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Título

NEUROLOGICAL ALTERATIONS RELATED TO VITAMIN B12 DEFICIENCY: A CASE REPORT

RESUMO

Case presentation: A 56-year-old male patient, in February 2012, presented a neurological condition showing irritability, paranoid delusions, evocation amnesia and apraxia when dressing and performing personal hygiene. Simultaneously, paresthesia and dysbasia in the lower limbs began due to imbalances of insidious onset. On examination, cognitive screening tests were initially unrealisable, and there was diffuse arreflexia, hypoesthesia in "boot" and ataxic gait. Laboratory evaluation demonstrated normal blood count, electrolytes, transaminases, nitrogen scores, folic acid, ESR and blood glucose levels, TSH 12.99 mUI/L, free T4 0.87 ng/dL, VDRL and anti-HIV 1 and 2 not reactive, serum vitamin B12 50.0 pg/ml. Magnetic resonance imaging of the skull showed a small cystic lesion in the right basal ganglia and mild leukoaraiosis. The patient started parenteral use of a compound of B complex vitamins - 5000 U, intramuscularly, once a week, for three months, associated with quetiapine, 50mg/day, and evolved with memory, behavioral disorders and balance improvement as well as functional autonomy, however remaining with a slight sensation of numbness in the feet. Discussion: Vitamin B12 deficiency usually causes megaloblastic anemia, which may be absent in one third of cases, associated with neurological symptoms, due to vascular alterations associated with the elevation of homocysteine, or alterations in methylation reactions, affecting myelin. Such alterations compromise axons of the ascending tracts of the posterior funiculus, descending pyramidal tracts and peripheral nerves. The treatment of the disease is carried out through parenteral replacement of the vitamin, with a maximum improvement generally occurring in the first six months, and its early initiation is of great importance to avoid possible neurological sequelae. Final Comments: This scenario, consisting of an amnesic and behavioral, apraxia, ataxia and sensory cognitive syndrome, representing subacute dementia, sensory ataxia and sensory polyneuropathy, has, in many cases, a secondary relation to vitamin B12 deficiency, based on its serum dosage, with the possibility of associated problems, such as the existence of a subclinical hypothyroidism, which was also verified in the patient.