THE PLANTAR REFLEX - RePub

1. Contraction of the tibialis anterior, voluntarily (patient 1) or as part of
the flexion reflex (patient 17): the toes go upward passively, without
contraction of the extensor hallucis longus. This is a classical pitfall
(Oppenheim, 1899; Kalischer, 1899).
2. A very active flexion reflex, combined with brisk plantar flexion of the
toes: once these bewildering movements have ceased, the big toe goes 'up'
(back) to the original position (patient 3 ).
3. Voluntary toe wriggling (patients 2, 16, 18). The jerky extensor
movements are inconstant and out of phase with the flexion reflex.
Involuntary movements caused by disease of the basal ganglia may also
confuse the examiner (C. and 0. Vogt, 1920; Dosuzkov, 1932).
4. The great toe is immobile, while the other toes go gently down; this may
create an optical illusion (patient 4).
5. Isolated fanning of toes (patient 15 ). This 'signe de I' even tail' also occurs
in normal subjects (Babinski, 1903 a; Noica and Sakelaru, 1906; Barre and
Morin, 1921) and can lead to errors of both observation and interpretation.
The reverence paid to this phenomenon is unnecessary from a historical as
well as from a practical viewpoint.
6. Anatomical variations which prevent toe flexion, although the flexor
hallucis brevis is active. In patient 8, both second (hammer) toes had been
amputated long before, probably with subsequent shift of the first
metatarsal bone and its tendons, as in hallux valgus (!ida and Basmajian,
1974). In patient 14, there seemed to be another abnormality of insertion
of the flexor hallucis brevis, as only isometric contractions could be
provoked by stimulating through the recording electrode; voluntary toe
flexion was possible, probably mediated by the flexor hallucis longus.
7. Peripheral lesions. It is an old notion that a false upgoing toe response
can occur by damage to the neuromuscular apparatus which mediates the
normal plantar reflex (Babinski, 1898; the gist of the relevant passage is
unfortunately inverted in the translation of Wilkins and Brody, 1967).
Most subsequent reports cite, like Babinski himself, cases of poliomyelitis
(Pfeifer, 1904; Salomon, 1921; Sicard and Seligman, 1925; Laignel-Lavastine,
1925; El Sherbini, 1971), although others have stressed that pyramidal
features can occur in poliomyelitis (Fuchs, 1905; Tournay, 1924; Souques
and Ducroquet, 1924; Sebeck and Wiener, 1926). Less often the phenomenon
has been encountered in lesions of nerve roots or plexus with
predominant affection of toe flexors (Sicard and Haguenau, 1919; Rouquier
and Couretas, 1926), in polyneuropathy (Lortat-Jacob, 1902), and even
in myopathy (Leri et al., 1923 ).
Despite the abundant literature on this 'peripheral pseudo-Babinski
sign', its occurrence is much less logical than it seems at first sight. The
Babinski sign is produced by pathological recruitment of extensor hallucis
longus motoneurones, and it is difficult to see how this is any more likely
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