Abstract:
Introduction: Deficiency of vitamin B12 produces protean effects on the nervous system, most commonlyneuropathy, myelopathy, cognitive and behavioral symptoms, and optic atrophy. Involuntary movements comprise a relatively rare manifestation of this readily treatable disorder. Both adults and infants deficient in vitamin B12 may present with chorea, tremor, myoclonus, Parkinsonism, dystonia, or a combination of these, which mayprecede diagnosis or become apparent only a few days after parenteral replacement therapy has begun. The pathogenesis of these movement disorders shows interesting parallels to certain neurodegenerative conditions. The clinical syndrome responds well to vitamin B12 supplementation in most cases, and an early diagnosis is essential to reverse the haematological and neurological dysfunction characteristic of this disorder Case Study: An 86- year-old woman with a history of cerebrovascular accident (CVA) and atrial fibrillation was admitted to our hospital Almak Nemer University hospital complaining of disturbance of consciousness and chorea-like involuntary movements of the extremities. The patient was diagnosed with encephalopathy due to vitamin B12 deficiency. Involuntary movements improved with parenteral vitamin B12 supplementation. Discussion: Vitamin B12 serve as cofactor for forming methionine from homocystiene. Decrease Vitamin B12 level lead to high level of homocystiene which appear to be toxic to endothelial cells. Methionine is further metabolized to Sadenosylmethionine (SAM). S-adenosylmethionine SAM influences serotonin, norepinephrine, and dopamine synthesis. This suggests that, in addition to structural consequences of vitamin B-12 deficiency, functional effects on neurotransmitter synthesis that may be relevant to mental status changes may occur. Conclusion: The present case is considered valuable in identifying the pathophysiology of involuntary movement due to vitamin B12 deficiency.
Description:
Introduction: Deficiency of vitamin B12 produces protean effects on the nervous system, most commonlyneuropathy, myelopathy, cognitive and behavioral symptoms, and optic atrophy. Involuntary movements comprise a relatively rare manifestation of this readily treatable disorder. Both adults and infants deficient in vitamin B12 may present with chorea, tremor, myoclonus, Parkinsonism, dystonia, or a combination of these, which mayprecede diagnosis or become apparent only a few days after parenteral replacement therapy has begun. The pathogenesis of these movement disorders shows interesting parallels to certain neurodegenerative conditions. The clinical syndrome responds well to vitamin B12 supplementation in most cases, and an early diagnosis is essential to reverse the haematological and neurological dysfunction characteristic of this disorder Case Study: An 86- year-old woman with a history of cerebrovascular accident (CVA) and atrial fibrillation was admitted to our hospital Almak Nemer University hospital complaining of disturbance of consciousness and chorea-like involuntary movements of the extremities. The patient was diagnosed with encephalopathy due to vitamin B12 deficiency. Involuntary movements improved with parenteral vitamin B12 supplementation. Discussion: Vitamin B12 serve as cofactor for forming methionine from homocystiene. Decrease Vitamin B12 level lead to high level of homocystiene which appear to be toxic to endothelial cells. Methionine is further metabolized to Sadenosylmethionine (SAM). S-adenosylmethionine SAM influences serotonin, norepinephrine, and dopamine synthesis. This suggests that, in addition to structural consequences of vitamin B-12 deficiency, functional effects on neurotransmitter synthesis that may be relevant to mental status changes may occur. Conclusion: The present case is considered valuable in identifying the pathophysiology of involuntary movement due to vitamin B12 deficiency.