Double magnetic stimulation of the motor cortex in amyotrophic lateral sclerosis

Objectives: To study the motor cortex circuitry and the motor interhemispheric influences with double magnetic stimulation in patients affected by amystrophic lateral sclerosis.Methods: We investigated the motor cortex in 21 amyotrophic lateral sclerosis patients (ALS, 10 with bulbar and 11 with spinal onset) with double magnetic stimulation (one shock in each hand area) with 2, 4, 6, 11 and 15 ms delay between shocks and paired magnetic stimulation (both shocks in the same area), with 4, 15, 25, 35, 55, 85, 100, 155, 200 and 255 ms delays, and compared the results with those obtained in normal subjects.Results: Double magnetic stimulation showed reduced interhemispheric facilitatory influences (maximal at 4 ms delay between shocks) when the test shock was applied on the left hemisphere in all patients; whereas no significant differences were observed compared to control (P>0.05) when it was applied on the right hemisphere in both forms. Inhibitory effects (maximal at 11 ms delay between shocks) were reduced in all patients for both hemispheres (P<0.05). Paired magnetic stimulations showed decreased inhibitory influences at 100–155 ms delay between shocks. Compared to control, the difference was significant in bulbar (P<0.05) and spinal onset, but not between onset forms (P>0.05). Inhibitory effects recorded with a short delay between shocks (4 ms) were not significantly modified in both forms of onset (P>0.05) as compared to control. There were no facilitatory influences at 15 and 35 ms delays between shocks.Conclusions: The results suggest that under these test conditions inhibition and facilitation were reduced in the motor cortex in ALS. As inhibitory effects were affected differently, two distinct cortical circuitries could be involved for short and long delays. As GABA neurons altered in ALS have been identified as a subpopulation reactive to parvalbumin, and since only inhibitory effects recorded with long delay between shocks were impaired in ALS, we suggest that this subpopulation of GABA neurons may be involved in the genesis of inhibitory effects recorded with a long delay between shocks.