Posterior cord syndrome occurs due to infarction of the posterior half of the spinal cord, from occlusion of the posterior spinal artery. Our patient presents with decreased sensation to pinprick below the level of the knees as well as walking with a wide-based gait, likely indicating loss of proprioception. The patient is also anemic with hyper-segmented neutrophils.

Hypersegmented neutrophils are typically caused by an inability to make enough DNA, caused by a lack of necessary precursors and vitamins including B9 (folate) and B12 (cobalamin). If the patient is folate deficient, we see elevated homocysteine deficiency. If the patient is B12 deficient, we see elevated methylmalonic acid and homocysteine levels. Hyperhomocysteinemia can increase thrombosis. Thrombosis in the posterior spinal artery can cause posterior cord syndrome. In addition, lack of vitamin B12 impairs myelin formation and leads to Subacute Combined Degeneration, which affects the Spinothalamic tract (accounting for decreased pinprick sensation), Corticospinal Tract, and Dorsal Column-Medial Lemniscus Tract (accounting for the reduced proprioception.

A) Anterior cord syndrome- loss of motor command, as well as bilateral loss of heat and pain, the patient has not lost motor function, so it cannot be this. B) Central cord syndrome- presents as a combination of motor and sensory loss, usually with bladder dysfunction. This patient does not display motor loss or bladder dysfunction. C) Hemicord syndrome- Also called Brown-Sequard, this is complete injury to either the left or right side of the spinal cord. It presents with motor dysfunction and reflex dysfunction ipsilaterally at the level of the lesion; loss of upper motor command below the lesion ipsilaterally (spastic paresis); loss of dorsal column-carried sensation ipsilaterally at and below the lesion; and loss of pain and temperature sensation contralaterally 2 to 3 vertebra below the lesion. E) Segmentary syndrome- a congenital failure to develop part of the spinal cord. The new onset of symptoms at 82 years old makes this an unlikely diagnosis,.

B12 deficiency leads to demylination of the DCML and ALS pathways (i.e. posterior cord syndrome).

Here is a good resource

https://www.amboss.com/us/knowledge/Incomplete_spinal_cord_syndromes

Personally my issue with this question is that I though B12 causes demyelination in both the LCST and the DCML (SCD) but they are testing the mechanism here really with the whole methylamonic acid bit and the impaired myelin synthesis

If you're curious

https://www.nature.com/articles/scsandc20166

But doesn't subacute combined degeneration lead to impairment in DCML, spinocerebellar and corticospinal tract? I get the ataxic gait - DCML/spinocerebellar. But the sensation to pinprick, wouldn't that be the spinothalamic tract? That is not usually affected in subacute combined degeneration.

Can someone explain what the picture is supposed to show? Is it supposed to be segmented neutrophils?

This question is incorrect. The reflexes are normal in the BLE. Subacute combines degeneration compromises the dorsal horns; which is why it got the name "combined" Can always count on Shit NBME questions.