THE PLANTAR REFLEX - RePub

jerks, which is a pyramidal feature (Chokroverty et al., 1975; Leestma and
Noronha, 1976). However, exaggeration of the flexion reflex and of
tendon jerks appeared to occur quite independently. A striking dissociation
between exteroceptive and proprioceptive hyperreflexia has also been
noted in, for instance, the Holmes-Adie syndrome (Swash and Earl, 1975).
This does not exclude the possibility that release of the flexion reflex is a
pyramidal sign, but one would still have to invoke different projections. An
argument for at least partial control of the flexion reflex by brain stem
centres is that flexor spasms are much more common after spinal lesions
than in cerebral disease. The presence of separate descending fibres to
control the segmental relay of myelinated and unmyelinated afferent fibres
(Kugelberg, 1948) has not been substantiated.
The reverse side of the question is which of the descending fibre systems
provide the normal facilitation of flexion reflex pathways that is disturbed
in spinal shock and in the acute phase of extensive cerebral lesions (case
13 ). Some evidence is furnished by the patients in this study who suffered
from acute spinal transection (table XXI). One patient (S4), with an
incomplete spinal cord lesion at C 7
, showed total inactivity of the flexion
reflex (including the hallux, which was down going), although he was able
to dorsiflex the great toe voluntarily. Hence we cannot easily ascribe
depression of reflex activity in this patient to an interruption of the
pyramidal tract. Another patient (S6), with progressive tentorial herniation,
showed bilateral Babinski signs until respiratory arrest occurred (the blood
pressure remained normal for a period). This suggests a 'permissive action'
for the Babinski sign from the lower brain stem.
BABINSKI SIGN: INTERACTION BETWEEN FLEXION REFLEX
AND DISTAL PYRAMIDAL CONTROL
Release at or near the motoneurone
We have seen that activation of flexion reflex pathways is necessary for
the appearance of the Babinski response, but that the Babinski response
can be released separately from the flexion reflex as a whole. We have also
seen that occurrence of the Babinski sign is almost invariably associated
with motor impairment of the foot, and that in some cases this motor
impairment is manifested only by the slowing down, dysrhythmia or
reduced fractionation of movements. The capacity for independent and fast
movements is probably mediated by direct cortical projections to individual
motoneurones (Kuypers, 1973 ). Because loss of this ability alone is
apparently sufficient to release the Babinski sign, the pyramidal 'shielding'
of extensor hallucis longus motoneurones from activity in the flexion
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