Body
Acute intermittent hypoxia (AIH) induces plasticity in spinal motor circuits through a serotonin-dependent mechanism that increases BDNF expression and strengthens synaptic input to motoneurons. This effect is well established after spinal cord injury.
Whether it occurs in MS is unknown, because demyelination degrades conduction in the same pathways on which AIH acts. This trial delivers AIH to people with and without MS and measures corticospinal excitability with transcranial magnetic stimulation, spinal reflex excitability, proprioception at the hand and wrist, and strength and fatigue in the upper limb.
Comparing the two groups will show whether the response to AIH is intact, reduced, or absent in MS.