Regression of ventral striatum hypometabolism after calcium/calcitriol therapy in paroxysmal kinesigenic choreoathetosis due to idiopathic primary hypoparathyroidism. Issue 5 (1st November 2001)

• Record Type: Journal Article
• Authors: Volonté, M A; Perani, D; Lanzi, R; Poggi, A; Anchisi, D; Balini, A; Comi, G; Fazio, F
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 71:Issue 5(2001)
• Page Start: 691
• Page End: 695
• Publication Date: 2001-11-01
• Subjects: paroxysmal kinesigenic choreoathetosis -- primary hypoparathyroidism -- ventral striatum -- movement disorders; Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp.71.5.691
• Languages: English
• ISSNs: 0022-3050

Abstract

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.