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.

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

ANCHISI, Davide;
2001-01-01

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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11390/852807
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