For the physician, and especially the neurologist, watching a patient's gait as they enter the consulting room still offers a wealth of fundamental semiological information. Longer life spans have amplified the socio-economic and medical problems of the “elderly who fall”. After rheumatic-orthopaedic causes, poor nutrition, sarcopenia, and visual deficits have been eliminated, it is time to seek a neurological aetiology.

Controlling gait and balance involves the primary motor cortex; the motor, premotor, and supplementary areas; and the basal ganglia, notably the mesencephalic locomotor region, including the pedunculopontine and cuneiform nuclei. This is the functional region that initiates and modulates autonomic locomotion. In addition to this motor control, the vestibular system and the cerebellum play a role in controlling posture in dynamic equilibrium; as John Russell Napier (1917–1987) put it: “Man's bipedal mode of walking seems potentially catastrophic because only the rhythmic forward movement of first one leg and then the other keeps him from falling flat on his face” [1].

The study of gait and walking goes back to antiquity and Hippocrates (460–356 BC) [2]. Countless authors over the centuries have sought to elucidate the causes of falling. For example, in 1733, Philippe Hecquet (1661–1737) suggested that “when there is a lack in the quantity of animal spirits, their power of movement [that of the muscles] is idle” [3].

It was not until the 19th century that the concept of astasia-abasia was formally and initially recognised as a deficiency of hysterical origin. But how did the pathology of astasia-abasia, considered functional and affecting children, become an organic gerontological pathology?