The reduced walking speed and the seeking of an increased base of support is a clear and well-known compensatory strategy to prevent the loss of balance. Indeed typical stumbling and unsteady ataxic gait reflects the poor ability to maintain balance in subjects affected by FRDA, but reflects the impairments of intra-limb coordination as well, as shown by Ilg and coll. Actually, FRDA pathophysiology is a mixed sensory and cerebellar ataxia resulting from spinocerebellar degeneration, peripheral sensory and optic neuropathy, cerebellar and vestibular pathology with a specific involvement of deep cerebellar nuclei (dentate, emboliform, globose and fastigial nucleus). The resulting walking pattern is the product of a complex interaction between cerebellar dysfunction and sensory loss, compromising balance control and multi-joint coordination.