THE PLANTAR REFLEX - RePub

ecruited and even interrupted by EHL activity, and there was no coactivation
of the TA. These features suggest that persistently insufficient
relaxation was the cause of the EHL activity, rather than a pathological
reflex mechanism.
Activity of the FHB was found in all control subjects with a downward
toe response on inspection, although the density of the electromyographic
pattern was not always proportional to the briskness of the clinical
response. These relative differences may be due to shortcomings of the
recording technique or to individual anatomical variations. Nine subjects in
the control group were judged to have absent plantar reflexes on clinical
grounds; three of these showed only minimal FHB activity, six none at alL
This means, at least for the subjects in this study, that clinically absent
plantar reflexes are genuinely absent and do not represent an undecided
tug of war between EHL and FHB.
Electrical stimulation: effects in EHL and FHB
Brief electrical stimuli to the plantar surface were applied in the same 15
patients and 40 controls, and the reflex effects are shown in Table IX
together with those after mechanical stimulation. A reflex was considered
to be present when potentials appeared repeatedly within 150 ms of
stimulation, showing an interference pattern that lasted for 50 ms at least.
These criteria are more or less arbitrary; the consequences of defining
them otherwise will be discussed below.
In five of the 15 patients with a Babinski sign, electrical stimuli failed to
activate the EHL. In one of them this failure was confirmed in three
subsequent experiments. He was a 56-year-old man with spastic paresis of
the right leg following haemorrhage from an arteriovenous malformation
in the left parietal parasagittal region. In another patient, a 50-year-old
man with a paraparesis probably due to multiple sclerosis, there were very
brisk flexor reflexes of both legs, which could be elicited even by stroking
the plantar surface with a finger pad. But electrical shocks were insufficient
to evoke a response even at maximal intensity (Figure 6, B). Of the three
remaining 'false-negative' patients, one had sustained a severe cerebral
concussion, both the others were suffering from paraparesis of unknown
ong1n.
In the control group, electrical stimuli evoked EHL reflexes in about one
out of every three subjects. One example (a healthy neurologist!) is shown
in figure 6,A. It could be possible that in these control subjects the stimulus
strength exceeded the intensities required for activating the EHL in
patients, and this was investigated further. The stimulus strength (mean
values when inconstant) was expressed in multiples of the tactile threshold
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