26th June 2023

Posterolateral Column Syndrome

Posterolateral column syndrome, also known as ‘Subacute Combined Degeneration of the spinal cord’ (SACD), is similar to a posterior column syndrome, but also involves the lateral corticospinal tracts. This is a slow and insidious spinal cord syndrome characterised by ascending bilateral limb paraesthesia, manifesting as loss of position and vibratory sense, progressing to weakness with ataxia, and eventually a bilateral spastic paresis. Pain and temperature sense is unaffected. Clinical findings may show a sensory ataxia with positive Romberg’s sign and bilateral spastic paresis with a positive Babinski sign.

It is usually caused by metabolic aetiology, most commonly a prolonged vitamin B12 deficiency. This is why a patient with folate deficiency should always have B12 levels checked, as symptoms of B12 deficiency can be exacerbated and masked if only the folate deficiency is treated. Subacute Combined Degeneration of the spinal cord can also be caused by vitamin E deficiency and copper deficiency, causing loss of myelin initially at the dorsal columns (governing vibration, coarse touch, and proprioception) and then at the lateral columns, including spinocerebellar and corticospinal tracts, but sparing the spinothalamic tracts.

Diseases which exacerbate these nutritional deficiencies, e.g. pernicious anaemia causing vitamin B12 deficiency, cystic fibrosis or abetalipoproteinemia causing loss of absorption of vitamin E, or Menkes disease, an X-linked recessive mutation in copper transport proteins, can all cause SACD. Of note, nitrous oxide administration (e.g. as anaesthesia, analgesia, or as a recreational drug) can induce a functional B12 deficiency and precipitate SACD in already B12 deficient individuals, by inactivating vitamin B12. This is assessed by checking methylmalonic acid (MMA) and homocysteine levels.

Treatment of SACD is with intramuscular hydroxocobalamin injections to replace vitamin B12 levels.