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Infantile encephalopathy due to vitamin deficiency in industrial countries

Ibrahim Abu-Kishk1, Marianna Rachmiel, Chen Hoffmann

  • 1Pediatric Intensive Care Unit, Assaf Harofeh Medical Center, Zerifin, Tel-Aviv 70300, Israel.

Child'S Nervous System : Chns : Official Journal of the International Society for Pediatric Neurosurgery
|July 9, 2009
PubMed

Insights

Severe vitamin deficiencies, specifically thiamine (B1) and cobalamin (B12), can cause life-threatening neurological issues in infants. Prompt diagnosis and treatment are crucial for recovery and minimizing long-term effects.

Area of Science:

  • Pediatric Neurology
  • Nutritional Science
  • Biochemistry

Background:

  • Severe vitamin deficiencies are rare in infants, typically associated with malabsorption or inadequate supplementation.
  • This case series highlights the potential for severe avitaminosis in infants without obvious risk factors.

Observation:

  • Two infants presented with unexplained neurological deterioration.
  • Initial work-up for infections and metabolic disorders did not yield a diagnosis.
  • Deterioration worsened with glucose administration in one infant, suggesting thiamine deficiency.

Findings:

  • Thiamine (B1) deficiency was confirmed by elevated cerebrospinal fluid lactate, improved transketolase activity post-treatment, and characteristic MRI/MRS findings.
  • Cobalamin (B12) deficiency was diagnosed in an infant of a vegetarian mother, presenting with megaloblastic anemia, low serum B12, and methylmalonic aciduria.
  • B12 treatment normalized methylmalonic acid levels.

Implications:

  • Avitaminosis should be considered in infants with atypical neurological symptoms, even in developed countries.
  • Early diagnosis and prompt vitamin repletion can lead to rapid recovery and reduced long-term neurological sequelae.
  • This underscores the importance of considering nutritional deficiencies in pediatric neurological presentations.
Abstract

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