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esult in disappearance of the Babinski sign, while it did abolish plantar flexion of the toes<br />
in normal subjects. Marinesco and Noica (191)) repeated Babinski"s experiment in a<br />
healthy volunteer, and found selective loss of distal power and of the ankle jerk. The<br />
hyperexcitability of the flexion reflex after ischaemia - providing the efferents are not<br />
blocked- was later attributed to a specific effect on afferent nerve fibres from the skin, with<br />
a reverse change in tendon reflexes and tone (Gilliatt, 1952).<br />
It is more difficult to explain why the reflex in the flexor muscles of the toes -provided<br />
this is still remnant in patients - recovers earlier from ischaemia than the response in irs<br />
more proximal antagonists. Marie and Foix (1912), who confirmed this finding, assumed<br />
that the muscles of the sole had a better vascular supply. Landau and Clare (1959)<br />
implicated mechanical compression of the lateral popliteal nerve against the head of the<br />
fibula, buc Babinski probably applied the bandage more proximally. Whatever its explanation,<br />
the difference in sensitivity to ischaemia between the normal and pathological plantar<br />
response does not detract from the identity of the Babinski sign with the flexion reflex. The<br />
dissociation only indicates that the normal response may still emerge under some circumstances.<br />
c) Upgoing toe without flexion reflex of the leg<br />
Whereas the two preceding categories were advanced by Babinski as instances of an<br />
exaggerated flexion reflex without dorsiflexion of the hallux, he also observed the reverse,<br />
if only by applying light stimuli. In this respect, Babinski was supported by Marie & Foix<br />
(1912, 1913), and not by them alone. Bing (1915) found that proximal reflex phenomena<br />
accompanied the upgoing toe sign in most patients with spinal lesions, but only exceptionally<br />
in cerebral disease. The occurrence of an isolated Babinski response was subsequently<br />
mentioned by Fulton and Keller (1932), Szapiro (1958) and also by Scholten (1964, 1965),<br />
who came to the surprising conclusion that only this constitutes the real Babinski sign,<br />
quite separate from the sign described by Babinski. Guillain and Dubois (1914) published<br />
the case history of a young woman with infantile hemiplegia in whom an upgoing toe<br />
phenomenon could be evoked from as far rosrrally as the ipsilateral face, while "the defence<br />
reflexes were nil'. In this last patient, the flexion reflex was probably masked by the<br />
concomitant spasticity of the extensor muscles in the leg - the extensor hallucis longus is<br />
the only physiological flexor muscle able to overpower its antagonists (Walshe, 1923 ).<br />
This explanation, however, probably does not account for all reported instances of an<br />
isolated Babinski sign. Walshe (1914) comends that in such cases a barely palpable<br />
contraction of the hamstring muscles or a just visible twitch of the musculus tensor fasciae<br />
latae has been overlooked. Although this follows from one of the most detailed studies on<br />
the subject, at this stage it must remain an open question whether this explanation is<br />
universally applicable (it will be referred to again in Chapter IV). That the recruitment<br />
order of muscles taking part in the flexion reflex could vary from one patient ro another<br />
was stressed by Bersot (1917- 1919), and by DimitrijeviC and Nathan (1968).<br />
Some authors, apparently quite unaware of the physiological discussions<br />
about the toe muscles, continued to connect the upgoing toe phenomenon<br />
to extensor synergies of the lower limb (Meyers, 1920; Armenise, 1924;<br />
Tournay, 1926; Salomon, 1921), or the normal plantar response to the<br />
flexion reflex (Goldflam, 1908; Waggoner and Ferguson, 1930; Yakovlev<br />
and Farrell, 1941; Morgenthaler, 1948).<br />
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