Cases reported "Vitamin B 12 Deficiency"

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1/8. Involuntary movements in infantile cobalamin deficiency appearing after treatment.

    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.
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keywords = involuntary movement, movement
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2/8. Involuntary movements associated with vitamin B12 deficiency.

    Involuntary movements are not a known feature of vitamin B12 (vB12) deficiency in adults, though they are a characteristic feature of vB12 deficiency in infants. This case report presents an adult patient with vB12 deficiency in whom, myoclonus-like muscular contractions appeared soon after the initiation of vB12 and disappeared after the first week of this therapy. To our knowledge, this is the first report of involuntary movements in an adult patient with vB12 deficiency. Although the mechanism remains unknown, involuntary movements similar to myoclonus should be considered as one of the extraordinary neurological manifestations of vB12 deficiency in adults.
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keywords = involuntary movement, movement
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3/8. Infantile cobalamin deficiency with cerebral lactate accumulation and sustained choline depletion.

    A remarkable, intermittent sudden-onset vigilance and movement disorder in an exclusively breast-fed infant is reported, which was caused by cobalamin depletion due to maternal vitamin B12 malabsorption. The lack of cobalamin caused a severe encephalopathy in the infant, whose brain displayed a striking loss of volume and a delay of myelination. Proton magnetic resonance spectroscopy revealed an accumulation of lactate in the gray and white matter of the brain and a sustained depletion of choline-containing compounds in the white matter, reflecting a reversible disturbance of oxidative energy metabolism in brain cells and a long-lasting hypomyelination disorder. The clinical picture in conjunction with MRI and spectroscopic data of this case study yields more insight into the functions of cobalamin in the cerebral metabolism.
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ranking = 0.00039209540866284
keywords = movement
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4/8. coma and respiratory failure in a child with severe vitamin B(12) deficiency.

    OBJECTIVE: Psychofunctional follow-up of severe vitamin B(12) deficit. DESIGN: Case report. SETTING: Pediatric intensive care unit. Patient: Ten-month-old boy. INTERVENTION: Follow-up at 3 yrs. MEASUREMENTS AND MAIN RESULTS: A 10-month-old boy was admitted to the pediatric intensive care unit with respiratory failure, muscular hypotonia, and involuntary movements. Although a central nervous system infection was excluded, computed tomography scan showed a diffuse cortical-subcortical atrophy. Vitamin B(12) deficiency was suspected because of a red-cell count of 1,350,000/mm(3) and a hemoglobin value 5.9 g/dL (MCV 116). The baby had been exclusively breast-fed, but his mother had been a strict vegan for 10 yrs. Chronic dietary vitamin B(12) deprivation was confirmed by blood and urinary samples. Treatment with vitamin B(12) led in 2 wks to rapid and complete hematological improvement and to partial regression of neurologic symptoms. During the following 3 yrs the boy had normal vitamin intake and underwent intensive rehabilitative treatment. The brain atrophy regressed, but linguistic and psychomotor delay persisted. CONCLUSIONS: Rapid clinical improvement after vitamin supply does not correlate with a complete recovery.
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ranking = 0.3322877455769
keywords = involuntary movement, movement
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5/8. Developmental regression as an early manifestation of vitamin B12 deficiency.

    Loss of previously attained developmental milestones in an infant is often associated with central nervous system tumor, neuromuscular disease, or an inborn metabolic error. An infant with developmental regression and involuntary movements who was found to be vitamin B12 deficient on the basis of unrecognized maternal vitamin B12 deficiency is described. The infant had a dramatic neurologic recovery after receiving vitamin B12. The case and a review of similar cases is presented.
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ranking = 0.3322877455769
keywords = involuntary movement, movement
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6/8. Nutritional vitamin B12 deficiency in infancy: three case reports and a review of the literature.

    Three cases of vitamin B12 deficiency that occurred during infancy are presented. These cases appeared to be the result of pre-existing maternal deficiency. All three infants demonstrated evidence of neurodevelopmental delay at presentation, and one had sustained loss of milestones and developed involuntary motor movements. Prior to the initiation of therapy, all three infants were anemic: one was thrombocytopenic and one pancytopenic. In all three cases the hematologic and neurologic abnormalities were corrected with vitamin B12 therapy. The literature is reviewed and discussed with respect to the mechanism of the infants' vitamin B12 deficiency and neurodevelopmental manifestations.
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keywords = movement
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7/8. paralysis of upward gaze as a presenting symptom of vitamin B12 deficiency.

    A 47-year-old woman presented with paralysis of upward gaze associated with Addison's pernicious anaemia. Administration of cyanocobalamin resulted in significant improvement of eye movements and haematological parameters. Isolated paralysis of upward gaze may be a feature of vitamin B12 deficiency.
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keywords = movement
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8/8. The neurological syndrome of infantile cobalamin deficiency: developmental regression and involuntary movements.

    Developmental regression is the presenting symptom of most infants with cobalamin (Vitamin B12) deficiency. We present a report of three infants with cobalamin deficiency in which the infants also developed a movement disorder. In each case the mother was a vegetarian and the infant was exclusively breast-fed. In two of the infants, a striking movement disorder consisting of a combination of tremor and myoclonus particularly involving face, tongue, and pharynx appeared 48 h after the initiation of treatment with intramuscular cobalamin. This was associated with marked changes in plasma amino acid levels. Paradoxically, the onset of the movement disorder coincided with overall neurological improvement. The third infant had a persistent focal tremor, which appeared before the commencement of treatment. The movements slowly abated during a 3-6 week period. The presence of a movement disorder in cobalamin deficiency has received less attention than other features, but in a mild form is probably common. It may offer an early clue to the diagnosis before the onset of profound neurological deterioration. The cause of the severe movement disorder that can appear after treatment is not known.
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ranking = 1.3315035547596
keywords = involuntary movement, movement
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