This study provides evidence that there is a differential pattern of paraspinal muscle recruitment between individuals with and without osteoporotic vertebral fractures and these changes are present at commonly fractured levels in the mid-thoracic spine and thoracolumbar junction. This finding may partly help to explain the complex and worrying clinical problem of the ‘vertebral fracture cascade’. Most notably, individuals who had sustained a vertebral fracture demonstrated delayed activation and a shorter time to reach maximum amplitude of the paraspinal muscles compared to individuals with no history of vertebral fracture.
The rapid arm movement paradigm used in this study provides an opportunity to investigate the strategy implemented by the central nervous system (CNS) to manage a sudden change in trunk equilibrium [3
]. The differential neuromuscular responses observed may be associated with greater vertebral loading in the fracture group given that muscle force is delivered over a shorter time, and thus point to a mechanism underlying the vertebral fracture cascade. However, the decision by the CNS to adopt this neuromuscular response may also be an adaptive/protective strategy. The longer time to initiate a response and shorter time to reach maximum amplitude may highlight a mechanism aimed at minimising the duration of vertebral loading. Further studies using a detailed anatomic model driven by EMG would be required to clarify the nature of these loading strategies.
A consistent pattern of activity was observed in longissimus thoracis during the arm movement task; onsets of T6 and T12 EMG activity occurred 25–50 ms after those of the non-fracture group, except in the flat base condition for T6 in which both groups demonstrated a significant rise in EMG activity above baseline at epoch
5. Results of this study are consistent with those reported previously using surface EMG in individuals with osteoporotic vertebral fractures [14
]. That study demonstrated a delay in activation of the erector spinae muscle at T7 in individuals with vertebral fractures by 50 ms, and a reliance on trunk muscle co-contraction to maintain equilibrium. Co-contraction contrasts to the alternating trunk muscle activity patterns reported in younger populations during similar tasks [2
Trunk muscle activity may be regarded as ‘feed-forward’ if onsets occur between 100 ms before to 50 ms after the onset of deltoid [21
]. Thus, results of the present study agree with previous reports that suggest a feed-forward pattern for erector spinae and multifidus activation relative to deltoid onset [3
]. A major element of the present study is that EMG recordings were made at commonly fractured sites, and from the paraspinal muscles, which are known to contribute significantly to compressive vertebral loading due to their short moment arm, particularly in individuals with vertebral fractures [13
]. Although EMG was not collected from participant-specific fracture levels, the majority of fractures sustained by participants in this study occurred at T6, in agreement with previous reports [7
For multifidus, the onset of EMG activity in the non-fracture group preceded that of the fracture group in the flat base condition; however the opposite pattern was noticed in the short base condition. Consistent with previous research, the deep multifidus was active prior to deltoid [31
]. The reason for earlier activation of the multifidus in the fracture group of 25 ms during the short base condition is uncertain; however we propose three possible explanations. First, it may be that individuals with osteoporotic vertebral fractures experience greater spinal instability therefore requiring a more rapid activation of the multifidus muscle compared to those without fractures. Second, the earlier response of multifidus may be necessary to accommodate for the delayed response of the more superficial long erector spinae muscles in the thoracic spine. Third, EMG of the lumbar multifidus was collected at L4 and vertebral fractures rarely occur at this level. Findings presented in this study may indicate that neuromuscular changes in the trunk extensors occur specifically at commonly fractured levels or that a CNS adaptation has occurred in the fracture group to increase lumbar intersegmental stability by recruiting multifidus relatively earlier.
As expected, muscle responses varied according to the task. In general, paraspinal muscles were recruited earlier in the short base condition (75–50 ms) compared to the flat base condition (50–25 ms), although little difference was observed in EMG amplitude between bases. This may reflect a greater demand placed on the CNS in the short base condition that required more rapid activation of the paraspinal muscles. On a flat base, the body rotates as a rigid mass about the ankle joints to maintain equilibrium in response to sagittal plane perturbations [24
]. The short base decreases the ability for individuals to use an ankle strategy (ankle torques) to maintain postural control, and equilibrium is maintained by generation of horizontal shear forces from hip and trunk movement [24
]. Muscular responses in the trunk therefore become more pronounced. Indeed, difficulty in executing postural tasks, particularly involving balance, has been reported previously in the elderly population [46
The delay in recruitment of the paraspinal muscles and its likely consequence, a shorter time to reach maximum amplitude, may have several implications. A previous study showed greater segmental loading in upright stance in individuals who had sustained a vertebral fracture [6
]. Combining higher static vertebral loads with a higher loading rate may be sufficient to cause vertebral failure by increasing trabecular strains [25
]. Alternatively, cyclic repetitions of this neuromuscular response may fatigue trabecular bone and accelerate disc degeneration, thereby increasing subsequent fracture risk [8
]. However, the neuromuscular contribution to these degenerative mechanisms may only be viewed as speculative at this time given the current knowledge in the literature. Importantly, the generally shorter time to reach maximum amplitude displayed by the fracture group may represent a compensatory strategy employed by the CNS to overcome the delay in activation and maintain trunk equilibrium, or minimise the duration of muscle loading.
The mechanisms explaining the delayed paraspinal muscle activity in the fracture group are uncertain. Inhibition of muscle function due to pain may be attributable to symptomatic fractures, while subtle changes in thoracic kyphosis may have altered the mechanical properties of the muscles [39
]. Previous research has confirmed changes in muscle recruitment as a consequence of pain [19
]. Other factors related to vertebral fractures such as decreased mobility and fear of falling could also influence muscle activation characteristics [35
]. Furthermore, individuals with vertebral fractures demonstrate lower back-extensor and systemic strength compared to individuals without fractures [9
]. In the presence of weakened musculature a more rapid response to reach maximum amplitude may be required to in order to satisfy the equilibrium requirements. Indeed, this hypothesis may help to explain the reduced risk of subsequent vertebral fracture seen after a programme of back-extensor strengthening [40
Previous studies have established that back-extensor strengthening, orthoses and proprioceptive re-education are beneficial in reducing the risk of osteoporotic vertebral fractures [39
]. However, care should be taken when prescribing paraspinal-strengthening exercises in order to minimise compression forces through already weakened vertebrae, and orthoses should not replace the role of active muscles in the long-term to avoid muscle deconditioning. The findings presented in this study have clinical significance and may help to optimise musculoskeletal rehabilitation for this population. This study provides evidence of the existence of altered neuromuscular patterns in individuals who have sustained vertebral fractures compared to those who have no history of vertebral fracture and this may be interpreted as one of the sequelae of vertebral fractures. Future research examining the efficacy of interventions directed towards modifying this neuromuscular response and the longitudinal efficacy in reducing fracture risk is therefore warranted. Neuromuscular retraining in individuals with low back pain has proved to be effective in reducing pain and improving function [34
], thus benefits, particularly a reduction in the vertebral fracture cascade, may be seen in the population of individuals with osteoporotic vertebral fractures. However, we cannot be sure whether changing the response will decrease fracture risk as it not yet known whether the altered neuromuscular responses are an adaptive strategy employed by the CNS. The cross-sectional design of the study precludes a cause-effect inference between an altered neuromuscular strategy and vertebral fracture, thus future research should adopt a longitudinal design to overcome this limitation. Future research should also utilise biomechanical trunk models driven by EMG to elucidate the influence of neuromuscular strategies on vertebral loading in this population. Temporal activation in this study was limited to specific epochs
, thus more specific information might be obtained from identifying accurate onset/offset times.