Brain, Vol 120, Issue 6 991-1003, Copyright © 1997 by Oxford University Press
R Mazzocchio and A Rossi
Changes in the excitability of the soleus H-reflex are were studied after
oral administration of L-acetylcarnitine, a cholinomimetic substance, in
eight healthy control subjects and 23 spastic patients presenting with
slowly progressive paraparesis (n = 10), a cord lesion (n = 9) and a
cerebral lesion (n = 4). Changes in the amount of recurrent inhibition of
soleus motor neurons at rest were also estimated in order to assess the
level of activity of Renshaw cells before and after L-acetylcarnitine
administration. Recurrent inhibition elicited by a conditioning reflex
discharge (H1) was assessed by a subsequent test reflex (H'). Four patients
lacked an H' reflex. In approximately 50% of the remaining patients,
recurrent inhibition was normal, while in the other half there was evidence
of reduced or absent inhibitory activity at rest. Pooling the data relative
to the effect of L-acetylcarnitine on the H-reflex in relation to the
strength of recurrent inhibition disclosed that the ratio of peak-to-peak
amplitude values of the maximum H reflex to maximum M wave responses
(Hmax:Mmax) was reduced in all the cases in which the recurrent inhibition
at rest was normal, while such a reduction was never observed in the
patients in whom recurrent inhibition was found to be decreased at rest. In
the former cases, the size of the H' reflex evoked by the same conditioning
H1 discharge was further depressed after L-acetylcarnitine, pointing to a
potentiating effect of the drug on Renshaw cells; in the latter cases no
such effect was seen. A significant decrease in the mean Hmax:Mmax ratio
after L-acetylcarnitine intake was also seen in the healthy control
subjects. Possible changes in the amount of presynaptic inhibition on Ia
terminals on soleus motor neurons after L- acetylcarnitine were ruled out.
It is proposed that the differential effect of the drug on the H-reflex
excitability is directly related to the level of Renshaw cell activity, a
reduction of which probably follows a lesion interrupting reticulo-spinal
pathways with tonic facilitatory influences on Renshaw cells. These
findings support the hypothesis that Renshaw cell excitability is set via
cortico-reticulo- spinal systems.
ARTICLES
Involvement of spinal recurrent inhibition in spasticity. Further insight into the regulation of Renshaw cell activity
Unita di Malattie del Sistema Motorio e Scienze del Movimento, Universita di Siena, Italy.
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