-year-old girl has worsening bladder control and a foot deformity during a growth spurt. Her conus medullaris ends at L4, anchored by a short, thick, fat-containing filum terminale. What is the main mechanism of her symptoms?
Answer: Stretching and ischaemia of the conus
In tethered cord syndrome a thick or fatty filum anchors the conus low, below the normal L1–L2 level. As the vertebral column grows faster than the cord, and with flexion, the fixed conus is stretched. Stretching narrows its small vessels and impairs oxidative metabolism of the neurones, causing progressive bladder dysfunction, leg weakness, foot deformity and back pain, typically during growth spurts.
Tethered cord
- Conus below L2 in an adult-sized spine
- Thick or fatty filum (over 2 mm)
- Growth stretches the conus
- Bladder, foot deformity, growth spurts
Remember Low conus plus growth spurt: tethered cord.
Exam trap Look for a skin marker over the lower back, such as a hairy patch or dimple, which often accompanies tethering.
Why the other options are wrong
- Compression of the cord by a disc Disc disease is rare in children and would not lower the conus.
- Demyelination of the dorsal columns Not the mechanism of a low-lying conus.
- Infarction in the anterior spinal artery territory Gives sudden paraplegia, not slow progression with growth.
- Blocked CSF flow at the foramen magnum Relevant to Chiari malformation and syrinx, not a low conus.
A 22-year-old student who inhales nitrous oxide from cream chargers every weekend develops tingling feet and an unsteady gait in the dark, from degeneration of the dorsal columns. How does nitrous oxide cause this?
Answer: It oxidises the cobalt of vitamin B12
Nitrous oxide oxidises the cobalt atom of methylcobalamin, inactivating vitamin B12. This blocks methionine synthase, reducing methionine and S-adenosylmethionine needed for myelin methylation, and methylmalonyl-CoA mutase activity also falls. The result is subacute combined degeneration of the dorsal columns and lateral corticospinal tracts, with vacuolar myelin loss, even when serum B12 is normal.
Nitrous oxide myelopathy
- Oxidises cobalt in B12
- Blocks methionine synthase
- Dorsal and lateral columns degenerate
- Serum B12 may be normal
Remember Cream chargers plus dorsal column loss: B12 inactivation.
Exam trap Serum B12 can be normal; raised homocysteine and methylmalonic acid confirm functional deficiency.
Why the other options are wrong
- It blocks folate absorption in the jejunum Folate absorption is not affected by nitrous oxide.
- It causes direct toxic cord ischaemia There is no vascular mechanism; it is metabolic.
- It triggers antibodies to intrinsic factor That is the mechanism of pernicious anaemia, not nitrous oxide.
- It depletes thiamine in neurones Thiamine deficiency causes Wernicke encephalopathy and neuropathy.
The spinal cord of a 6-week-old baby with a sacral dimple can be examined by ultrasound through the back, but this is no longer possible by about 6 months. What is the anatomical reason?
Answer: Posterior arches are still unossified
In the first few months of life the posterior elements of the vertebrae are largely cartilage and the spinous processes are not yet ossified, so ultrasound passes through to show the canal, cord, conus and filum. As the posterior arches ossify, bone reflects and absorbs the beam and the window closes, usually by about 4 to 6 months, after which MRI is needed. The two halves of each neural arch fuse with each other during the first years of life.
Neonatal spinal ultrasound
- Posterior arches still cartilage
- Gives an acoustic window
- Shows conus level and pulsation
- Window closes by 4 to 6 months
Remember Before ossification, ultrasound sees the cord.
Exam trap A conus at or above L2–L3 in a term infant is normal; lower suggests tethering.
Why the other options are wrong
- Infant cord contains more water Water content does not open an acoustic window through bone.
- Infant dura is absent over cord The dura is present at all ages.
- Infant CSF transmits sound faster Sound speed in CSF is similar at all ages and not the reason.
- Infant cord lies outside the canal The cord always lies inside the vertebral canal.
A 38-year-old woman has a headache that appears within minutes of standing and eases on lying flat, caused by a spinal CSF leak. Her cranial dura becomes thickened and engorged, and the venous sinuses enlarge. What explains these dural changes?
Answer: Dural veins engorge to replace lost CSF
This is spontaneous intracranial hypotension from a spinal CSF leak. By the Monro–Kellie doctrine, the total volume of brain, blood and CSF inside the rigid skull is constant, so when CSF volume falls the venous compartment expands. The dural veins and sinuses engorge and the dura thickens and enhances smoothly. The brain sags, stretching pain-sensitive structures when upright and causing orthostatic headache.
Intracranial hypotension
- Spinal CSF leak
- Orthostatic headache
- Monro–Kellie: veins expand
- Engorged dura, sagging brain
Remember Low CSF volume: veins fill the space.
Exam trap Opening pressure may be normal; the problem is low CSF volume.
Why the other options are wrong
- Bacteria infect the dura through the leak Infection would cause fever and meningitis, not an orthostatic picture.
- Tumour cells coat the meninges Malignant meningeal disease is nodular and not orthostatic.
- Blood leaks into the subdural space Subdural collections may follow but do not explain diffuse dural engorgement.
- CSF pressure stretches the arachnoid villi Arachnoid villi absorb CSF; pressure here is low, not high.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Spine, Spinal cord, meninges and blood supply of the cord