Frontal lobe ataxia

Gait abnormalities often result from disorders intrinsic to the cerebellum. Gait difficulties resulting from frontal lobe disease are less common but well recognized. The pathophysiologic mechanism of this type of ataxia is not well understood. One promising explanation implicates involvement of the frontopontocerebellar tract (Arnold's bundle). This tract originates in the frontal lobe in Brodmann's area 10 and carries information on intended movement to the contralateral cerebellum via the pontocerebellar peduncle. Interruption of this tract deprives the cerebellum of this information, thus impairing coordination and locomotion.

A patient is described with a large bilateral, medialorbital, frontal lobe lesion, progressive gait impairment, and dysarthria. The lesion is defined by magnetic resonance imaging (MRI) and positron emission tomography (PET) using 18-fluorodeoxyglucose. The cystic component of the lesion was drained surgically.

The PET scan using 18-fluorodeoxyglucose showed a normal metabolic rate in the brain stem, a 10%-15% decrease in metabolism in the thalmus and a symmetric decrease of only 15% in the cerebellum bilaterally. The MRI of the cerebellum did not show any significant atrophy. The patient's speech improved, but there was minimal change in her gait ataxia after surgical drainage and partial removal of the cystic frontal lobe lesion.

The patient's syndrome supports the view that frontal lobe ataxia is an established although rare clinical entity, and this report adds original information defining the syndrome with MRI and PET studies. The 15% metabolic decrease in the cerebellum with PET is highly supportive of the syndrome of frontal lobe ataxia and not pathology intrinsic to the cerebellum. The syndrome of frontal lobe ataxia in this patient is due to interruption of the frontopontocerebellar pathway originating in Brodmann's area 10.