Infantile Tremor Syndrome: A Vitamin B12 Deficiency Syndrome in Infants

Garewal, G.; Narang, Anil; Das, Kusal K

doi:10.1093/tropej/34.4.174

Cited by 65 publications

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“…24,26,34 Tremors have been described to occur as a distinct entity in children of north and central India -The infantile tremors syndrome. 3,35 Similar cases with tremors have recently been described from other countries. 36 These cases mostly have macrocytic anemia and developmental regression in addition to tremors.…”

Section: Clinical Profile: Anemia and Beyondsupporting

confidence: 64%

Megaloblastic anemia: Back in focus

Chandra

2010

Indian J Pediatr

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Megaloblastic anemia (MA), in most instances in developing countries, results from deficiency of vitamin B(12) or folic acid. Over the last two to three decades, incidence of MA seems to be increasing. Of the two micronutrients, folic acid deficiency contributed to MA in a large majority of cases. Now deficiency of B(12) is far more common. In addition to anemia, occurrence of neutropenia and/or thrombocytopenia is increasingly being reported. Among cases presenting with pancytopenia, MA stands out as an important (commonest cause in some series) cause. This article focuses on these and certain other aspects of MA. Possible causes of increasing incidence of MA are discussed. Observations on other clinical features like neurocognitive dysfunction, associated hyperhomocysteinemeia and occurrence of tremors and thrombocytosis during treatment are highlighted.

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Section: Clinical Profile: Anemia and Beyondsupporting

confidence: 64%

Megaloblastic anemia: Back in focus

Chandra

2010

Indian J Pediatr

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“…In the present study more patients <2 years of age presented with neurologic symptoms than those aged ≥2 years (p<0.05). Numerous case reports have reported neurologic symptoms in patients with vitamin B12 deficiency in infants [26][27][28][29][30] and 2 large series from Turkey reported various neurologic symptoms in infants [31,32]. These findings might be due to the fact that myelinization of the central nervous system is incomplete and ongoing during the first 2 years of life.…”

Section: Discussionmentioning

confidence: 99%

Long-term outcome in children with nutritional vitamin B12 deficiency

Evim

Erdol²,

Özdemır³

et al. 2011

Turk J Hematol

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Objective: Vitamin B12 deficiency is frequently observed in developing countries. Herein we report the long-term clinical and laboratory outcomes in 45 children presented with various symptoms of vitamin B12 deficiency. Materials and Methods: Symptoms and physical findings, and percentiles for weight, height, and head circumference at presentation were recorded. The educational level of the patients' mothers, vitamin B12 deficiency-related diseases and family income data were collected. Complete blood count, serum vitamin B12, folate, iron, iron binding capacity and ferritin, and plasma homocysteine levels were recorded measured at presentation. The patients were treated with vitamin B12, as follows: 1 mg/d IM for 1 week, followed by 1 mg IM QWK for 2 weeks, and then monthly 1mg injections. Patients were neurologically and hematologically re-evaluated after treatment. The visual evoked potential (VEP) test was used to examine the integrity and function of the visual pathway. Brainstem evoked potential (BAEP) responses were used to analyze auditory function. Neuromotor development was assessed using Denver II Development Screening Test. Results: The mean age of 20 male and 25 female patients was 5.6±5.9 years (range: 1.4 months-17 years). The most common symptoms at presentation were weakness, failure to thrive, and hematologic manifestations (pallor, petechiae, ecchymosis). Abnormal neurologic findings at presentation were observed in 20% of the patients, and were more commonly observed in those <2 years. VEP, BAEP, and Denver II Development tests were performed in 66% of the patients one year after vitamin B12 replacement was started. VEP and BAEP interval prolongation was observed in 37% and 17% of the cases, respectively. Denver II Development Test results showed developmental delay in 20% of the patients tested. Conclusion: All the patients achieved full hematologic recovery within 1 month of treatment onset. Neurological symptoms resolved following B12 administration; however, during long-term follow-up ranged from 17% to 37% of the tested patients had persistent VEP; BERA, and Denver II abnormalities. Neurological symptoms resolved following B12 administration; however, during long-term followup 33% of the patients had persistent VEP, BERA, and Denver II abnormalities. As such, clinicians should continue to follow-up such patients even after hematologic and clinical improvement are obtained in order to assess their neurologic status. (Turk J Hematol 2011; 28: 286-93)

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“…Although variations in the timing are described, movements often appear a few days after initiation of cobalamin injections (Garewal et al 1988;Emery et al 1997;Avci et al 2003;Benbir et al 2007;Yavuz 2008). Movements are described as a combination of tremor and myoclonus and may affect extremities as well as face and tongue, making feeding difficult.…”

Section: Treatmentmentioning

confidence: 99%

Cobalamin status in children

Bjørke‐Monsen

Ueland

2010

J of Inher Metab Disea

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Cobalamin and the metabolic markers methylmalonic acid and total homocysteine undergo marked changes during childhood. In breastfed infants a metabolic profile indicative of cobalamin deficiency is common. Symptoms of cobalamin deficiency in children differ with age, presenting a continuum from subtle developmental delay to life-threatening clinical conditions. The symptoms may be difficult to detect, particularly in infants, and there tends to be a diagnostic delay of several months in this age group. Several reports show that even moderate deficiency in children may be harmful, and long-term consequences of neurological deterioration may persist after cobalamin deficiency has been treated. Given the crucial role of cobalamin for normal growth and development, possible widespread infantile deficiency needs attention. Cobalamin deficiency should be considered a differential diagnosis in children with subtle symptoms, and strategies to prevent cobalamin deficiency in mothers and children should be addressed.

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Infantile Tremor Syndrome: A Vitamin B12 Deficiency Syndrome in Infants

Cited by 65 publications

References 0 publications

Megaloblastic anemia: Back in focus

Megaloblastic anemia: Back in focus

Long-term outcome in children with nutritional vitamin B12 deficiency

Cobalamin status in children

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