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North American Congress on Biomechanics Canadian Society for Biomechanics - American Society of Biomechanics University of Waterloo Waterloo, Ontario, Canada August 14-18, 1998 |
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Low back pain (LBP) is the leading major cause of industrial disability. In the United States, one million back injuries occur per year. 100 million work days are lost each year, and LBP accounts for 20 percent of all work related injuries. Hulshof and van Zanten (1987) reviewed the positive relationship between LBP and WBV.
This review paper discusses several novel methods used by the authors to gain insight into the aetiology of WBV-caused LBP
In Vivo Measurements. We measured WBV by transducers rigidly fixed to the L3 spinous process. The frequency spectra were subjected to a triangular smoothing filter. Pope et al.(1987) introduced a platfomm suspended by soft springs and guided by two linear bearings. The impact was applied by a pendulum to the center of the platform. In Pope et al.(1987), tests are described in which a subject is placed in different controlled sitting postures, erect posture, relaxed posture and erect posture with valsalva and the transmissibility and phase angle determined. Similar studies investigated the dynamic response of the standing subject. These conditions included modification of posture, increase of the trunk load moment, the wearing of different types of shoes and standing on different foam material (Pope et al., (1986b)).
Electromyographic Activity (EMG). The phasic activity of the right and left erector spinae (ES) muscles under WBV at discrete frequencies between three and ten Hz were measured in six males (Seroussi et at. 1989). The relationship of the electromyographic signal to a given torque demand on subjects was found by measuring the EMG while performing an isometric pull. The amplified ES were sampled at 500 Hz for four s. The signals were high-pass filtered, rectified ensemble averaged and then converted to torque using the EMG-torque calibration. The phase relationship between the input and the resulting torque was established.
The development of fatigue was studied through the median frequency from contracting back muscles (Hansson et al., 1991). EMG were recorded using surface electrodes on 6 males. The subjects were exposed to 1) whole body vibration of five Hz and 0.29 RMS acceleration, and 2) static sitting. These signals were amplified and filtered by a spectrum analyzer.
In Vivo Creep. Spinal height changes were measured by means of an LVDT (Magnusson et al., 1992). The transducer was mounted on top of a column which was tilted slightly backwards. The column was equipped with posture controls for the tnunk and head. The transducer registered height changes continuously during the exposure. Height changes were measured in twelve female subjects exposed to static sitting and seated whole body vibrations. The vibration input was five Hz frequency and 0.19 RMS acceleration.
Biochemical measurements. In another series of studies we measured biochemical changes due to WBV (Pope et al. 1994). The von Willebrand factor (vWf) is a complex protein whose release is a marker for endothelial damage; serum levels of its antigen (vWFAg) can be used as a marker for such changes. We measured the levels of back discomfort and vWFAg in 11 subjects following 25-min periods of (1) lying down, (2) sitting upright, (3) vibrating whilst sitting and (4) sitting upright. The subject was then vibrated at 5 Hz at levels of 3.5 m/s2 for 25 min in an upright unsupported posture. This vibration exposure was at the level of the fatigue ISO, decreased proficiency limit.
In Vivo. The subjects in the relaxed seated posture experience a transmissibility peak at L-3 at five Hz coupled with an attenuation peak between six to 8.5 Hz. In the erect posture the response curves had the same general forrn, except that the peaks were more marked in the relaxed posture. The Valsalva increased in height the five Hz peak of transmissibility, and beyond that point there was decreasing gain with frequency. Contraction of the glutei resulted in a response curve which was between that of the relaxed and the Valsalva. Placing a block under the pelvis to offer rotationai support reduced the gain peak and the gain valley. In erect standing, there was a single transmissibility peak at 5.5 Hz. The at-ease posture gave a slightly reduced peak, and a knee-bent posture attenuated the response. A pelvic tilt and Valsalva cause the peak to move to 6.5 Hz and seven Hz respectively, while the adoption of a tip toe stance moved the peak to three Hz.
EMG. Higher average EMG levels, or muscle torque, were found for the vibration condition compared to the static condition, except at three, four, and ten Hz. The time lag between the input displacement and the peak torque varied from 30 ms to 100 ms at three Hz. At ten Hz there was a trend for the muscle contraction again becoming in phase (or 360° out of phase) with the input signal. At all other frequencies, it was out of phase.
The mean frequency of the EMG signals obtained from the erector spinae muscles, at both the thoracic and lumbar level, decreased with time. The decease was accentuated by whole body vibration.
In Vivo Creep. Height loss was significant for both vibration and static sitting (p<0.0005). A larger height loss was demonstrated when the subjects were exposed to vibration, than when not (p< 0.03).
Biochemical. Back discomfort and vWf levels were significantly increased following sitting upright, compared with lying flat, and increases further following WBV. They fell thereafter with a period of sitting still upright. These results demonstrate that WBV has a significant effect in increasing back discomfort and the serum levels of vWFAg, and it is possible that WBV may induce vascular.
In vivo, studies demonstrate that the first resonance occurs within a band of 4.5 to 5.5 Hz. Similar, but less tightly defined resonances, are also identified in the 9.4 to 13.1 Hz range. The resonance at 4.5 to 5.5 Hz is markedly affected by the peivis-buttocks system. The timing of the back muscle response with respect to the vibration stimulus is such that the muscles are not able to protect the spine from adverse loads. At many frequencies, the muscles' response are far out of phase, their forces are added to those of the stimulus. The fatigue that is found in muscles, after WBV, is indicative of the loads in the muscles. It was demonstrated that WBV in itself, always caused increased height loss in the subjects. The spinal height change reflected increased spinal load. We also found biochemical changes that could be used as a measure of tissue damage.
Blann AD, Pope MH, Kaigle AM, Weinstein JN, Wilder DG, Jayson MIV: The effects of vibration on plasma levels of von Willebrand factor antigen: a preliminary study. Proc Soc for Back Pain Res, Oxford, UK, Mar 1991.
Hansson T. Magnusson M, and Broman H (1991) Back muscle fatigue and seated whole body vibrations. An experimental study in man. Clin. Biomech, 6:173-179.
Hulshof C, van Zanten BV (1987) Whole body vibration and low back pain. Int Arch Occup Environ Health 54:205-220.
Magnusson M, Almqvist M, Broman H. Pope MH, and Hansson T (1992) Measurement of height loss during whole body vibration. J. Spinal Disorder, 5(2):198-203.
Pope MH, Wilder DG, Jorneus L, Broman H. Swensson M, Andersson GBJ (1987) The response of the seated human to sinusoidal vibration and impact. J Biomech Eng, 109:279-284.
Seroussi R. Wilder D, Pope MH (1989) Trunk muscle electromyography and whole body vibration. J Biomech 22(3):219-229.