• Andrew M Briggs, Alison M Greig, Kim L Bennell, and Paul W Hodges.
• Centre for Health, Exercise and Sports Medicine, School of Physiotherapy, The University of Melbourne, Melbourne, VIC 3010, Australia. abriggs@cabrini.com.au
• Eur Spine J. 2007 Aug 1; 16 (8): 113711441137-44.

AbstractThe high risk of sustaining subsequent vertebral fractures after an initial fracture cannot be explained solely by low bone mass. Extra-osseous factors, such as neuromuscular characteristics may help to explain this clinical dilemma. Elderly women with (n = 11) and without (n = 14) osteoporotic vertebral fractures performed rapid shoulder flexion to perturb the trunk while standing on a flat and short base. Neuromuscular postural responses of the paraspinal muscles at T6 and T12, and deep lumbar multifidus at L4 were recorded using intramuscular electromyography (EMG). Both groups demonstrated bursts of EMG that were initiated either before or shortly after the onset of shoulder flexion (P < 0.05). Paraspinal and multifidus onset occurred earlier in the non-fracture group (50-0 ms before deltoid onset) compared to the fracture group (25 ms before and 25 ms after deltoid onset) in the flat base condition. In the short base condition, EMG amplitude increased significantly above baseline earlier in the non-fracture group (75-25 ms before deltoid onset) compared to the fracture group (25-0 ms before deltoid onset) at T6 and T12; yet multifidus EMG increased above baseline earlier in the fracture group (50-25 ms before deltoid) compared to the non-fracture group (25-0 ms before deltoid). Time to reach maximum amplitude was shorter in the fracture group. Hypothetically, the longer time to initiate a postural response and shorter time to reach maximum amplitude in the fracture group may indicate a neuromuscular contribution towards subsequent fracture aetiology. This response could also be an adaptive characteristic of the central nervous system to minimise vertebral loading time.

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