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K.W. Andreason, J.B. Kerrison, D.E. Holck, S.M. Blaydon, J. Lancaster, L.A. Richardson, J.C. Morrison, F.E. Zamarripa, P.T. Fox; PET Scanning in Essential Blepharospasm . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2722.
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Purpose: Essential blepharospasm (EB) is a disorder characterized by involuntary bilateral episodic contractions of the orbicularis oculi muscles. It is classified as a primary focal dystonia. It can be difficult to diagnose in its early stages, and its pathophysiology is not well understood. Prior studies using positron emission tomography neuroimaging with 18fluorodeoxyglucose (PET(18FDG) ) in EB patients demonstrate abnormal metabolism in the frontal cortex, striatum, thalami, pons, and cerebellum. The purpose of this study is to localize in the brain, using PET (18FDG ), differences in glucose metabolism between patients with EB and controls. Methods: PET(18FDG) neuroimaging was performed in 11 EB patients and 11 controls matched for age and gender. Standard PET software region-of-interest anaylsis and a 3D global analysis, normalizing brain metabolism and size in Talairach space, were performed. Results: Global analysis of PET(18FDG) neuroimages demonstrated multiple cortical and subcortical differences from controls. Cortical areas with the largest and most significant clusters of increased glucose uptake were the inferior frontal gyri, right posterior cingulate gyrus, left middle occipital gyrus, fusiform gyrus of the right temporal lobe, and left anterior cingulate gyrus. Cortical areas with the largest and most significant clusters of decreased glucose uptake were the inferior frontal gyri, ventral to the area of increased glucose metabolism. Subcortical abnormalities, consisting of increased glucose uptake, involved the right caudate, and consisting of decreased glucose uptake, involved the left inferior cerebellar hemisphere and thalamus. Conclusions: Global analysis of PET (18FDG ) neuroimaging in EB patients in comparison with controls demonstrates a pattern of abnormalities involving several cortical and subcortical areas that control blinking, including the inferior frontal lobe, caudate, thalamus, and cerebellum. EB may arise from an aberrant flow or harnessing of the neural network which controls blinking. With further studies, these identified regional differences may aid in the diagnosis, grading and evaluation of treatment response in patients with EB.
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