Funding agencies: This work was supported by the Benign Essential Blepharospasm Research Foundation and Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (21791725 to Y.S.; 20591038 to K.I.).
Article first published online: 16 FEB 2012
Copyright © 2012 Movement Disorder Society
Volume 27, Issue 4, pages 519–525, April 2012
How to Cite
Shimizu, M., Suzuki, Y., Kiyosawa, M., Wakakura, M., Ishii, K., Ishiwata, K. and Mochizuki, M. (2012), Glucose hypermetabolism in the thalamus of patients with hemifacial spasm. Mov. Disord., 27: 519–525. doi: 10.1002/mds.24925
Relevant conflicts of interest/financial disclosures: Nothing to report.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 4 APR 2012
- Article first published online: 16 FEB 2012
- Manuscript Accepted: 3 JAN 2012
- Manuscript Revised: 28 NOV 2011
- Manuscript Received: 31 JAN 2011
- cerebral glucose metabolism;
- hemifacial spasm;
- positron emission tomography;
The purpose of this study was investigate functional alteration in the brains of patients with hemifacial spasm using positron emission tomography (PET). We studied cerebral glucose metabolism using PET with 18F-fluorodeoxyglucose in 13 patients with right lateral hemifacial spasm and 13 with left lateral hemifacial spasm. All patients underwent 2 PET scans before treatment (active state) and after treatment (suppressive state) with the botulinum neurotoxin type A. At the time of the PET scans, the severity of the spasm was rated according to the Jankovic Disability Rating Scale. We also used magnetic resonance imaging to evaluate the grade of neurovascular compression in each patient using scores of 1 to 3 (1 = mild, 3 = severe). Fifty-two normal volunteers were examined as controls. Compared with controls, patients with right and left hemifacial spasm showed bilateral cerebral glucose hypermetabolism in the thalamus in both the active and suppressive states. However, thalamic glucose metabolism after the suppressive state was significantly reduced compared with that in the active state using region of interest analysis. There was a positive correlation between the severity of the spasm in the active state and the score of neurovascular compression (rs = 0.65) that was estimated using Spearman order correlation coefficient. We observed bilateral cerebral glucose hypermetabolism in the thalamus of patients with hemifacial spasm. The thalamic glucose hypermetabolism may be attributed to multiple sources, including afferent input from the skin and muscle spindle, antidromic conduction of the facial nerve, and secondary alteration in the central nervous system. © 2012 Movement Disorder Society