Frontal lobe ataxia.

Abstract

The precise anatomy and physiology of human walking remains poorly understood. The frontal lobes appear crucial, and, on the basis of clinical observation, contribute to the control of truncal motion, postural responses, and the maintenance of equilibrium and locomotion. The rich repertoire of frontal gait disorders gives some indication of this complexity. Variable combinations of disequilibrium with a wide stance base, increased body sway and falls, loss of control of truncal motion, locomotor disability with gait ignition failure, start hesitation, shuffling, and freezing are encountered in diseases of the frontal lobes. Furthermore, the pattern of gait may change as the frontal disease progresses. The slowness of walking, lack of heel-shin or upper limb ataxia, dysarthria or nystagmus distinguishes the wide stance base from cerebellar gait ataxia. A lively facial expression, normal voluntary movements of the upper limbs, upper motor neuron signs, and the absence of a rest tremor distinguish the hypokinetic elements from Parkinson's disease. Poor truncal mobility, impaired postural responses, and falls after the slightest perturbation eventually make walking impossible even though simple leg movements may still be possible while seated or lying. One or more of these features usually predominates in the initial presentation of a frontal gait syndrome. Accordingly, there is considerable variation in the manner of presentation and evolution of frontal gait disorders. The gait syndrome is accompanied by frontal motor and cognitive changes, which may be subtle or overshadowed by the gait disorder. This complexity of clinical presentation accounts for the plethora of descriptions from "frontal ataxia" to "gait apraxia". As suggested in the original descriptions of frontal ataxia, the spectrum of gait disturbance is likely to be due to damage to frontal cortex and its connections with subcortical structures including the basal ganglia, cerebellum, and the brainstem.