Oxygen treatment reduces neurological deficits and demyelination in two animal models of multiple sclerosis.

Aims: The objective of the study is to explore the importance of tissue hypoxia in causing neurological deficits and demyelination in the inflamed CNS, and the value of inspiratory oxygen treatment, using both active and passive experimental autoimmune encephalomyelitis (EAE).

Methods: Normobaric oxygen treatment was administered to Dark Agouti rats with either active or passive EAE, compared with room air-treated, and naïve, controls.

Results: Severe neurological deficits in active EAE were significantly improved after just 1 h of breathing approximately 95% oxygen.

Deep brain stimulation of the midbrain locomotor region improves paretic hindlimb function after spinal cord injury in rats.

In severe spinal cord injuries, the tracts conveying motor commands to the spinal cord are disrupted, resulting in paralysis, but many patients still have small numbers of spared fibers. We have found that excitatory deep brain stimulation (DBS) of the mesencephalic locomotor region (MLR), an important control center for locomotion in the brain, markedly improved hindlimb function in rats with chronic, severe, but incomplete spinal cord injury. The medial medullary reticular formation was essential for this effect.