Neuropathic pain is caused by either damage or disease in parts of the nervous system.
Its exact symptoms vary from person to person, and they range from odd sensations to intense pain.
In some individuals, a light breeze can trigger significant discomfort, whereas in others, moving just a single hair can provoke excruciating pain.
Affecting as many as 1 in 10 individuals in the United States, neuropathic pain still has no safe and effective treatments that work for everyone.
Most commonly, people with neuropathic pain will manage their symptoms with nonsteroidal anti-inflammatory drugs, opioids, or anti-epileptics, all of which have unpleasant side effects and none of which are effective for all. Also, famously, opioids carry a significant risk of addiction.
Can we treat neuropathic pain?
Earlier research endeavors hunting for potential treatments have focused on targeting specific molecules that are involved in pain pathways. Although there has been some headway, this approach has not yet come up trumps.
The reason seems to be that when you block one or two of the molecules that generate pain, others move in and take their place.
Researchers from the European Molecular Biology Laboratory in Rome, Italy, have designed an innovative approach to neuropathic pain. Their latest findings were published recently in the journal Nature Communications.
The research, led by Paul Heppenstall, Ph.D., uses an entirely new approach. Rather than searching for molecular messengers, they identified the subgroup of nerve cells that are responsible for oversensitivity to pain, and they concentrated their efforts on quietening the guilty cells.
They found that a subpopulation of sensory neurons that express a receptor called tropomyosin receptor kinase B (TrkB) are responsible for generating disproportionate levels of pain.
To influence these nerves, the team designed a light-sensitive chemical that specifically binds to TrkB receptors. They injected this chemical into the skin of mice with neuropathic pain.
Once the chemical had bound to the receptors, they blasted it with near-infrared light. This caused the nerve endings to retract from the surface of the skin, making them less likely to be triggered.
"It's like eating a strong curry, which burns the nerve endings in your mouth and desensitizes them for some time."
Paul Heppenstall, Ph.D.
Does it work?
After the nerve endings were shrunk back, the researchers assessed how well the intervention had worked by measuring the pain responses of the mice.
Most often, mice with neuropathic pain quickly withdraw their paw following just a light touch.
But once the light therapy had been carried out, the mice's reflexes returned to normal.
Importantly, the treatment was effective for a number of weeks — until the pruned nerve endings grew back.
This method is useful because, among the huge variety of nerve cells in the skin, it only targets the important ones. As Heppenstall explains, "The nice thing about our technique is that we can specifically target the small subgroup of neurons causing neuropathic pain."
Of course, the current study was carried out in a mouse model and, therefore, may not apply in the same way to humans. To take a preliminary look at this, the researchers investigated human skin. They found that the neurons targeted in mice seem to be similar to their counterparts in humans, which gives hope for the future.
Heppenstall and colleagues plan to continue their work. He concludes, "[O]ur aim is to solve the problem of pain in both humans and animals," which is a long and noble road to follow.