Glucose hypometabolism in medial frontal cortex of patients with apraxia of lid opening.
PURPOSE: To determine whether regional cerebral functional abnormalities exist in patients with apraxia of lid opening (ALO). METHODS: Cerebral glucose metabolism was examined by positron emission tomography (PET) in 11 patients (8 women and 3 men, age 48-69 years); 10 with ALO accompanied by blepharospasm and 1 patient with pure ALO. Eleven normal volunteers (6 women and 5 men, age 45-66 years) were examined as controls. A comprehensive ophthalmological examination, magnetic resonance imaging (MRI), and PET were performed. The cerebral glucose metabolism was evaluated by the relative uptake of [fluorine-18]fluorodeoxyglucose by PET. The mean +/- two standard deviations of the normal controls was defined as the normal range for cerebral glucose metabolism. RESULTS: MRI revealed no particular lesion except for an infarction in the unilateral basal ganglia in two patients. Decreased glucose metabolism was observed in a wide area of the medial frontal lobe (six cases) and primary visual cortex (PVC) (four cases). Group multiple comparisons revealed a significant decrease ( P<0.0035) in the bilateral anterior cingulate gyrus, left supplementary motor area (SMA), and bilateral PVC. CONCLUSION: The results support the hypothesis that ALO is associated with hypofunction in the SMA and/or anterior cingulate gyrus.[1]References
- Glucose hypometabolism in medial frontal cortex of patients with apraxia of lid opening. Suzuki, Y., Kiyosawa, M., Ohno, N., Mochizuki, M., Inaba, A., Mizusawa, H., Ishii, K., Senda, M. Graefes Arch. Clin. Exp. Ophthalmol. (2003) [Pubmed]
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