Vitamin B12 deficiency can manifest with hematological and neurological abnormalities, though intracranial involvement is less common than spinal cord or peripheral nerve manifestations. We report the case of a man in his 70s who developed acute cognitive decline over 4 days, accompanied with left lower limb weakness and visual disturbances. Neurological examination revealed reduced verbal output, dysarthria, significant cognitive impairment (Mini-Mental State Examination score, 7/30), and left lower limb weakness (Medical Research Council grade, 4/5). Laboratory tests showed pancytopenia (white blood cell count, 2.7 × 10 9 /L; red blood cell count, 1.34 × 10 12 /L; hemoglobin level, 6.3 g/dL; platelet count, 55 × 10 9 /L), with macrocytic anemia (mean corpuscular volume, 134 fL; mean corpuscular hemoglobin, 47 pg) and markedly low serum vitamin B12 levels (<83 pg/mL). Brain magnetic resonance imaging demonstrated distinctive bilateral periventricular hyperintensities on T2‑weighted and diffusion‑weighted imaging, suggestive of cytotoxic edema, a finding often associated with metabolic disturbances. A diagnosis of acute metabolic encephalopathy due to vitamin B12 deficiency was established. Following vitamin B12 supplementation, the patient’s symptoms resolved completely (Mini-Mental State Examination score: 24/30, Montreal Cognitive Assessment score, 23/30, adjusted for educational level). This case illustrates that vitamin B12 deficiency can present with acute cognitive dysfunction and may manifest on magnetic resonance imaging as symmetrical periventricular brain cytotoxic edema. Early recognition and treatment are crucial for achieving both clinical and radiographic recovery.
Xiong et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: