THE PLANTAR REFLEX - RePub

noticed no special features, and of Holmes (1915): ' ... a simple flexion of
the great toe ... differs from the normal flexor response in that it is slower
and smaller in range .. .'. Subsequent early reports came from Collier
(1916) and from Guillain and Barre (1917). These French authors also
stressed the slowness of the response, but differed from Holmes' observations
in remarking that the downward toe movement was often ample, and
had a long latency and duration. Finally, Riddoch (1917) showed in a
comprehensive study how this initial plantar flexion was gradually
replaced by a Babinski sign in the course of a few weeks, as the flexion
reflex of the leg emerged from spinal shock. This transition had also been
noted by Holmes (1915 ), but he inferred - perhaps still influenced by
Bastian's law - that the transverse lesion was probably not complete in
patients with toe reflexes.
Quite to the contrary, in the course of time an initial downward response
of the toes has come to indicate a poor prognosis for recovery (Editorial,
1960), although it has been reported in a functionally incomplete lesion
(Minkowski, 1923 ). With the wide-spread introduction of assisted ventilation,
the reflex has also been reported in brain death (Ivan, 1973 ). As far as
spinal functions are concerned, primary brain death is comparable to a
transection at C 1
. In another series of such patients, toe responses were
not found (Jmgensen, 1973).
Why does the downward toe response 'escape' from spinal shock?
Holmes (1915) argued that it was a unisegmental reflex, as opposed to the
complex intersegmental mechanism of the flexion reflex. Moreover, it was
pointed out by Riddoch (1917) and Guttmann (1952, 1976) that sacral
segments of the cord suffered less depression than rostral segments: reflex
activity of the external sphincters disappeared only for a short time or not
at all, and ankle jerks were also found in the earliest phase after injury.
This gradient in spinal shock had been noted earlier in animals (Sherrington,
1906).
The mechanism of reflex depression has remained elusive, although it
became clear long ago that Goltz's hypothesis (1876) of inhibition by
irritation from the lesion was untenable (Sherrington, 1906). Most
information stems from animal experiments. The Sherringtonian concept
of a diminished central excitatory state (Liddell, 1934; Ruch 1942) has
been confirmed by demonstration of hyperpolarisation of motoneurones
(Barnes et al., 1962). This is compatible with loss of excitation as well as
with release of postsynaptic inhibition (van Harreveld, 1940). The morphological
findings of Illis (1967) -temporary disorganisation of the synaptic
zone - favour a negative causation. In man, conclusions have ranged from
depressed fusimotor activity (Weaver et al., 1963) or depressed fusimotor
activity plus initial decrease of motoneurone excitability (Diamantopoulos
and Olsen, 1967) to increased presynaptic inhibition (Ashby et al., 1974).
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