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Involuntary movements in infantile cobalamin deficiency appearing after treatment
E A Ozer1, M Turker, A R Bakiler
1Clinic of Pediatrics, SSK Tepecik Teaching Hospital, Yenisehir, Izmir, Turkey.
Insights
Infantile cobalamin (vitamin B12) deficiency can cause neurological issues. A rare movement disorder, including tremor and myoclonus, may emerge after treatment, improving with clonazepam.
Area of Science:
- Neurology
- Pediatrics
- Nutritional Science
Background:
- Infantile cobalamin (vitamin B12) deficiency is a treatable condition that can lead to severe neurological impairment.
- Neurological symptoms, including involuntary movements, are common in infants with cobalamin deficiency.
Observation:
- Two breast-fed infants with cobalamin deficiency developed a severe movement disorder characterized by tremor and myoclonus shortly after initiating cobalamin treatment.
- The involuntary movements primarily affected the tongue, face, pharynx, and legs.
Findings:
- Neurological symptoms, including the striking movement disorder, showed improvement within days of administering clonazepam.
- Maternal cobalamin deficiency was identified as the cause in both cases, highlighting the importance of maternal nutritional status.
Implications:
- This case report highlights a rare but notable adverse effect of cobalamin treatment in infants, necessitating increased clinical attention.
- While the exact cause remains unknown, the potential for post-treatment movement disorders warrants consideration for additional therapeutic strategies if symptoms are severe.
Abstract:
Involuntary movements may be a symptom in most infants who present with neurologic syndrome of infantile cobalamin (vitamin B12) deficiency. In this report, two infants with cobalamin deficiency are presented. These patients also developed a striking movement disorder that appeared a few days after treatment with intramuscular cobalamin. The movement disorder was characterized by severe involuntary movements, which were a combination of tremor and myoclonus particularly involving tongue, face, pharynx, and legs. The neurologic symptoms improved within a few days after the administration of clonazepam. In each patient the mother was also cobalamin deficient and the infant was solely breast-fed. The cause of involuntary movements that can appear rarely after treatment in infantile cobalamin deficiency is not known. Besides initial neurologic presenting symptoms of cobalamin deficiency, the occurrence of involuntary movements after treatment should also receive attention. This movement disorder may disappear spontaneously, or an additional treatment may be an alternative approach if the symptoms are severe.