It is an indicator of damage or injury along the corticospinal tract.
Of all the neurologists whose name is commemorated in everyday use, Babinski’s may not surpass Romberg in frequency, but rather overshadows all of his dramatic impact and clinical implication.
Wartenberg was said to have evoked his name by rejecting the engagement with an emotional “By the great Babinski, no!” The sign is generally attributed to a lesion of the pyramidal tract
Joseph Felix Francois Babinski was born in Paris to Polish parents in 1857, two years after his brother Henri, with whom he was destined to spend most of his life.
In 1879 he was appointed to a general medical position as “interne des hôpitaux”, during which he published anatomical studies on the muscle spindle and the pathology of multiple sclerosis .
In 1885 he became the “clinic chef” for Jean-Martin Charcot, who became the first professor of neurology in France in 1882 at La Salpetriére, a gunpowder factory in the 17th century that became an asylum and later into a hospital, becoming one of the world’s great centers for the study of neurological diseases.
In 1890, Babinski passed the “Médecin des Hôpitaux” exam and the path seemed clear for a career in academic neurology. The next step would be an associate professorship (agrarian professor), but this was not due to what appears to have been an act of professional jealousy by Charles Bouchard.
Bouchard was trained by Charcot and their names are linked as “Charcot-Bouchard aneurysms” that precede cerebral hemorrhage in hypertensive patients. After Bouchard became a professor of pathology in 1879, his relationship with Charcot deteriorated.
It may have been a coincidence that Bouchard presided over the exam for the agrarian professor when Babinski was a failed candidate, while three of the five who passed were Bouchard’s students.
Babinski never tried the exam again. In 1895 he became head of service at the Hôpital de la Pitié, which is located next to Salpetriére, and he remained in that position until he retired in 1922 at the age of 65.
He wrote on a wide variety of subjects, and his fame attracted neurologists from overseas, including SAK Wilson, CG Chaddock, and Robert Wartenberg.
He provided a boost to neurosurgery, particularly by reporting on the successful removal of intracerebral tumors and the localization of spinal cord tumors on clinical grounds. He encouraged some of his students, including Clovis Vincent, to become neurosurgeons.
Babinski died in 1932.
In 1896, Babinski presented a short article to the Paris Biological Society, translated as “On the cutaneous plantar reflex in certain organic disorders of the nervous system.”
He had observed that the prick of the sole of the foot on the healthy side of a patient with hemiplegia or monoplegia of the lower extremity caused the withdrawal of the lower extremity with flexion of the toes on the metatarsal bones.
In contrast, the same stimulus applied to the sole on the affected side caused extension of the toes at the metatarsophalangeal joints, even in patients who were unable to move them voluntarily.
He later referred to “stroking” of the single stimulus rather than pricking as an appropriate stimulus, a point not to be missed by today’s registrars or residents, many of whom warn their patients that they are about to get rid of their feet. or use some other potentially intimidating term.
Babinski’s definitive description appeared in 1898. An English translation is included in van Gijn’s monograph. He stated that the “toe phenomenon” can be more easily obtained from the lateral aspect of the sole of the foot and that the anatomical extensor reaction is most evident in the first or first two toes.
He demonstrated the extensor response in hemiplegic and paraparhetic patients and stated that he had observed it in Friedreich’s ataxia.
He attributed the sign to dysfunction of the pyramidal tract and noted that it was generally associated with exaggeration of tendon reflexes and clonic movements, but that “this relationship is far from indissoluble.”
He concluded by calling attention to the presence of the sign in the Newborn, an association that had not escaped the attention of a Renaissance artist.
The reversal of the plantar flexor response occurs at variable times from the age of seven months to one year or more, who concluded that the relationship of this change with the start of walking was probably indirect.
Confusion can arise in infants because the grasping reflex, which is most easily produced by stimulating the ball of the foot, involves flexing the toes. It usually disappears between six and 12 months of age and appears to be related to the age of standing.
Babinski had noted that the sign appeared transiently on the affected side in a man during a Jacksonian attack and bilaterally in another patient suffering from strychnine poisoning.
I had the opportunity to observe such a brief disturbance in a child of mine subject to night terrors. As I tried to comfort her, I ran my thumb lightly against the side aspect of her sole like one does and saw a definite response from Babinski.
As soon as the paroxysm ended, the response became flexor.
In 1903, Babinski commented during a case presentation that abduction of the toes could accompany the extension of the fingers in a pyramidal injury, but was by no means constant. This was later known as “le signe de l’éventail”.
