El Síndrome Pospoliomielitis es ocasionado por la muerte de las terminales de nervios individuales en las unidades motoras el desarrollo de una debilidad muscular, atrofia muscular y fatiga muscular nueva que no son explicables por otra causa médica-
Traumatic brain injury causing neuropathic pain is unfortunately a daily reality for millions of Americans. This condition generally occurs after injury to the central nervous system and it is a malfunction in the nervous system that can become chronic. Individuals can suffer pain even from a light touch or suddenly feel freezing from slight changes in temperature.
Currently, researchers believe that neuropathic pain comes from spinal nerve cells that release the neurotransmitter GABA. GABA is the main inhibitory neurotransmitter in the brain and is responsible for preventing over excitation in the brain. In this case, GABA neurons have been damaged or completely disabled allowing for pain impulses to go out of control.
If these GABA neurons could be kept alive after injury to the nervous system, it’s possible that an individual could forgo neuropathic pain.
Researchers at the University of Texas Medical Branch at Galveston (UTMB) have discovered a way to keep these neurons alive. They found that the key to keeping GABA cells alive is to keep oxidative stress at bay.
According to UTMB professor Jin Mo Chung, senior author of a paper on the research, “GABA neurons are particularly susceptible to oxidative stress, and we hypothesized that reactive oxygen species contribute to neuropathic sensitization by promoting the loss of GABA neurons as well as hindering GABA functions.”
The researchers tested this hypothesis by conducting experiments in mice that had been surgically altered to simulate the condition of neuropathic pain. In a particular experiment, they treated mice with an antioxidant for a week after surgical treatment to simulate neuropathic pain and compare them to mice that were untreated. These researchers report that mice treated with antioxidant demonstrated less pain-associated behavior and had more GABA neurons than untreated mice.
Chang reports that, “So by giving the antioxidant we lowered the pain behavior, and when we look at the spinal cords we see the GABA neuron population is almost the same as normal. That suggested we prevented those neurons from dying, which is a big thing.”
However, Chung also reported that there was one complication. There was a “moderate quantitative mismatch” between the behavioral data and the GABA-neuron counts. Apparently the anti-oxidant mice displayed less pain behavior but their behavioral improvement wasn’t as substantial as their GABA neuron count was higher than expected. He offers an explanation that the surviving neurons were somehow impaired which seemed to be supported by electrophysiological data.
At this time no clinical trials are planned, however, Chung believes that anti-oxidants have a great potential as a therapy for neuropathic pain. Chung adds, “If this is true and it works in humans — well, any time you can salvage neurons, it’s a good thing. Neuropathic pain is very difficult to treat, and I think this is a possibility, a good possibility.”