The calcium channel blocker, Nimodipine, inhibits spinal reflex pathways in humans

Voltage-sensitive calcium channels contribute to depolarization of both motor- and interneurons in animal studies, but less is known of their contribution to human motor control and whether blocking them has potential in future antispasmodic treatment in humans. Therefore, this study investigated the acute effect of Nimodipine on the transmission of human spinal reflex pathways involved in spasticity. In a double-blinded, cross-over study, we measured soleus muscle stretch- and H-reflexes, and tibialis anterior cutaneous reflexes in nineteen healthy subjects before and after Nimodipine (tab-let 60mg) or Baclofen (tablet 25mg). Baclofen was used as a control to compare Nimodipine's effects with known antispastic treatment. Changes in the size of the H_max/M_max-ratio, stretch- and cutaneous reflexes following intervention of Nimodipine and Baclofen, respectively, were analysed using a one-way RM-ANOVA. Nimodipine significantly reduced the H_max/M_max-ratio (F(2.5,42)=15; p<0.0001) and the normal-ised soleus stretch reflex (F(2.6,47)=4.8; p=0.0073) after administration. A similar tendency was seen following Baclofen (H_max/M_max-ratio: F(2.1,39)=4.0; p=0.024; normalised stretch reflex: F(2.8, 50)=2.4; p=0.083). The M_max-response was unaffected by either intervention. Interestingly, during voluntary soleus activation, the stretch reflex remained unchanged with either treatment. For the cutaneous reflexes, there was a trend toward reduced early inhibition (F(1.6,9.3)=4.5; p=0.050) and subsequent facilitation (F(1.3,8.0)=4.3; p=0.065) after Nimodipine. No severe adverse effects were reported after Nimodipine. These findings suggest that Nimodipine acutely reduced electrophysiological measures related to spasticity in healthy individuals. The effect seemed located at the spinal level, and voluntary contraction counterbalanced the reduction of the stretch reflex, highlighting its relevance for future studies on antispastic therapies.