The normal plantar response to cutaneous stimuli from the sole of the foot can be viewed as a superficial reflex, such as abdominal and cremasteric reflexes that are abolished by upper motor neuron injury. It is then replaced by Babinski’s answer.
The upturned toe is anatomically considered an extension of the big toe, but physiologically it is part of a flexor reflex, apparently uninhibited by the loss of control of the upper motor neuron, and its receptive field can extend in some cases to the leg or thigh.
This led to the description of many “reflections,” such as the Chaddock and Oppenheim signs, which were simply different ways of obtaining the Babinski sign.
Although the sign generally accompanies spasticity, and has been described as caused by an infarction apparently limited to a medullary pyramid in three cases cited by van Gijn, its cause has been questioned due to lesions of the pyramidal tract.
Nathan and Smith studied the patients before and after spinal cord operations (anterolateral cordotomy), correlating the clinical findings with the extent of the surgical injury.
They found that destruction of the anterior half of the spinal cord may be associated with a Babinski response, whereas the sign could be absent with histologically verified lesions of the lateral (pyramidal) corticospinal tract.
Later, Nathan and Smith reported 44 patients undergoing chordotomy for cancer pain relief. Overall, the Babinski response was found to be present after corticospinal tract injuries and not with other umbilical cord injuries.
However, a transient Babinski response could be observed after previous lesions, and some patients with tract lesions retained normal plantar responses.
There is an important difference compared to the spinal debraded cat that sheds some light on the matter.
In the decerebrate cat, the stretch reflex of the quadriceps muscle becomes more active as the degree of stretch (i.e., the length of the muscle) increases.
In contrast, in those chronic preparations of animals with increased muscle tone, the quadriceps reflex response progressively decreases as the degree of stretch increases, analogous to the clasp and knife response in human spasticity.
Since the reverse applies to the flexor muscles (i.e., increasing muscle stretch improves reflex response) it appears that stretch-sensitive receptors, such as group II afferent fibers, inhibit the stretch reflex of the hindlimb extensors. .
This in turn facilitates the flexors as long as the stretch is maintained.
These flexor reflex (ARF) afferents are normally suppressed by the dorsal reticulospinal system that arises from the pontomedullary reticular formation and descends into the dorsolateral funiculus of the spinal cord.
Burke et al made discrete lesions in the reticular formation and upper quadrant sections in the spinal cord of the decerebrate cat, which transformed the length-dependent facilitation of stiffness of the decerebrate into a length-dependent inhibition of spinal spasticity.
These experimentally observed changes can easily be applied to the human situation.
Using the H reflex as an indicator of motor neuron excitability in spastic patients, it was shown that stretching of the calf muscles decreased the amplitude of the H reflex recorded in the calf, while stretching of the pretibial flexor muscles increased. the H reflex of those muscles.
That is, the afferents of the flexor reflex have been released in spastic patients, as in the chronic spinal cat.
This explains the clasp-knife phenomenon in human spasticity, in which the tonic stretch reflex in the quadriceps is inhibited by increasing muscle length beyond the midpoint of knee flexion.
It also explains the improvement in the protective response of the flexor, including the Babinski sign.
In cats, the reticulospinal inhibitory pathway is directed from the motor cortex by parapyramidal fibers that descend medially from the internal capsule and the medial area of the midbrain dorsal to the cerebral peduncle.
If it can be extrapolated to humans from these studies in the cat, any alteration in the function of this cortico-reticulospinal tract, which is closely applied to the pyramidal tract along its course from the cortex to the segmental levels of the spine, it will release the flexor reflexes, including the Babinski.
Therefore, it appears that the Babinski sign is an indication of the withdrawal of supraspinal control of the flexor reflexes in the lower extremities.
Clinically it can be equated with the inactivation, transient or permanent, of the upper motor neuron, a term that implies corticoreticulospinal fibers as well as the pyramidal tract anywhere on its way from the cerebral cortex to the termination of the cord.
Flexion reflexes are prominent in newborns and young babies. In order for the baby to stand up, the flexor reflexes in the lower extremities must be controlled by the dorsal reticulospinal tract.
For the baby to walk, the synergy of the flexor must be used in the motor cortex as part of the walking pattern. With the maturation of the upper motor neuron pathways, the Babinski sign disappears and the big toe descends as the sole is stimulated.
If upper motor neuron control is temporarily suspended, as in an epileptic seizure, or eliminated by disease, Babinski’s sign reappears.