Case Presentation: A 79-year-old male presented to the emergency department after a witnessed episode of unresponsiveness, jerking motions, urinary incontinence and post-ictal confusion. The patient’s wife denied a history of epilepsy but reported several months of progressive dysarthria and gait ataxia, for which he had been evaluated nine months earlier. Work-up was negative for hemorrhage, mass effect, hydrocephalus or acute infarct. Serum vitamin B12 level was undetectable (< 150 pg/mL), however cobalamin supplementation was not started and patient was lost to follow up. Neurologic exam on admission was remarkable for dysarthria, akathisia, dysmetria, decreased proprioception and vibration sense affecting bilateral lower extremities. There was no cogwheel rigidity. CT head showed no acute infarct. Electroencephalogram revealed no epileptiform discharges. Laboratory findings included hemoglobin 11.8 g/dL, MCV 100.0 fL, undetectable serum B12 and serum folate (< 3.5 ng/mL). Methymalonic acid level was normal (250 nmol/L) and homocysteine was moderately increased (15.8 μmol/L). Rapid plasma reagin was non-reactive. Peripheral blood smear showed macrocytosis and a hyper-segmented neutrophil with seven lobes. Anti-intrinsic factor was elevated (13.6 AU/mL). Esophagogastroduodenoscopy showed non-bleeding duodenal erosions with pathology negative for Helicobacter pylori and celiac sprue. MRI brain showed restricted diffusion in the cerebellar vermis and pons, concerning for subacute stroke. Based on the lesion’s subcortical location, neurology rejected stroke as the primary source of seizure. The patient was treated with cobalamin 1000 units IM daily and folic acid 1mg PO daily. His dysarthria, akathisia and dysmetria resolved after several days. His proprioception and gait abnormalities persisted, therefore he was discharged to subacute rehab.
Discussion: Although uncommon, prior case reports detail vitamin B12 deficiency as an etiology of seizures. Neurologic symptoms of vitamin B12 deficiency typically include loss of proprioception and vibration sense, symmetric paresthesias and ataxia. The pathogenesis involves neuronal demyelination in the central and peripheral nervous systems. Methylcobalamin, a B12 analogue, has demonstrated a protective effect in cortical neurons against glutamate toxicity, suggesting that demyelinated neurons are more susceptible to glutamatergic excitation and epileptogenesis. While our patient’s diagnosis is confounded by the discovery of a subacute stroke, the subcortical location of the lesion makes it unlikely to be an etiology of seizure.
Conclusions: Guidelines for the management of first seizure in adults do not recommend assessment for vitamin B12 deficiency. This case adds to growing literature suggesting clinicians should maintain vigilance for central and peripheral neurologic symptoms indicative of B12 deficiency when evaluating new-onset seizures.