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首页> 外文期刊>Brain & Development >Exacerbation of idiopathic paroxysmal kinesigenic dyskinesia in remission state caused by secondary hypoparathyroidism with hypocalcemia after thyroidectomy: Evidence for ion channelopathy
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Exacerbation of idiopathic paroxysmal kinesigenic dyskinesia in remission state caused by secondary hypoparathyroidism with hypocalcemia after thyroidectomy: Evidence for ion channelopathy

机译:继发性甲状旁腺功能低下并发低钙血症的甲状腺切除术后继发性阵发性运动性运动障碍加重:离子通道病的证据

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摘要

Most reported cases of paroxysmal kinesigenic dyskinesia (PKD) are idiopathic or familial; however, hypoparathyroidism is another unusual cause of secondary PKD. The pathomechanism of PKD remains poorly understood, and the association between idiopathic and secondary PKD remains an enigma, and has yet to be clearly elucidated. We recently encountered a patient with idiopathic PKD whose symptoms were aggravated by secondary hypoparathyroidism with hypocalcemia after having undergone a thyroidectomy. The patient's paroxysms were ameliorated by the normalization of serum calcium levels. The results discussed herein may provide support for the hypothesis that PKD is associated with neuronal ion regulation.
机译:阵发性运动性运动障碍(PKD)的大多数报告病例是特发性或家族性的。然而,甲状旁腺功能低下是继发性PKD的另一个不寻常原因。 PKD的致病机理仍知之甚少,特发性与继发性PKD之间的关联仍是一个谜,并且尚未明确阐明。我们最近遇到一名患有特发性PKD的患者,在进行甲状腺切除术后,其症状因继发性甲状旁腺功能低下并伴有低钙血症而加重。血清钙水平正常化可减轻患者的阵发性疾病。本文讨论的结果可为PKD与神经元离子调节相关的假设提供支持。

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