Lid opening apraxia is associated with medial frontal hypometabolism

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Abstract
We used [18F]fluorodeoxyglucose with positron emission tomography to explore the functional basis of lid opening apraxia (LOA). We studied four patients with LOA without associated pyramidal or extrapyramidal motor dysfunction (mean age 65.5 ± 4.7 years). We compared measures of glucose metabolism with those calculated for 10 age‐matched normal volunteers (mean age 60.6 ± 11.4). All four patients demonstrated significant metabolic reductions (>2 SD) in the medial frontal lobe: bilaterally in two, unilaterally in two. Significant abnormal unilateral metabolic reductions in the left basal ganglia were evident in two patients. These findings suggest that medial frontal lobe hypometabolism is associated with LOA. Abnormal striatofrontal interactions may be involved in the pathogenesis of this condition.