THE PLANTAR REFLEX - RePub

Electromyographic recording from muscles that are active in the plantar
reflex could be of help in equivocal cases. Unfortunately, there is no
consensus on which muscle mediates the Babinski sign: the extensor
hallucis longus (Landau and Clare, 1959, in keeping with older notions), or
the extensor hallucis brevis (Kugelberg et a!., 1960; Grimby, 1963 a). In
the latter studies electrical stimuli were used, and the boundary between
the presence and absence of the Babinski sign was electromyographically
indistinct. Reviewers avow that the plantar response is 'not a simple
reflex' (Basmajian, 1974) and ·a manifold phenomenon' (Broda!, 1969).
Could not this complexity be caused by the use of electrical stimuli? This
question has been re-examined by recording from the roe muscles during
stroking of the sole, i.e. while the great roe is actually going up or down.
This done, we can go on to see whether electrical stimuli give the same
result. If not, studies in which electrical stimuli are used should be
interpreted with caution (Chapter Ill).
Once the electromyographic patterns accompanying normal and pathological
plantar responses are known, this technique can be applied to
equivocal plantar reflexes. Are the electromyographic results consistent?
This has been investigated by repetition and 'blind' interpretation, and the
outcome in each patient has also been checked with the eventual neurological
diagnosis. Then, clinical and electromyographic observations have been
compared, and I have tried tO deduce from the differences and similarities a
set of rules (and pitfalls) for the bedside interpretation of plantar reflexes
(Chapter IV).
The last main question in this study concerns the pathophysiology of the
Babinski sign. On which descending fibres does it depend, which segmental
pathways mediate it, and at what level in the lumbosacral cord do the
descending and segmental fibre systems interact? After an appraisal of
pathological studies, the termination of the descending fibres that are
involved in the appearance of the Babinski sign has been investigated
from a clinical angle: which other physical signs are most often associated
with the Babinski response? More precisely, is the appearance of the
Babinski sign linked tO motOr deficits, or rather tO segmental release
phenomena? If such correlations give insight into physiological and
anatomical relationships, can we conversely explain an unexpectedly
absent Babinski sign by the concurrent absence of some other pathological
features? Or can a dysfunction of intraspinal pathways also play a part?
Finally I have tried to consider whether the association patterns of various
pyramidal signs justify the concept of the 'upper motor neurone'
(Chapter V).
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