Spinal cord

What it normally does

• The cord tapers and stops at the L1-L2 level in an adult (conus medullaris). Below that the canal holds only a loose bundle of lumbar and sacral nerve roots floating in CSF (cauda equina).

  Explains why a lumbar disc damages roots and not cord — a flaccid, areflexic cauda equina syndrome instead of a myelopathy — and why a lumbar puncture at L3/4 or L4/5 is safe.

• Three tracts matter, and they cross in three different places. Movement comes down the side of the cord having already crossed in the medulla (lateral corticospinal tract). Fine touch, vibration and joint position run up the back of the cord on the same side and cross in the medulla (dorsal columns, via the internal arcuate fibres to the medial lemniscus). Pain and temperature cross inside the cord itself within a segment or two, through the anterior white commissure, then run up the opposite anterolateral quadrant (spinothalamic tract).

  Explains the sharp-edged sensory level and upper motor neuron signs of a compressed cord, why weakness and vibration loss sit on the side of the lesion while pain loss sits on the other (Brown-Sequard), and why B12 deficiency knocks out the back and the side of the cord together.

• Fibres are stacked by body part. In the lateral corticospinal and spinothalamic tracts the sacral fibres lie furthest out and the cervical/arm fibres closest to the centre (somatotopic lamination), and the pain and temperature fibres decussate in the anterior white commissure, just in front of the central canal.

  Explains a cape of lost pain and temperature over both arms with everything else intact in syringomyelia, and sacral sparing when the damage starts centrally.

• The cord runs the autonomic outflow and the reflex arcs. Sympathetic preganglionic fibres leave only between T1 and L2, bladder and bowel parasympathetics come from S2-S4, and every stretch reflex is a local loop that descending pathways normally hold down.

  Explains painless retention and saddle anaesthesia, the flaccid phase of spinal shock followed days to weeks later by spasticity and upgoing plantars, and autonomic dysreflexia in a lesion at or above T6.

What goes wrong

• Metastatic (malignant) spinal cord compression← from “Three tracts matter, and they cross in three d…”

  A vertebral metastasis (breast, lung, prostate, myeloma) collapses or expands into the epidural space and squeezes the cord — an epidural abscess, haematoma or a large disc does the same thing mechanically. Every tract crossing that level is compressed at once. The corticospinal fibres already crossed in the medulla, so weakness is below the lesion on the same side; the squeezed spinothalamic and dorsal column fibres give the sensory loss a sharp upper edge — a level. Descending inhibition is cut off, so reflexes below become brisk and plantars go up.

  New back pain in anyone with cancer plus any leg or bladder symptom means urgent whole-spine MRI (same day) and discussion with oncology/neurosurgery; guidelines advise starting dexamethasone as soon as compression is suspected rather than waiting for the scan. It affects roughly 5-10% of patients with metastatic cancer, and the power they walk in with is roughly the power they keep.

  You would find: Weeks of back pain that is worse lying flat and wakes them at night, then a band of altered sensation across the trunk with normal skin above it, brisk knee and ankle reflexes, upgoing plantars, and a bladder they cannot empty. Feel for a distended bladder or scan it.

• Cauda equina syndrome← from “The cord tapers and stops at the L1-L2 level i…”

  A large central disc at L4/5 or L5/S1 — or a tumour, haematoma or abscess — crushes the loose lumbosacral roots below the conus. These are peripheral nerve roots, not cord, so the picture is lower motor neuron: flaccid weakness with lost reflexes. The S2-S4 roots carrying bladder, bowel and perineal sensation run in that bundle and are affected early.

  Cord is brisk and upgoing; cauda equina is flaccid and absent. Saddle numbness with a large post-void residual means MRI now and urgent surgical referral for decompression — hesitation buys permanent incontinence.

  You would find: Sciatica down both legs, numbness over the buttocks, perineum and inner thighs (saddle anaesthesia), absent ankle jerks, lax anal tone, and painless retention then overflow — they never felt the bladder fill. Ask directly whether they can feel the toilet paper and whether they can feel themselves passing urine, then scan the bladder for a residual.

• Syringomyelia← from “Fibres are stacked by body part. In the latera…”

  A CSF-filled cavity expands inside the central cord, usually cervical, most often with a low-lying cerebellar tonsil (Chiari 1 malformation) or years after trauma. The first fibres it interrupts are the pain and temperature fibres decussating in the anterior white commissure. The dorsal columns sit at the back, untouched — so pain and temperature go while light touch and joint position stay (dissociated sensory loss). As the cavity grows outwards it reaches the anterior horn cells, then the corticospinal tracts.

  Cape distribution, pain and temperature gone, touch preserved — that is a syrinx until MRI says otherwise. Treatment is aimed at the cause (posterior fossa decompression or shunting), not at the numbness.

  You would find: Painless burns and cuts on the fingers the patient never felt, spread as a cape over both shoulders and arms, while light touch there is still normal. Later, wasted small hand muscles with lost arm reflexes, and stiff spastic legs below. MRI of brain and whole spine makes the diagnosis.

• Subacute combined degeneration (B12 deficiency)← from “Three tracts matter, and they cross in three d…”

  Without B12 the most heavily myelinated tracts fail first, and they fail together: the dorsal columns at the back and the lateral corticospinal tracts at the side — hence 'combined'. Causes are pernicious anaemia, gastric or ileal surgery, long-term metformin, strict vegan diets, and nitrous oxide, which oxidises the cobalt atom of cobalamin and so inactivates methionine synthase.

  Young person, tingling feet, unsteady in the dark — ask about nitrous oxide canisters, an increasingly recognised cause in Australian emergency departments. Replace B12 before giving folate: folate alone can correct the blood count while the cord keeps degenerating.

  You would find: Pins and needles in the feet and hands, a wide unsteady gait far worse in the dark or with eyes shut (Romberg positive), lost vibration and joint position sense at the toes. The giveaway is the mixed pattern: brisk knee jerks but absent ankle jerks (coexisting peripheral neuropathy) with upgoing plantars. The blood film and haemoglobin can be entirely normal.

• Spinal shock, then spasticity and autonomic dysreflexia← from “The cord runs the autonomic outflow and the re…”

  A cord injury cuts the descending inhibition. For days to weeks everything below is flaccid and areflexic with retention (spinal shock). Then the isolated cord's local reflex loops recover with no brake on them: tone returns as spasticity, with brisk reflexes, clonus and upgoing plantars. If the lesion is at or above T6 most of the sympathetic outflow is disconnected from brainstem control, so a noxious stimulus below the level fires a mass sympathetic discharge that descending pathways cannot switch off.

  Australian traumatic cord injury is mostly young men in road crashes, falls and shallow-water diving; Aboriginal and Torres Strait Islander people are injured at a substantially higher rate and travel much further to reach spinal services. In any cord-injured patient, hypertension with headache is dysreflexia until the catheter has been checked.

  You would find: A wheelchair user with a pounding headache and a blood pressure of 200/110 when their baseline is 90/60 — flushed and sweating above the lesion, pale and cold below, with a reflex bradycardia. Sit them up, loosen anything tight, and hunt the trigger: a blocked catheter is the usual answer, a loaded rectum or a pressure sore next.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.