Neuropathic pain erodes quality of life. In this chronic pain state, nerves in the central nervous system have become damaged, dysfunctional or injured, sending incorrect signals to other pain centers.

Nearly 50 million American adults have significant chronic pain or severe pain, according to a recent study prepared by the National Institutes of Health's National Center for Complementary and Integrative Health (NCCIH). Based on data from the 2012 National Health Interview Survey (NHIS), the study estimates that within a previous three-month period, 25 million U.S. adults had daily chronic pain, and 23 million more reported severe pain.

But help may be on the way, as researchers have discovered a connection between neuropathic pain and microglia cells.

Neuropathic pain, unlike physiologic pain, persists even after the injured nerve has healed and is often resistant to pain relievers like acetaminophen and naproxen. While opiates are used to alleviate pain, they have side effects and are not always effective for neuropathic pain patients.

Pain is a complex phenomenon. We know pain is present in multiple forms and is the most common reason for seeking medical assistance in the United States. As we know, acute pain usually starts suddenly and resolves quickly, serving as a warning of tissue damage, injury or a threat to the body.

On the other hand, chronic pain persists even after an injury has healed and becomes a debilitating condition, imposing both physical and emotional effects on affected individuals. Chronic pain is not a simple extension in time of acute pain; instead, the transition from acute to chronic pain involves neuronal plasticity in both peripheral and central nervous systems.

In terms of neuropathic pain, Long-Jun Wu, a professor of cell biology and neuroscience at Rutgers University, and his researchers believe this pain could be reduced or even eliminated by targeting those brain cells that are supposed to provide immunity but instead do the opposite. They discovered that chronic neuropathic pain — resulting from nerve damage after an injury, surgery or a debilitating disease like diabetes or cancer — can be greatly reduced in animals if the injury was treated targeting microglia within one to five days.

In laboratory studies on mice, Wu and his colleagues used chemotherapy drugs to prohibit the microglia brain immune cells from proliferating, similar to the treatment used by oncologists to prevent cancer cells from multiplying. The results showed this chemotherapy drug reduced the amount of pain the mice experienced after the injury occurred.

According to Wu, the microglia cells need to be prevented from multiplying in the first place. It had been thought that these cells were beneficial in a normal brain, but Wu's research discovered how these cells function under neuropathic pain condition and initiate the problem.

Although scientists have studied microglia cells in relationship to neuropathic pain for the past two decades, Wu and his team are the first to pinpoint the exact role the cells have in the initiation and maintenance of the condition. By discovering that the proliferation of these types of cells is one of the major contributors of microglial pain, developing more effective painkillers with fewer side effects may be possible.