An experimental drug has been shown to restore function to nerves damaged by spinal cord compression injuries and shows potential for future treatment of spinal cord trauma, according to new research from Purdue University.
As recently detailed in the Journal of Neurophysiology, the chemical compound, 4-aminopyridine-3-methyl-hydroxide, was used to treat pig spinal cord tissue that was simulated to experience the stresses that occur in spinal cord compression injuries, which stretch rather than sever the nerves and can lead to paralysis.
As confirmed in the research findings, spinal cord compression injuries damage the myelin sheath, a thick insulating layer that protects axons, the slender fibers that extend from nerve cells and transmit signals in the spinal cord via rapid electrical impulses.
According to the researchers, “fast potassium channels” that reside in the axons and play a crucial role in the transmission of nerve impulses are exposed following damage to the myelin sheath, thus impairing normal signal transmission and nerve function.
However, in treating the damaged axons with 4-aminopyridine-3-methyl-hydroxide, the researchers learned that this experimental drug acted as a “potassium channel blocker” that prevented these channels from exposure following compression injuries and restored nerve function without slowing down the firing time between pulses.
The researchers added how 4-aminopyridine-3-methyl-hydroxide, which is 10 times stronger than 4-aminopyridine alone, could result in lower doses and fewer side effects than other drugs given to patients with spinal cord injuries, and even be used to treat nerve damage from multiple sclerosis, a chronic and often-disabling disease that also damages myelin.