The calcium channel blocker nimodipine inhibits spinal reflex pathways in humans

Voltage-sensitive calcium channels contribute to depolarization of both motor neurons and interneurons in animal studies, butless is known of their contribution to human motor control and whether blocking them has potential in future antispasmodictreatment in humans. Therefore, this study investigated the acute effect of nimodipine on the transmission of human spinal reflexpathways involved in spasticity. In a double-blinded, crossover study, we measured soleus muscle stretch reflexes and Hreflexes and tibialis anterior cutaneous reflexes in 19 healthy subjects before and after nimodipine (tablet 60 mg) or baclofen(tablet 25 mg). Baclofen was used as a control to compare nimodipine’s effects with known antispastic treatment. Changes inthe size of the maximum H reflex (Hmax)/maximum direct motor response in muscle (M max) ratio and stretch and cutaneousreflexes following intervention with nimodipine and baclofen, respectively, were analyzed with a one-way repeated-measures(RM) ANOVA. Nimodipine significantly reduced the Hmax /Mmax ratio [F(2.5,42) ¼ 15; P < 0.0001] and the normalized soleusstretch reflex [F(2.6,47) ¼ 4.8; P ¼ 0.0073] after administration. A similar tendency was seen after baclofen [H max/Mmax ratio:F(2.1,39) ¼ 4.0, P ¼ 0.024; normalized stretch reflex: F(2.8,50) ¼ 2.4; P ¼ 0.083]. The M max response was unaffected by eitherintervention. Interestingly, during voluntary soleus activation, the stretch reflex remained unchanged with either treatment. Forthe cutaneous reflexes, there was a trend toward reduced early inhibition [F(1.6,9.3) ¼ 4.5; P ¼ 0.050] and subsequent facilita-tion [F(1.3,8.0) ¼ 4.3; P ¼ 0.065] after nimodipine. No severe adverse effects were reported after nimodipine. These findingssuggest that nimodipine acutely reduced electrophysiological measures related to spasticity in healthy individuals. The effectseemed located at the spinal level, and voluntary contraction counterbalanced the reduction of the stretch reflex, highlighting itsrelevance for future studies on antispastic therapies.
NEW & NOTEWORTHY
The calcium channel antagonist nimodipine significantly reduces the size of the soleus H reflex andstretch reflex in healthy individuals without affecting maximum direct motor response (M max) or the stretch reflex during voluntaryactivation. This underscores the importance of exploring nimodipine as a potential antispastic medication in the future.