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

J Neurol Neurosurg Psychiatry. 2001 Nov;71(5):691-5. doi: 10.1136/jnnp.71.5.691.

Abstract

A [(18)F]-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 [(18)F]-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 [(18)F]-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.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Basal Ganglia / diagnostic imaging
  • Basal Ganglia / metabolism*
  • Basal Ganglia / pathology
  • Brain Diseases, Metabolic / chemically induced*
  • Calcitriol / adverse effects*
  • Calcium / adverse effects*
  • Chorea / drug therapy*
  • Chorea / etiology*
  • Fluorodeoxyglucose F18
  • Glucose / metabolism
  • Humans
  • Hypothyroidism / complications*
  • Magnetic Resonance Imaging
  • Male
  • Radiopharmaceuticals
  • Tomography, Emission-Computed

Substances

  • Radiopharmaceuticals
  • Fluorodeoxyglucose F18
  • Calcitriol
  • Glucose
  • Calcium