Early nerve damage caused by repetitive strain injuries can trigger "sick worker" syndrome

Early nerve damage caused by repetitive strain injuries can trigger "sick worker" syndrome - characterized by malaise, fatigue and depression, and often mistaken for poor performance, according to a study by Ann Barr, Ph.D., and Mary Barbe, Ph.D., at Temple University's College of Health Professions.

The study, "Increase in inflammatory cytokines in median nerves in a rat model of repetitive motion injury," is published this month in the Journal of Neuroimmunology.

Repetitive strain injuries are the nation's most common and costly occupational health problem, affecting hundreds of thousands of American workers and costing more than $20 billion a year in worker's compensation, so employers have long been interested in the connection between the two conditions.

The purpose of the study was to observe early changes in nerves caused by repetitive strain that lead to chronic pain and eventual degenerative problems such as carpal tunnel syndrome, tendonitis, tennis elbow or other serious neural and musculoskeletal injuries. The Temple researchers hope the findings could one day lead to early intervention techniques that would prevent permanent damage.

They discovered that nerve injuries caused by low-force, highly repetitive work can be blamed on an onslaught of cytokines -- proteins that help start inflammation. These cytokines, known also to spark symptoms of malaise, appear in injured nerves as early as three weeks after the first signs of cell stress -- much earlier than previously believed. As the nerve injury progressed, ever greater numbers of cytokines were made at the injury site.

Unexpectedly, the researchers also found that the cytokines affected the rats' psychosocial responses. With so many cytokines entering the blood stream so early, some apparently traveled to the brain, sparking the rat version of "sick-worker" syndrome. "At three weeks, even before the rats experienced pain from their wrist injuries, we watched them self-regulate their work behavior," said Barr. "With inflammatory proteins in the bloodstream, they began to slack off from completing their tasks."

By five weeks to eight weeks, when cytokine production reached "peak" levels, some rats curled up in a ball and slept in between tasks.

The researchers theorize that as early as three weeks -- as cytokines first appear in the newly injured nerve -- signs of "sick-worker" syndrome may begin. Employees may call out sick because of undefined symptoms, or slow down their work production. A low-grade depression may set in.

The connection between this "off" feeling and possible neural and musculoskeletal injuries may not be immediately apparent to the employee or employer, since actual pain is rare at this early stage of injury. Over months, however, as inflammation worsens, chronic pain will eventually lead workers to seek clinical help.

While some employers might see the cytokine connection as a simple opportunity to slack off work, Barbe disagrees.

"Cytokines are self-protective," she says. "This undefined feeling of malaise may be telling the body to take some time off to heal, before things get worse."

The next step for the researchers is to look more specifically at the psychosocial component of cytokines and their effect. To do this, they have been awarded a $1.3 million grant from the National Institute of Occupational Safety and Health at the Centers for Disease Control and Prevention.

They are also in the process of translating their research into human subjects. In an earlier rat study, Barr and Barr observed increases in circulating blood levels of serum cytokines. They are now finishing a study in which they are examining blood collected from humans diagnosed with repetitive strain injuries for these cytokines. Positive findings could aid earlier diagnosis and therefore earlier treatment.