26th June 2023

Posterior Column Syndrome

Distribution of vibration and proprioception loss in posterior column syndrome of the cervical spinal cord.

Image Source: Dr D Chang – own work

Posterior column syndrome is the most uncommon incomplete spinal cord syndrome, manifesting as a loss of proprioception and vibratory sense, and two-point discrimination distal to the lesion, deep tendon areflexia and a sensory ataxia (due to loss of joint position sense). Romberg sign is positive, and a stomping gait is present which can be exacerbated by removing visual cues, e.g. by closing eyes. There is hypotonia in limbs distal to the lesion, but power is usually preserved. If the lesion is at the level of the cervical cord, it can be associated with Lhermitte’s sign, in which neck flexion elicits neuropathic pain and paraesthesia down the arms.

The aetiology or posterior cord syndrome is classically due to neurosyphilis with tabes dorsalis, but can happen due to thrombosis or occlusion of the posterior spinal arteries, mechanical causes such as localised compression from epidural tumours, haematomas or abscesses, and inflammatory causes such as multiple sclerosis. Friedreich’s ataxia (see the section below) can also manifest primarily as a posterior cord syndrome before progressing to involve corticospinal tracts.

In the case of tabes dorsalis as a late complication of neurosyphilis, posterior column degeneration is also accompanied by dorsal root ganglion demyelination. Tabes dorsalis progressively develops over years, manifesting with the posterior cord syndrome as above, accompanied with lancinating pain and dysesthesias and can progress to cause bladder dysfunction, Argyll Robertson pupils (see Cranial Nerve Disorders section) and can cause a Charcot arthropathy. Treatment is with intramuscular benzylpenicillin, noting that patients undergoing treatment may experience a Jarisch Herxheimer reaction where the death of the Treponema pallidum spirochetes release endotoxins that provoke pyrexia, tachycardia, rigors, and rashes 6 to 48 hours post initiation of therapy.