Early nerve damage caused by repetitive motion on the job can cause “sick worker” syndrome, a fatigue or depression that can be mistaken for poor work performance, according to a study published in this month’s Journal of Neuroimmunology.
The study done on rats found that nerve injuries caused by low-force, highly repetitive movement -- common to typists, pianists and meatpackers, among other professions -- can be blamed on increased production of proteins known as cytokines.
Cytokines show up in injured nerves as early as three weeks after the first signs of cell stress, much earlier than previously thought, researchers at Temple University found.
Cytokines also are known to spark symptoms of malaise and the study concludes that an onslaught of these proteins affected the rats’ psychosocial responses, the researchers said.
With so many cytokines entering the blood stream so early, some apparently traveled to the brain, sparking the rat version of “sick worker” syndrome, the study said.
“At three weeks, even before the rats experienced pain from their wrist injuries, we watched them self-regulate their work behavior,” researcher Ann Barr said. “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 study said.
The researchers theorized that as cytokines first appear in the newly injured nerve of workers who perform the same physical movement over and over, signs of “sick worker” syndrome begin. People may call in sick with undefined symptoms, or slow down their work production or a low-grade depression may set in, the researchers said.
Some bosses might see the cytokine connection as an excuse for employees to slack off work, but Temple researcher Mary Barbe disagrees.
“Cytokines are self-protective,” she said. “This undefined feeling of malaise may be telling the body to take some time off to heal, before things get worse.”