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Título

EXTENSIVE LEUKOENCEPHALOPATHY SECONDARY TO VITAMIN B12 DEFICIENCY: CASE REPORT

RESUMO

Presentation: A 43-year-old male patient with a history of sudden cervical pain irradiating to the lower limbs followed by paraplegia 11 years before, with a slight improvement of motor déficit, remained restricted to bed for 2 years, when he presented spontaneous recovery of functionality, without complaints for the following 2 years when he acutely presented symmetrical paraparesis with episodes of daily kinesiogenic painful dystonia in the lower limbs with clonus, associated to paresthesia with a sensory level not clearly defined in the T5 topography. The condition has remained stable with no improvement in weakness up to the present day. Personal history: SAH. On examination: alert, oriented, mild intellectual impairment, isochoric and photoreagent pupils, paraparesis (grade 1), spastic tone, normotrophic, superficial hypoesthesia at T5, distal hypopalesthesia with patellar hyperreflexia, Babinski sign on the right and bilateral Hoffman sign. Mini mental with score below the value for the degree of education (27/30). Serum vitamin B12 dosage <148, with macrocytic and hyperchromic red blood cells, without anemia; MRI of the neuroaxis showing confluent punctiform foci in subcortical and deep white matter, U-shaped cortical fibers and diffuse medullary atrophy, with hypersignal on T2 and STIR in the posterior cord at the level of D2 to D5, suggestive of vitamin B12 deficiency. Discussion: The combined clinical signs of pyramidal syndrome, with clear predominance of lower limb involvement, sensory changes with spinal cord sensory level suggestive of myelopathy, and quantified cognitive decline, necessitated the need for CNS imaging study that showed extensive leukoencephalopathy pattern and signal enhancement of the posterior spinal cord, which, together with the finding of serum hypovitaminosis B12 and gastric atrophy on AGE, strengthened the hypothesis of specific metabolic myelopathy. Commenst: Vitamin B12 is directly linked to neuropsychiatric functions due to its participation in DNA synthesis and neuronal myelination, and, thus, its deficiency can cause alterations in the central and peripheral nervous system. The above patient presented an atypical clinical picture, with spastic paraparesis and fluctuating painful dystonias, with a surge pattern, extensive radiological involvement, suppressed serum dosage of this substrate, and a definite digestive disabsorptive etiology, consistent with the diagnosis of cyanocobalamin deficiency encephalomyelopathy.

Palavras Chave

Leucoencefalopatia