Sensory pathways: dorsal column and spinothalamic

What it normally does

• Fine touch, vibration and joint position sense (proprioception) enter the cord and run straight up the back of it on the SAME side, only crossing the midline far higher up, in the lower medulla, as the internal arcuate fibres leaving the gracile and cuneate nuclei (dorsal column-medial lemniscus pathway).

  A lesion of one half of the cord loses vibration and position sense on the same side as the lesion, below it.

• Pain and temperature fibres enter the cord, travel only one or two segments up or down in Lissauer's tract, then synapse in the dorsal horn. The second neurone crosses the midline and ascends on the OPPOSITE side (spinothalamic or anterolateral pathway).

  That same one-sided lesion loses pin and temperature on the opposite side, and because of that short climb before crossing, the loss starts a segment or two below the level of the lesion.

• Those crossing pain and temperature fibres squeeze through the middle of the cord, just in front of the central canal (anterior white commissure).

  Anything expanding outward from the centre of the cord hits pain and temperature first and spares the dorsal columns until the cavity is large.

• The thick, heavily myelinated dorsal column fibres depend on vitamin B12. B12 is the cofactor for two enzymes: methionine synthase, which regenerates methionine and so keeps S-adenosylmethionine available for the methylation reactions myelin maintenance needs, and methylmalonyl-CoA mutase, which converts methylmalonyl-CoA to succinyl-CoA. Failure of the methylation arm is thought to be the main driver of the myelin damage; the older explanation, that odd-chain fatty acids accumulate and are built into the sheath, remains a hypothesis.

  B12 deficiency picks off the dorsal columns and the corticospinal tracts and largely spares the thin pain and temperature fibres.

What goes wrong

• Brown-Sequard syndrome (hemisection of the cord)← from “Fine touch, vibration and joint position sense…”

  One half of the cord is cut or crushed. The dorsal column fibres on that side have not crossed yet, so vibration and position sense are lost below the lesion on the SAME side. The spinothalamic fibres running past have already crossed from the other side, so pin and temperature are lost on the OPPOSITE side, beginning one or two segments below. The lateral corticospinal tract crossed much higher, at the pyramids of the medulla, so the fibres cut here are already the ones supplying the same side of the body, and the weakness is ipsilateral too.

  Weakness and vibration loss ipsilateral; pin and temperature loss contralateral starting one to two segments lower. Pure hemisection is rare; incomplete Brown-Sequard from trauma, disc or tumour is what you actually see, and it has the best prognosis of the incomplete cord syndromes.

  You would find: A patient after a stab wound or with a lateral cord tumour who has a weak, stiff leg that cannot feel a tuning fork, and on the other side a leg that walks well but feels nothing to pinprick or a cold swab. There is often a narrow band of total sensory loss, sometimes with lower motor neurone signs, at the level itself.

• Syringomyelia (fluid cavity in the centre of the cord)← from “Those crossing pain and temperature fibres squ…”

  A cavity expands from the central canal, usually in the cervical cord. It first destroys the pain and temperature fibres crossing in front of the central canal. Those fibres are gone bilaterally at those segments, but the dorsal columns sitting at the back are untouched, so touch and vibration remain normal. This split is dissociated sensory loss.

  Cape-like bilateral loss of pain and temperature with intact vibration equals a central cord cavity until proven otherwise. A large proportion sit with a Chiari 1 malformation; MRI the whole neuraxis, not just the painful bit.

  You would find: A young adult who keeps burning or cutting their hands without noticing, with painless scars. Loss of pin and temperature in a cape distribution over both shoulders, upper arms and upper chest, with normal light touch and vibration in the same skin. Wasted small hand muscles, from the cavity reaching the anterior horns, and scoliosis if it spreads.

• Subacute combined degeneration (vitamin B12 deficiency)← from “The thick, heavily myelinated dorsal column fi…”

  Without B12 the myelin of the dorsal columns and the lateral corticospinal tracts degenerates, which is why it is called combined. Losing the dorsal columns means the brain no longer knows where the feet are, so the patient falls back on vision to stay upright. Losing the corticospinal tracts adds an upper motor neurone picture. A peripheral neuropathy is common as well, which is why the ankle jerks can be absent.

  In Australia think metformin, long-term proton pump inhibitors, vegan diet, bariatric surgery, pernicious anaemia, and heavy nitrous oxide (nang) use in young people. Nitrous oxide inactivates B12-dependent methionine synthase while the serum B12 level can read normal, so check methylmalonic acid and homocysteine. Treat on suspicion: axons lost do not come back.

  You would find: Loss of vibration at the great toe on a 128 Hz fork is the earliest sign. Unsteady wide gait that gets much worse in the dark or with eyes shut (positive Romberg). Brisk knee jerks with absent ankle jerks and upgoing plantars in the same patient. Anaemia and macrocytosis may be completely absent.

• Anterior spinal artery occlusion (anterior cord syndrome)← from “Pain and temperature fibres enter the cord, tr…”

  The single anterior spinal artery supplies the front two-thirds of the cord: both spinothalamic tracts and both corticospinal tracts. The dorsal columns sit in the territory of the two posterior spinal arteries and survive. So pain, temperature and power are lost below the level on both sides while vibration and position sense stay intact.

  Dissociated loss again, but the mirror image of a syrinx: pin and temperature gone, vibration preserved, and power gone too. If vibration is preserved in a paraplegic patient, think vascular front-of-cord, not compression.

  You would find: Sudden paraplegia with a sensory level to pin and cold, plus retained vibration and joint position sense in the same numb legs. Classically after aortic surgery, aortic dissection or profound hypotension. Bladder goes early.

• Diabetic peripheral neuropathy (length-dependent, small and large fibre)← from “Pain and temperature fibres enter the cord, tr…”

  Chronic hyperglycaemia damages the longest axons first, before the pathway even reaches the cord. The thinly myelinated A-delta and unmyelinated C fibres that feed the spinothalamic tract die back, giving burning pain and loss of pin and temperature in the feet. The thick A-beta fibres that feed the dorsal columns go too, giving loss of vibration and unsteadiness. Damaged nociceptors fire spontaneously, so the patient has both numbness and pain in the same foot.

  Diabetes is common in Australia and Aboriginal and Torres Strait Islander people carry a markedly higher burden of type 2 diabetes, foot ulceration and lower limb amputation, so an annual foot check with a 10 g monofilament is not optional.

  You would find: Glove-and-stocking loss that starts at the toes and creeps up symmetrically. Burning feet worse at night. A painless ulcer under a callus on the sole because the patient cannot feel the pressure. Loss of 10 g monofilament sensation marks loss of protective sensation and is the standard screening test.

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.