vitamin-b-12 and Encephalomyelitis

Pernicious anemia is uncommon in Africa. The purpose of this report is to describe a case of pernicious anemia observed in Madagascar. The revealing manifestation was encephalomyelitis with combined medullar sclerosis that responded favorably to vitamin B12 replacement therapy. Clinical symptoms included paresthesia associated with allodynia of all four extremities and with tetrapyramidal syndrome, medullar ataxia and minor cognitive disturbances ongoing for 5 months. Hemogram testing revealed macrocytic anemia. Serum cobalamin level was low. Anti-intrinsic factor antibody was detected. Spinal cord magnetic resonance imaging showed diffuse high-signal intensity along the posterior spinal cord extending from C1 to C4. Vitamin B12 replacement therapy led to full regression of clinical signs after six weeks. Association of central nervous system involvement with macrocytic anemia suggests vitamin B12 deficiency and pernicious anemia should be suspected. This disease can be considered as a curable form of myelitis in Africa and Madagascar.

Topics: Anemia, Pernicious; Encephalomyelitis; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Tropical Climate; Vitamin B 12; Vitamins

We report a 39-year-old man who developed seizures as a predominant symptom of vitamin B12 deficiency. About a month before admission to our hospital, he experienced flickering vision, and had generalized convulsive seizures about ten times a day. On admission, he presented with visual disturbance and paralysis of the left leg. Brain MRI revealed a tumor-like lesion in the medial side of the right frontal lobe. Follow-up MRI about 2 weeks after admission demonstrated multiple lesions in the periaqueduct, the medial side of the bilateral thalami, the bilateral frontal lobes, and the bilateral occipital lobes. After administration of antiepileptic drugs, his condition was well-controlled. Paralysis of his left leg was gradually improved, and abnormal findings on brain MRI disappeared except that in the right frontal lobe cortex, which was considered to be cortical laminar necrosis. 123I-IMP-SPECT showed hyperperfusion in the bilateral occipital lobes. About 3 months after the first admission, he was readmitted because of ataxic gait and numbness in the extremities. Laboratory tests revealed macrocytic anemia and vitamin B12 deficiency. Spinal MRI revealed typical findings of subacute combined degeneration. Brain MRI showed multiple new lesions in the bilateral dorsal sides of the medulla, cerebellar hemispheres, interthalamic adhesion, and left frontal cortex. After the initiation of vitamin B12 supplementary therapy, the symptoms were improved, and the abnormal MRI findings disappeared. Serum anti-gastric-parietal-cell antibody and anti-intrinsic-factor antibody were positive. 123I-IMP-SPECT demonstrated hypoperfusion in the bilateral occipital lobes, possibly reflecting visual disturbance. To the best of our knowledge, this is the first report indicating that vitamin B12 deficiency may insult various brain regions as well as the spinal cord with reversibility. Vitamin B12 deficiency should be also considered in the differential diagnosis of the causes of epilepsy.

Topics: Adult; Brain; Diagnosis, Differential; Encephalomyelitis; Humans; Magnetic Resonance Imaging; Male; Seizures; Treatment Outcome; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Animals; Carcinoma, Hepatocellular; Encephalomyelitis; Liver Neoplasms; Neoplasms; Rats; Vitamin B 12