2012
DOI: 10.1016/j.braindev.2012.01.014
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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

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Cited by 8 publications
(7 citation statements)
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“…On the other hand, if red flags which are not common in primary PKD patients are present, more careful assessment will be needed to differentiate primary PKD from other paroxysmal dyskinesias or secondary PKD. Brain CT/MRI is recommended for all PKD‐suspected patients, because PKD has several secondary etiologies, such as multiple sclerosis, trauma, metabolic derangements, and inadequate brain perfusion . Genetic screening is optional, because PKD is a relatively benign disease with spontaneous remission and effective medications to control attacks.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…On the other hand, if red flags which are not common in primary PKD patients are present, more careful assessment will be needed to differentiate primary PKD from other paroxysmal dyskinesias or secondary PKD. Brain CT/MRI is recommended for all PKD‐suspected patients, because PKD has several secondary etiologies, such as multiple sclerosis, trauma, metabolic derangements, and inadequate brain perfusion . Genetic screening is optional, because PKD is a relatively benign disease with spontaneous remission and effective medications to control attacks.…”
Section: Discussionmentioning
confidence: 99%
“…Brain CT/MRI is recommended for all PKD-suspected patients, because PKD has several secondary etiologies, such as multiple sclerosis, trauma, metabolic derangements, and inadequate brain perfusion. [29][30][31][32][33][34] Genetic screening is optional, because PKD is a relatively benign disease with spontaneous remission and effective medications to control attacks. For patients who undergo genetic screening, mutations of the following genes reported to be associated with PKD should be initially tested: PRRT2, PNKD, SLC2A1, SCN8A, KCNMA1, KCNA1, and DEPDC5.…”
Section: Genetic Features Of Paroxysmal Kinesigenic Dyskinesiamentioning
confidence: 99%
“…PKD was initially considered to be an ion channelopathy due to its clinical features and high sensitivity to small doses of sodium channel blockers [ 13 , 14 ]. However, proline-rich transmembrane protein 2 ( PRRT2 ) was the first disease-causing gene identified in 2011 by Chinese scholars, which likely explained the pathogenesis of familial PKD [ 15 ].…”
Section: Discussionmentioning
confidence: 99%
“…Secondary PKD has been described in the setting of hypocalcemia, as has exacerbation of symptoms in a patient with a history of idiopathic PKD in childhood. 84,90 This may relate to the role of disrupted ion channels in the pathophysiology of the disease, as has been seen in other paroxysmal movement disorders. 90…”
Section: Infectious/para-infectiousmentioning
confidence: 98%