Richard L. Bruno is chairperson of the International Post-Polio Task Force and director of The Post-Polio Institute at Englewood Hospital and Medical Center. Please e-mail questions directly to him at ppseng@aol.com.
Note: This column is for information purposes only and is not intended as a substitute for professional medical advice.
Q: I heard that a study found that magnets do not help people who have back pain. But I read on the Internet that magnets cure back pain in polio survivors. What's the real story?
A study in the March 8, 2000, issue of the Journal of the American Medical Association found that wearing a magnet or an identical-looking nonmagnetic pad produced no significant relief in patients who had experienced low back pain for at least six months. In 1997 Carlos Vallbona of Baylor College of Medicine examined the effect of magnets in polio survivors. First, he identified places anywhere on polio survivors' bodies that hurt. He then caused pain "by firm application of a blunt object" to the area, asking subjects to rate the pain from zero to 10. Pain was rated as "nine" on average. Then either a magnet or a nonmagnetic pad was placed over the painful area for 45 minutes, and the blunt object was again pressed into the skin. Subjects wearing the magnet rated their pain as "four" on average while those wearing the nonmagnetic pad rated their pain "eight."
Q: With cadaver stem cells being used to grow new neurons in the laboratory in hopes of curing spinal cord injury, could new nerves be implanted into spinal cords of polio survivors to reduce prior nerve damage or even cure PPS?
The hope with spinal cord injury is that stem cells might "bridge the gap" in severed spinal cord axons, which are like long telephone wires that connect brain motor neurons to spinal cord motor neurons, and once again allow the brain to "tell" muscles to move. This would require intact motor neurons below the injury level. In contrast, the poliovirus killed off at least 60 percent of motor neurons in the spinal cord. Stem cells injected into the spinal cord would have to become new motor neurons, not bridge a gap. Those new neurons would then have to send out axons to activate muscles paralyzed when the original axons disappeared 40-plus years ago at the time poliovirus-infected neurons died. These axons would have to find the appropriate muscles to activate by burrowing inches, and in the case of foot muscles, three feet through the tissues in the leg. Finally, the brain's motor neurons would have to send out new axons as well, since their axons also deteriorated after the spinal cord motor neurons died. These axons would have to burrow through the lower part of the brain, down through the spinal cord to newly-implanted motor neurons--a daunting task!
In summary, while reconnecting a spinal cord damaged by injury would require the physiological "home run" of bridging a gap between cut axons, the idea of rebuilding a polio-damaged spinal cord would be the equivalent of a "hat trick": creating new spinal motor neurons, new axons from brain to spinal cord, and yet more new axons growing from spinal cord to muscles.