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

A [F-18]-FDG PET study was performed in a 44 year old man with proximal kin esigenic choreoathetosis (PKC) secondary to idiopathic primary hypoparathyr oidism (IPH) before and 1 year after calcium/calcitriol therapy. The [F-18] -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 o f PKC episodes, the [F-18]-FDG PET did not show the previously detected hyp ometabolism. The hypometabolism of the ventral striatum secondary to hypoca lcaemia seems to play a crucial part in the pathogenesis of paroxysmal kine sigenic choreoathetosis associated with JPH.