BMJ 1996;313:1029-1030 (26 October)

Editorials

The Babinski sign: 100 years on

Still rivals current technology in its precision, reliability, convenience, and cost

In this age of information explosion and high technology, the neurological examination is still the gold standard for defining clinically relevant neurological disease. This is the centenary of the Babinski sign, known to every medical student and almost synonymous with the neurological examination.

Before Joseph Babinski's discovery in 1896, knowledge about reflexes was limited. Although reflex activity was recognised as an involuntary response of the nervous system by Descartes as early as 1662, it was not until the 19th century that clinicians began to understand the underlying mechanisms. Motor and sensory roots were described in 1811, followed by the neurone theory in the latter half of the century. Cutaneous and tendon reflexes were defined in rapid succession from 1875. Flexion reflex withdrawal of the lower limb was recognised as indicative of a pyramidal syndrome, but little attention was given to the movement of the toes.

Thus the stage was set for Babinski's eloquent and lucid discovery described in two presentations in 1896 and 1898.1 2 The abstract dated 1896 and the paper dated 1898, which was recently translated and published in English,3 differ in their description of the manoeuvre for eliciting the sign. Babinski changed from recommending a pin prick to stroking the sole. In the paper he emphasised the site, the predominance of the first two toes in dorsiflexion, the transient appearance of the sign in epileptic seizures, and its value in excluding hysterical paralysis. He also stated that it occurs only in pyramidal lesions, which may be severe or transient, and appears in normal infants due to an immature pyramidal system.

The paper was followed by worldwide confirmation, and so popular was the sign that no less than 14 rival or alternative methods of eliciting it appeared in the literature over the next few years. Physicians trained during the era of eponyms will smile in recollection of the Chaddock, Gordon, Oppenheim, and Gonda signs. Bitter controversy raged for a decade, in large part due to the recent descriptions of the "neurone doctrine and the spinal reflex,"4 which defined the reflex arc from sensory fibres to spinal cord neurones to motor fibres.

Controversy erupted again on the occasion of the 60th anniversary of Babinski's discovery, when several authors disputed "the relationship of the sign of Babinski to pyramidal defect."5 6 7 8 Sir Francis Walshe, the renowned British neurologist, was quick to point out the errors in these criticisms.8 9 He subsequently indicated that the literature had been inadequately reviewed by these critics and that there was ample evidence that focal demyelination without tract degeneration was sufficient to produce pyramidal dysfunction.

Today it is well accepted that a positive Babinski sign is indicative of dysfunction of fibres within the pyramidal tract.3 The fibres that control the foot and toes are the most likely to be dysfunctional if the Babinski sign is present, and over 90% of patients will have some degree of motor deficit in the foot.10 These fibres probably terminate at or near the motor neurones because they are responsible for independent and fast movement of the toes and foot.11 That such precise localisation can be achieved so reliably, easily, and inexpensively makes one wonder if the current technology will endure the next 100 years as well as the Babinski sign has.

Although a student of Charcot, Joseph Babinski devoted his clinical and research career to establishing findings that distinguished organic disease from hysterical paralysis. In this context he disagreed with his teacher and claimed the difference between the two was "not a ditch but an abyss." His brother Henri was his lifelong friend, valet, secretary, chef, and companion, and they lived together until their deaths one year apart in 1931 and 1932.3

JOHN F DITUNNO Professor of rehabilitation medicine

RODNEY BELL Professor of neurology

Jefferson Medical College of Thomas Jefferson University, 111 South 11th Street, Philadelphia, PA 19107-5098, USA

John F Ditunno, Rodney Bell 


  1. Babinski J. Sur le reflexe cutane plantaire dans certaines affections du systeme nerveux central. Comptes Rendus des Sciences et Memoires de la Societe de Biologie 1896;207-8.
  2. Babinski J. Du phenomene des orteils et de sa valeur semiologique. Semaine Medicale 1898;18:321-2.
  3. Van Gijn J (1996) The Babinski sign--a centenary. Utrecht: Universiteit Utrecht, 1996.
  4. Landau WM, Clare MH. The planter reflex in man, with special reference to some conditions where the extensor response is unexpectedly absent. Brain 1959;82:321-55. [Free Full Text]
  5. Hoff HE, Breckenridge CG. Observations on the mammalian reflex prototype of the sign of Babinski. Brain 1956:79:155-66.
  6. Lassek AM. The pyramidal tract: its status in medicine. Oxford: Blackwell Scientific, 1954.
  7. Nathan PW, Smith MC. The Babinski response: a review and new observations. J Neurol Neurosurg Psychiatry 1955;18:250-9.
  8. Walshe F. Further critical studies in neurology and other essays and addresses. Edinburgh: Livingstone, 1965.
  9. Walshe FMR. The Babinski planter response, its forms, and its physiological and pathological significance. Brain 1956;79:529-56. [Free Full Text]
  10. Van Gijn J. The Babinski sign and the pyramidal syndrome. J Neurol Neurosurg Psychiatry 1978;41:865-73. [Abstract]
  11. Kuypers HGJM. The anatomical organisation of the descending pathways and their contributions to motor control especially in primates. In: Desmedt JE, ed. New developments in electromyography and clinical neurophysiology. Vol 3. Basel: Karger, 1973:38-68.

This article has been cited by other articles:

  • Rayner, P H W, Hughes, T. (1997). The Babinski sign. BMJ 314: 374-374 [Full text]  

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