The Babinski sign

Babinski's life and the story of the Babinski sign are summarised. The physiological basis of the sign is discussed.     

Babinski sign

Despite all of the medical advances, Babinski sign has proved reliable in precise localization of central nervous system dysfunction. It is well accepted that Babinski sign is indicative of dysfunction of fibers within the pyramidal tract. Joseph Fran?ois Félix Babinski first described the clinical significance of the reflex in 1896. He showed that the extensor plantar response was indicative of pyramidal dysfunction and that it was absent in hysteria. He also illustrated that it was present in infancy and transiently appeared in epilepsy and strychnine poisoning. Babinski also pointed to the existence of "formes frustes" of his reflex and recognized its occasional absence in patients with other clinical signs of pyramidal lesions. The sign emerges when the dysfunction of the pyramidal tract involves the fibers that project on motoneurons of foot muscles and is mediated by extensor hallucis longus. Babinski sign may not be present acutely after transverse lesions of the spinal cord or acute brain lesions because of temporary inexcitability of spinal motoneurons.     

The Babinski sign and the pyramidal syndrome.

The presence or absence of a Babinski sign can be puzzling, but in the light of existing pathological studies it is more fruitful to consider which pyramidal tract fibres release it than whether they release it. This was investigated clinically, by looking for correlations with other reflex changes and with motor deficits in the leg. A survey of 50 patients with a unilateral Babinski sign and six patients who lacked it in spite of other pyramidal tract signs was supplemented with follow-up of the patients who had acute lesions. Appearance of the Bibinski sign proved to depend on the interaction of two factors: (1) activity (not necessarily hyperactivity) in the segmental pathways of the flexion synergy; (2) a motor deficit of the foot, in some cases consisting only in an impairment of rapid foot movements, and probably representing a disturbance of direct pyramidal tract projections to distal motoneurones.