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ilateral operations). Adding this to the less startling fact that normal<br />
plantar responses were found in other patients who eventually showed<br />
severe descending degeneration of the lateral tracts (I shall discuss this<br />
problem separately), the authors arrived at the iconoclastic conclusion:<br />
'any lesion of the lateral and ventral columns of the cord may, or may not,<br />
cause the Babinski response'.<br />
However, the question of Babinski signs in the absence of obvious<br />
corticospinal degeneration is only a pseudo-problem, as Walshe (1956)<br />
was quick to point out. The fallacy is to assume that a non-degenerated<br />
pyramidal tract is the same thing as a normal pyramidal tract, particularly<br />
for patients in whom a cordotomy lesion borders upon pyramidal fibres:<br />
focal demyelination can produce severe loss of function without Wallerian<br />
degeneration. The experimental demonstration of conduction block by<br />
focal demyelination in the central nervous system is only a recent<br />
milestone in neurology (McDonald and Sears, 1970).<br />
From the clinico-pathological side, however, it had been noted long<br />
before that demyelinating lesions with preservation of axis cylinders could<br />
produce neurological deficits, and Babinski was also a pioneer in this<br />
particular field (Babinski, 1885), together with Holmes (1906). It is<br />
therefore hardly surprising that he described patients with the toe<br />
phenomenon in whom the pyramidal tracts were not degenerated<br />
(Babinski, 1898, 1899 a, 1911 a). Nathan and Smith (1955) comment that<br />
Babinski, by these lines, disproved his own supposition about the relation<br />
between pyramidal tract and upgoing toe sign; this interpretation is<br />
inappropriate, as Babinski was very much alive to the relative importance<br />
of absent secondary degeneration - some of his cases were paraplegic!<br />
Walshe (1956) also gives Babinski too little credit in this respect, although<br />
the latter was not always fully consistent in that he sometimes explained<br />
an absent toe phenomenon by referring to undegenerated lateral tracts<br />
(Babinski, 1906 b, 1911 a).<br />
In summary, the evidence that Babinski signs can result from lesions<br />
outside the pyramidal tract rests on incorrect premises. But of course this is<br />
a negative conclusion which does not prove the reverse.<br />
'Pure' pyramidal lesions<br />
Anatomical evidence from lesions caused by disease is often ambiguous,<br />
not only because absence of secondary degeneration does not necessarily<br />
imply functional integrity, but also because most lesions interfere with<br />
more than one fibre system. For this reason a number of studies were<br />
wholly or partially devoted to the plantar reflex after experimental lesions<br />
in monkeys and apes.<br />
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