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February 2008 Issue

Jun-Ming Zhang, MD, is studying inflammation and how its effects on sensory neurons in the low back cause persistent chronic pain.
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UC Awarded $1.7 Million for Low Back Pain Study

Published February 2008

Back pain is the leading cause of disability in Americans younger than 45 years old and is experienced by 50 to 80 percent of adults at some point in their lives.

UC researchers have been awarded $1.7 million from the National Institute of Neurological Disorders and Stroke to study the condition that costs Americans $50 billion a year. They are focusing their five-year study on inflammation and how its effects on sensory neurons in the low back cause persistent chronic pain.

The anesthesiology department team, led by Jun-Ming Zhang, MD, director of UC’s Pain Research Center, believes small molecules called chemokines are key factors in the development of pain.

Chemokines are a family of small cytokines—chemical “messenger” molecules used by immune and nerve cells to communicate with other cells.

“If we can determine the role these chemokines play in the development of back pain we can hopefully develop better medications to treat the problem,” says Zhang.     

Zhang says acute (short-term) pain can actually be beneficial.

“Acute pain responses to potentially dangerous stimuli—like the neural circuitry that tells you to pull your hand away from a hot stove—are essential for survival,” says Zhang.

But when pain becomes chronic, it “serves no useful purpose,” he says, and often affects a person’s quality of life.

Back pain can be caused by physical trauma such as a sports injury, lifting heavy items or from a car accident, Zhang explains.

For others, medical conditions such as a herniated disc cause pain. But many people experience back pain for no apparent reason.

“When a patient goes to the doctor for low back pain, they may undergo an MRI or an X-ray. Sometimes these tests show anatomical reasons for the pain such as a herniated disc. But for some patients, tests don’t show any physical evidence for why they are experiencing low back pain,” he says.

Zhang adds that the lack of physical evidence can be very frustrating for patients and make it more difficult for doctors to help a patient effectively manage their pain through medication and other treatment therapies.

“That’s why we hope to identify specific molecules that contribute to low back pain development. Our goal is to develop a non-opiod analgesic targeting those molecules to alleviate pain,” says Zhang.

In previous research, Zhang and his team, including Judith Strong, PhD, coinvestigator for the new study, found that pain-sensing neurons can become abnormally sensitive or “fire” spontaneously in the absence of stimuli. This early spontaneous activity plays a key role in setting up the pathological pain state.

“We found that by blocking the early spontaneous activity of an injured nerve we can completely prevent the development of chronic pain. This technique could be extremely useful for combat nerve injuries and amputations that often lead chronic pain,” he says.

In this study, the team will explore how inflammation may contribute to the development of low back pain by intentionally causing this abnormal neuronal firing.

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