3845

J Physiol 594.13 (2016) p 3845

The Journal of Physiology

Neuroscience

LETTER

Limitations of the F-wave test in

monitoring spinal motoneurone
excitability
The interesting and intriguing paper
by Khan et al. (2016) investigated
the changes of excitability in spinal
motoneurones following both sustained
voluntary contractions (with different
intensities) and repetitive peripheral nerve
electrical stimulations (with different
frequency). The Authors made use of
the F wave, that is the electromyographic
counterpart of the recurrent discharge
(Eccles, 1955), to assess these excitability
changes.
They did not take into account, however,
some limitations of the F-wave test
in monitoring the spinal motoneurones
excitability, which have been reported, even
recently, in the literature (Gogan et al. 1984;
Hultborn & Nielsen, 1995; Espiritu et al.
2003; Burke, 2014; Balbi et al. 2014).
Prompted by the unexpected results Khan
and colleagues found, and in the light of
such F-wave limitations, I will try to provide
some further and alternative interpretations
of their interesting and original data.
Firstly, when an antidromic wave is set
in all the motor fibres of a peripheral
nerve by means of a distal supramaximal
stimulus, it is conducted without interruption to the initial segment of each
motor axon. Depending on what happens
at the junction between axonal initial
segments and motoneurone somata, three
distinct sets of neurones can be theoretically
distinguished, in which (1) the antidromic
action potential (AP) fails to invade the
soma, (2) the antidromic AP invades
the soma after a junctional delay able to
start a recurrent discharge, and (3) the
antidromic AP invades the soma but no
recurrent discharge develops (too short
a junctional delay). Among these three
distinct sets, the second one is responsible
for the F wave and accounts for about
25% of the entire motoneurone pool
(Kimura, 2001). The relative proportions
of these three sets of neurones, which are
undetectable, depend on the biophysical
features of single neurones and on the net
sum of the excitatory and inhibitory inputs.
In these conditions it is not always true

that a reduced excitability throughout the

motoneurone pool results in a smaller size
of the second set (i.e. reduced amplitude
or area, or persistence of the F wave), as
initially expected by Khan and colleagues.
A reduced generalized (i.e. assumed
equally distributed through the motoneurone pool) excitability, indeed, will shift
some neurones from set 2 to set 1: in
some neurones which formerly exhibited
the recurrent discharge, the backfiring is
now absent because the antidromic invasion
of the soma does not any more occur.
The same reduced excitability will shift
some other neurones from set 3 to set 2:
a prolongation of the junctional delay in
neurones of set 3 happens, to the point that
in some of them a recurrent discharge can
develop. Paradoxically, if the second transition (from set 3 to set 2) is wider than
(or equal to) the first one, an increase (or
no modifications) of the F-wave parameters
will be detected in the presence of a reduced
generalized excitability.
That is just what happens, in my opinion,
with experiment 2 in the paper by Khan
and colleagues, when a diffuse hyperpolarization is induced by the repetitive
peripheral stimulation of the ulnar nerve,
but no F-wave depression develops. In
fact, this finding can represent a direct
experimental proof of the limited role of
the F wave in unidirectionally detecting
excitability changes of the motoneurone
pool.
Secondly, the fraction of the motoneurone
pool which is responsible of the F wave
(representing only a minor portion of
the entire motoneurone pool) and the
one activated by the voluntary contraction
are presumably two different and only
partially overlapping sets of neurones.
Therefore, it appears unlikely that the
behaviour of a small (and in the interpretation above described, variable) set of
spinal motoneurones can provide faithful
information on the direction and amount
of the excitability changes of the entire
motoneurone pool.
The limitations of the F-wave test here
described show how a reliable method
to directly detect the motoneurones
excitability is still lacking, even though the
present and past brilliant work by Khan and


C 2016 The Authors. The Journal of Physiology 
C 2016 The Physiological Society

colleagues undoubtedly sheds light on the

complex central mechanisms of voluntary
motor control and on the correct interpretation of classical neurophysiological
tests.
Pietro Balbi
Department of Neurorehabilitation
Salvatore Maugeri Foundation, Scientific
Institute of Pavia, IRCCS, via Boezio 28,
Pavia, Italy
Email: pbalbi@fsm.it
References
Balbi P, Martinoia S, Colombo R & Massobrio P
(2014). Modelling recurrent discharge
in the spinal -motoneuron: Reappraisal
of the F wave. Clin Neurophysiol 125,
427429.
Burke D (2014). Inability of F waves to control
for changes in the excitability of the
motoneuron pool in motor control studies.
Clin Neurophysiol 125, 221222.
Eccles JC (1955). The central action of
antidromic impulses in motor nerve fibres.
Pflugers Arch 260, 385415.
Espiritu MG, Lin CS-Y & Burke D (2003).
Motoneuron excitability and the F wave.
Muscle Nerve 27, 720727.
Gogan P, Gustafsson B, Jankowska E &
Tyc-Dumont S (1984). On re-excitation of
feline motoneurones: its mechanism and
consequences. J Physiol 350, 8191.
Hultborn H & Nielsen JB (1995). H-reflexes and
F-responses are not equally sensitive to
changes in motoneuronal excitability. Muscle
Nerve 18, 14711474.
Khan SI, Taylor JL & Gandevia SC (2016).
Unexpected factors affecting the excitability of
human motoneurones in voluntary and
stimulated contractions. J Physiol 594,
27072717.
Kimura J (2001). The F wave and the A wave. In
Electrodiagnosis in Diseases of Nerve and
Muscle: Principles and Practice, 3rd edn, ed.
Kimura J, pp. 439465. Oxford University
Press, New York.

Additional information
Competing interests

None declared.

DOI: 10.1113/JP272442