Can Paralysis Be Cured Using Neuroscience?
Can paralysis be cured using neuroscience? About 6 million people in the United States suffer from some serious form of paralysis. Major causes include stroke, spinal cord injury, and multiple sclerosis. Strokes damage the brain control centers for movement, while spinal cord injuries and multiple sclerosis damage neural axons that either control muscles directly or transmit signals from the brain to control muscles.
As with most medical conditions, the best solution is prevention — reducing accidents or the trauma in accidents — and curing paralyzing diseases like multiple sclerosis and vascular damage that leads to strokes. But future cures don’t help people currently afflicted with these conditions. The best types of cures would be biological — regrowing damaged axons or their insulating myelin sheaths, or inducing neural cell division to reconstitute damage brain areas. The last resort is the brain–computer interface to replace lost function.
Slow progress is being made toward biological cures. It used to be thought that there was virtually no new neuron births (neurogenesis) of adult neurons with the exception of olfactory receptors. However, recent research has demonstrated neurogenesis in the hippocampus associated with memory formation, and this process may occur to a limited extent elsewhere in the nervous system. Genetic and pharmacological techniques are being studied that may initiate this process.
A long-standing puzzle about axon myelination that is degraded in diseases like multiple sclerosis is that peripheral axons, sheathed by a type of glial cell called a Schwann cell, regrow following transection, but central nervous system axons, sheathed by oligodendrocytes, do not. Considerable efforts are underway to understand the biochemical differences between these two glial cell types with the hope of inducing regeneration in central nervous system axons damaged by traumatic injuries and strokes.
While people who suffer from paralysis wait for research to generate needed biological cures, some more immediate hope lies with brain–computer interfaces that may allow the capture of brain command signals to move limbs and the direct electrical stimulation of muscles either directly or via surviving motor neurons. In the case of limb loss, similar brain–computer interfaces may control prosthetic arms and legs. Rapid advances in computer technology are making the possibility of realizing such devices more likely in the very near future, and prototype brain–computer control for limbs and artificial prosthetic limbs are under development.
An interesting hybrid technology that has emerged recently is brain–computer interface augmentation. In some cases of nerve damage, some brain signal reaches the muscles, but it’s too reduced to allow sufficient strength for a person to stand upright, for example. A computer-controlled exoskeleton can amplify the person’s own motor commands supplying the missing force needed for standing and walking.
One possible advantage of this approach is that amplifying normally controlled movement may, via neural plasticity, not only reduce long-term neural degeneration that typically accompanies paralysis, as well as itself inducing regeneration of both muscles and neural connections. An exciting possibility is the use of such augmentation devices with pharmacological or genetic modifications to enhance neural plasticity that might be triggered by the use of such devices.