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  • Regression of ventral striatum hypometabolism after calcium/calcitriol therapy in paroxysmal kinesigenic choreoathetosis due to idiopathic primary hypoparathyroidism

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Regression of ventral striatum hypometabolism after calcium/calcitriol therapy in paroxysmal kinesigenic choreoathetosis due to idiopathic primary hypoparathyroidism
  1. M A Volontéa,
  2. D Peranid,
  3. R Lanzib,
  4. A Poggia,
  5. D Anchisid,
  6. A Balinib,
  7. G Comia,
  8. F Fazioc,d
  1. aMovement Disorder Unit, Department of Neuroscience, Istituto Scientifico Ospedale San Raffaele, Via Olgettina 60, 20132 Milano, Italy, bDepartment of Internal Medicine, cDepartment of Nuclear Medicine, dInstitute of Neuroscience and Bioimaging, CNR, Italy
  1. Dr M A Volonté

Abstract

A [18F]-FDG PET study was performed in a 44 year old man with proximal kinesigenic choreoathetosis (PKC) secondary to idiopathic primary hypoparathyroidism (IPH) before and 1 year after calcium/calcitriol therapy. The [18F]-FDG PET performed before the start of the therapy disclosed a significant bilateral hypometabolism in the ventral striatum. One year later, with the patient still under calcium/calcitriol therapy and free of any occurrence of PKC episodes, the [18F]-FDG PET did not show the previously detected hypometabolism. The hypometabolism of the ventral striatum secondary to hypocalcaemia seems to play a crucial part in the pathogenesis of paroxysmal kinesigenic choreoathetosis associated with IPH.

  • paroxysmal kinesigenic choreoathetosis
  • primary hypoparathyroidism
  • ventral striatum
  • movement disorders

https://doi.org/10.1136/jnnp.71.5.691

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