Sensory peripheral neuropathy of vitamin B12 deficiency: A primary demyelinating disease?

Abstract

In five patients with peripheral neuropathy due to vitamin B12 deficiency, electrodiagnostic studies demonstrated severe reduction in sensory nerve conduction velocities compatible with a demyelinating disorder affecting sensory nerve fibres. It is suggested that in some patients lack of vitamin B12 may cause primary sensory demyelinating neuropathy.

Vitamin B-12 treatment of asymptomatic, deficient, elderly Chileans improves conductivity in myelinated peripheral nerves, but high serum folate impairs vitamin B-12 status response assessed by the combined indicator of vitamin B-12 status

“…The neuropathologic findings include a diffuse, multifocal pattern of axonal loss and demyelination that is most severe in the cervical and thoracic spinal cord (6,7). Sensory polyneuropathy is also observed in vitamin B-12 deficiency (8) and involves myelinated large-caliber afferent fibers (7,8). Although the clinical and neurophysiologic features of symptomatic vitamin B-12 deficiency in patients with neurologic manifestations have been reported (6,9), most reports have been from case studies of elderly subjects with pernicious anemia who received a variety of treatments and different followup assessments (10)(11)(12)(13) or have only studied small groups of participants (7,(14)(15)(16).…”

The neurology of cobalamin deficiency in an elderly population in Israel

“…Indeed, in a recently published study only 16 out of 23 patients with peripheral neuropathy and CblD had abnormal nerve conductions indicating sensory axonal neuropathy [14]. This form of neuropathy is considered characteristic for CblD [1,11,15].…”

Axonal and demyelinating neuropathy with reversible proximal conduction block, an unusual feature of vitamin B12 deficiency

“…13 In our patient the finding of conduction block in four nerves (which improved shortly after commencing treatment) is interesting not only because it has not been reported before, but because it provides good demonstration of segmental demyelination, consistent with the findings in histopathological studies of animals fed on vitamin B12 deficient diets. [14][15][16] The clinical progress and marked improvement on treatment in the presence of normal cerebrospinal fluid parameters, negative family history and normal metabolic screening tests suggest that the proximal conduction block was a direct result of the deficiency state and not due to an alternative pathology. It is also interesting to note that the nerve segments…”