Neurologic involvement is typically present in B12 deficiency and not in folate deficiency. Which statement best describes this contrast?

Neurologic involvement is typically present in B12 deficiency and not in folate deficiency. Which statement best describes this contrast?

• A. Neurologic involvement is present in both B12 and folate deficiencies.
• B. Neurologic involvement is typically present in B12 deficiency and not in folate deficiency.
• C. Neurologic involvement is present in folate deficiency but not in B12 deficiency.
• D. Neurologic involvement is never seen in either deficiency.

Answer: (B)

Neurologic involvement in B12 deficiency arises from its role in myelin maintenance and methylation reactions. B12 is a cofactor for methionine synthase, which helps regenerate methionine and supports the methylation of myelin proteins and phospholipids. When B12 is deficient, this remethylation is impaired, and methylmalonyl-CoA mutase activity is reduced, leading to demyelination—especially in the dorsal columns and lateral columns of the spinal cord. This causes neurologic signs such as paresthesias, ataxia, weakness, and cognitive changes, collectively known as subacute combined degeneration. Folate deficiency, on the other hand, primarily disrupts DNA synthesis and cell division, producing macrocytic anemia with hypersegmented neutrophils but not demyelination. As a result, neurologic symptoms are typically present with B12 deficiency and not with folate deficiency. (Note: folate can mask the hematologic signs of B12 deficiency, but does not prevent the potential neurologic damage from B12 deficiency.)

Neurologic involvement in B12 deficiency arises from its role in myelin maintenance and methylation reactions. B12 is a cofactor for methionine synthase, which helps regenerate methionine and supports the methylation of myelin proteins and phospholipids. When B12 is deficient, this remethylation is impaired, and methylmalonyl-CoA mutase activity is reduced, leading to demyelination—especially in the dorsal columns and lateral columns of the spinal cord. This causes neurologic signs such as paresthesias, ataxia, weakness, and cognitive changes, collectively known as subacute combined degeneration. Folate deficiency, on the other hand, primarily disrupts DNA synthesis and cell division, producing macrocytic anemia with hypersegmented neutrophils but not demyelination. As a result, neurologic symptoms are typically present with B12 deficiency and not with folate deficiency. (Note: folate can mask the hematologic signs of B12 deficiency, but does not prevent the potential neurologic damage from B12 deficiency.)