On the basis of neurological evidence that autistic patients have fewer
Purkinje and granule cells in the cerebellum as well as vermal cerebellar
hypoplasia, the authors tested the hypothesis that autistic patients have
cerebellar hypofunctioning. They used positron emission tomography of the
cerebellum with 18F-labeled 2-deoxyglucose to study seven autistic patients
and eight age-matched control subjects. The results showed no significant
difference in mean cerebellar glucose metabolism between the two groups,
but all mean glucose rates of the autistic patients were either equal to or
greater than those of the control subjects. The implications of these
findings are discussed.Abstract Teaser