ABSTRACT
Experimental studies of locomotion in quadrupeds indicate a prominent role of brainstem structures and spinal cord networks. The role of the cerebral cortex appears relatively small compared with that of subcortical structures, although the cortex and corticospinal tract are important for adept placement of the feet during locomotion. The applicability and scope for any generalization of these studies to human bipedal locomotion has frequently been questioned. This conundrum is well illustrated by the concept of frontal and higher level gait disorders. Experimental models of locomotion do not predict the complex range of gait disturbances encountered in diseases of the frontal lobes and the subcortical circuits connecting the frontal lobes, basal ganglia, cerebellum and brainstem. The mechanisms of these gait disturbances are poorly understood, and in many cases it is simply the association with frontal pathology that leads to the designation ‘frontal gait disorder’. As a result, the nomenclature and classification of frontal gait disorders remains the subject of debate.1 The term ‘higher level’ gait disorder has also been used to describe gait disorders associated with disease of the frontal lobes and their connections, distinguishing these gait patterns from middle-level disorders caused by lesions of the corticospinal tracts (paraparesis or hemiparesis), the cerebellum (ataxia), or basal ganglia (parkinsonian and dyskinetic gaits) and lower level disorders affecting the peripheral neuromuscular apparatus.1
