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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.

Abstract
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.
AuthorsDongkwan Jin, Won Tae Yoon, Bum Chun Suh, Heui-Soo Moon, Pil-Wook Chung, Yong Bum Kim
JournalBrain & development (Brain Dev) Vol. 34 Issue 10 Pg. 840-3 (Nov 2012) ISSN: 1872-7131 [Electronic] Netherlands
PMID22361453 (Publication Type: Case Reports, Journal Article)
CopyrightCopyright © 2012 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
Chemical References
  • Calcium
Topics
  • Adult
  • Calcium (blood)
  • Channelopathies (complications)
  • Chorea (etiology)
  • Dystonia
  • Humans
  • Hypocalcemia (etiology)
  • Hypoparathyroidism (etiology)
  • Male
  • Remission Induction
  • Thyroidectomy (adverse effects)

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