When the average person feels pain in his leg, the problem can usually be solved with rest, over-the-counter drugs, stretching or other simple remedies. The situation, however, becomes much more complicated when that pain is in a leg that is no longer there or totally paralyzed.

Researchers at the School of Medicine and Veterans Administration Rehabilitation Research and Development Center in West Haven have made progress towards understanding the likely source of phantom pains. They have also been able to suppress these pains in rats.

Dr. Stephen Waxman, chair of the Neurology Department and the senior author of the study, said the scientists studied rats with spinal cord injuries that caused a certain sodium channel to become spontaneously active, creating sensations of pain in paralyzed limbs. He said this discovery might eventually be applied to humans to alleviate phantom pain in amputated or paralyzed limbs.

“Some patients with spinal cord injuries have no perception in their limbs,” Waxman said, “but they sometimes have phantom sensations, which can be very unnerving.”

Physicians said these findings will be relevant not only for patients with spinal injuries, but also for those with amputated limbs who still feel pain in their removed appendages.

“Unfortunately we end up performing lots of amputations on patients because they have peripheral vascular disease [a condition where blood vessels in the leg become clogged],” said Dr. Bauer Sumpio, section chief of vascular surgery.

About one-fourth to one-third of amputees develop phantom pain that last for a substantial amount of time, he said.

Patients suffering from phantom pain often go from doctor to doctor in search of relief, Waxman said. He said the plight of these individuals drove him to find the true source of these pains and treat them on a molecular basis.

“If you have a headache, you take an aspirin. There’s no aspirin for this pain,” Sumpio said.

There are three pathways of neurons involved in the transmission of pain, beginning with those that relay information from the skin’s surface to the spinal cord, then from the spinal cord to the thalamus, the brain’s pain center. The final pathway connects the thalamus to the primary sensory cortex, Waxman said. The pain sensation only results once the signal reaches the cortex. The signals are transferred through various sodium channels, he said, which have only recently been distinguished from one another.

Whereas the first two pathways had been previously studied in relation to phantom pains, the third had not, so the researchers focused on a synapse closer to the cortex.

“We looked at the thalamus — a pain center,” Waxman said. “We found that after a spinal cord injury the neurons of the Nav1.3 [sodium channels] became spontaneously active. They responded abnormally high to a small stimulus.”

As a result of this discovery, the researchers were able to design molecular agents to reduce phantom pain signals by targeting and reducing the presence of Nav1.3 sodium channels.

Sumpio said these findings take advantage of recent developments in molecular neurology and mark the start of a relatively new sort of approach to phantom pain treatment — a scientific, rather than purely empirical, methodology.

“Neurology has traditionally been focused on incurable diseases, but I want to change that,” Waxman said. “I’m using the molecular approach.”

Though he said the research has not produced clinical applications and it will be much longer before these results can be put into practice, Waxman said he is encouraged by what he thinks is a very important step forward.