Exposure to hand-arm vibration through the use of power hand-tools can result in the development of hand-arm vibration syndrome (HAVS), which is characterized by a reduction in tactile sensitivity in the fingers and hands of workers. The etiology underlying the development of HAVS is unknown. The goal of this study was to use a rat-tail model of HAVS to characterize progressive changes in sensory nerve function that occur with repeated exposures to vibration. Rats were exposed to tail vibration, restraint or control conditions 4 h/day, 5 days/week for 5 weeks. A-beta, A-delta and C-fiber function was assessed using transcutaneous electrical stimulation at 3 different frequencies. Thresholds were measured before and after the last exposure each week. Analyses revealed that between week 1 and week 2, A-beta and A-delta fiber thresholds declined by about 50% in vibrated rats, indicating an increased sensitivity to mechanical and pain stimuli. Vibration also caused an additional transient reduction in A-beta fiber thresholds immediately following exposures during weeks 4-5. No changes were seen in C-fiber thresholds over time. Although HAVS is associated with a reduction in tactile sensitivity, this loss of sensory function may be preceded by hyperalgesia to mechanical stimuli. Thus, this increase in pain sensitivity may serve as an early marker of vibration-induced nerve damage, and non-invasive tests to detect mechanical hyperalgesia could be used to identify workers that may be at risk for developing HAVERSUS.