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Neuromotor Habituation As A Mechanism For Vibration Induced Low Back Pain - Introduction; Proceedings Of The First American Conference On Human Vibration
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  • Description:
    Occupational exposure to whole body vibration has long been associated with increased incidence of low back pain and low back injuries1. A number of studies have investigated transmissibility of seat pan vibration 5, 6. While transmissibility has been well researched, the mechanism by which vibration may induce injury has not been thoroughly studied. Winter et al. identified increased reflex response delay after vibration exposure and speculated that muscular fatigue may be the cause of this increase9. However, a mechanism has yet to be demonstrated completely. A potential mechanism that may explain the increased risk is neuromotor habituation. Muscle spindle organs have been shown in the extremities to be sensitive to muscle and tendon vibration. Rapid length changes in muscle have been shown to result in kinesthetic illusions as the regular firing of the muscle spindles is interpreted as muscle lengthening4, 7. These illusions have also been demonstrated in the paraspinal musculature2. With removal of vibration, research in the extremities has demonstrated increased positioning errors, probably due to neuromotor habituation8. In this research, it has been hypothesized that neuromotor habituation after exposure to occupational vibration will increase positioning errors. It is further hypothesized that these errors can be shown to be linked to increased reflex response time. Such increased reflex response time could, in turn, decrease spinal stability and increase low back injury risk. Methods Both positioning error and sudden load response were measured before and after exposure to 20 minutes of 5 Hz, 0.223 m/s2 RMS seat pan vibration. Subjects were asked to sit on an unpadded seat without a backrest. Throughout the whole body vibration period, subjects were instructed to put their hands on a stable hand rest and feet on an adjustable stable footrest. The subjects were instructed to assume a comfortable and relax sitting posture for the duration of the exposure. Positioning error was measured using an active-active reposition sense protocol. Electromagnetic markers (Motionstar, Ascension Tech, Burlington, VT) were used to track trunk motion. With markers attached to the skin at the T10 vertebra, the S1 vertebra and manubrium, trunk flexion (the angle from vertical of the line connecting T10 and S1) and lumbar curvature (the difference in inclination of the T10 and S1 markers) were tracked. In the reposition sense protocol, subjects were asked to maintain an upright trunk flexion and to rotate their pelvis and lumbar curvature to assume a target lumbar curvature. In the protocol subjects completed training trials, where they were asked to match their lumbar curvature using a visual display, and assessment trials, where they were asked to reproduce the lumbar curvature from memory. After two initial training trials, training trials and assessment trials were alternated for a total of 3 assessment trials. Reposition error was defined as the absolute difference between the target lumbar curvature and the lumbar curvature the subject assumed during the assessment trials.

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