Neuromuscular electrical stimulation reduces spinal excitability in Multiple Sclerosis patients with spasticity symptoms

Background: The use of neuromuscular electrical stimulation (NMES) has been recently proposed in patients with neurological diseases, such as spinal cord injuries and stroke, to improve symptoms of spasticity, resulting in both increased control of voluntary movements and improved functional ability in daily activities. Despite several authors suggest that these results could be related to a reduced spinal excitability, which is known to be higher in spastic patients, no previous studies investigated the neurophysiological mechanisms underlying the effect of NMES in reducing spasticity. In addition, there are no studies in the literature adopting NMES to improve spasticity in patients with Multiple Sclerosis (MS). Therefore, this study aims at comparing acute responses in spinal excitability, as measured by H-reflex, between MS patients with and without spasticity, following three experimental conditions: 1) isometric voluntary contraction (ISO) of the ankle plantar flexor muscles; 2) NMES passively applied (pNMES) to the ankle plantar flexor muscles; and 3) NMES superimposed onto isometric voluntary contraction (NMES+) of the same muscles. Methods: 15 MS patients with spasticity (MS+) and 15 MS patients without spasticity (MS-) took part in a single experimental session, which consisted in the application of NMES to the ankle plantar-flexor muscles in the most spastic and compromised leg. Following the assessment of maximum voluntary isometric contraction (MVIC), participants were asked to perform 15 repetitions of 6 s at 20 % of MVIC, with 6 s of recovery between repetitions, during the three experimental conditions (ISO, pNMES, NMES+). Before and after each condition, soleus (SOL) H-reflex amplitudes were recorded by using surface electromyography (sEMG). Results: In MS+, H-reflex amplitude significantly decreased after both pNMES (p = 0.007) and NMES+ (p = 0.003), while it was unaltered after ISO (p = 0.829). In MS-, H-reflex amplitude did not change under any experimental condition (ISO: p = 0.383; pNMES: p = 0.328; NMES+: p = 0.087). Conclusion: The reduction of H-reflex after pNMES and NMES+ can be attributed to a reduced spinal excitability in spastic MS patients, which may be attributed to presynaptic inhibition, recurrent inhibition, gamma-aminobutyric acid activity and persistent inward current. These results are highly relevant from both neurophysiological and clinical point of views, suggesting new approaches to manage spasticity symptoms in neurological patients.