13th November 2014
Journal of Electromyography and Kinesiology (in press)
Van Damme, Benedicte; Stevens, Veerle; Perneel, Christiaan; Van Tiggelen, Damien; Neyens, Ellen; Duvigneaud, Nathalie; Moerman, Luc; Danneels, Lieven
Its great to see new research coming out to support out clinical observations of movement control tests.
The purpose of this study was to develop a statistical model, based on logistic regression analysis, to differentiate patients with NS-CLBP presenting a flexion-related MCI from healthy subjects. That is a hard task!
However we found it a somewhat confusing paper. It initially discusses the use of movement control tests to subgroup patients with chronic non-specific low back pain into flexion control impairments, extension control impairments, and rotation control impairments, or combinations of to all three of the above. They note that there is a link between pain being provoked by a particular direction of movement and deficiency in the muscles that have control of the movement.
The aim of this study was to develop an objective statistical method to differentiate patients with chronic low back pain who demonstrate flexion movement control impairments from healthy subjects, based on trunk muscle recruitment patterns measured by surface EMG.
They started with 116 subjects which reduced to 69 subjects with movement control impairments based on the Kinetic Control classification. They stated testing both in the Kinetic Control principles is very similar to the method used by O’Sullivan (2005), but offers a more structured evaluation model. They eventually ended up with 36 subjects with flexion related movement control impairments (flexion, flexion-rotation or multidirectional MCI with a dominant flexion pattern). There were 53 healthy controls.
All participants performed six movement control tests from the Kinetic Control system. They were asked to maintain a neutral lumbar spine alignment whilst performing specific movements of the limbs or trunk.
Seated uni- and bilateral knee extension
Standing uni-lateral hip extension
Seated uni-and bilateral shoulder flexion
Seated hip flexion
Surface EMG was placed on 4 trunk muscles:
2 deep stabilisers: lumbar multifidus (LMF) and internal abdominal oblique (IO) and two superficial torque producing mobilisers: iliocostalis lumborum thoracicis (ICLT) and external abdominal oblique (EO)
Normalised EMG ratios of stabiliser: mobiliser recruitment were calculated (IO/EO and LMF/ICLT)
Three tests appear to identify that patients with flexion related MCI can be distinguished from healthy subjects based on trunk muscle recruitment patterns. They stated that “this underlines that both in the clinical setting in research, the choice of exercises is very crucial to detect differences between populations”.
Tests 1 and 2 were predictive of identifying patients with flexion related MCI. They demonstrate that these patients have increased stabiliser muscle co-contraction (stabiliser > global mobiliser). The subjects demonstrate additional muscular stabilisation in order to maintain a neutral spine and to compensate for reduced spinal stiffness. Patients co-contract more flexor muscles than extensor muscles compared to controls. Patients appeared to have increased recruitment of lumbar multifidus and decreased recruitment of the external obliques to stiffen the spine in these two tests.
Asymmetry between right and left abdominal muscle recruitment ratios predicted increased likelihood of being the patient.
In contrast, test 3 demonstrated that higher recruitment ratios (indicating co-contraction) decrease the probability of being a patient. The authors suggested that this may be related to subjects being asked to maintain a neutral rather than usual sitting position.
There are some apparent discrepancies within how the Kinetic Control process of identifying the flexion movement control impairment would be done in the performance of these tests in this study.
Tests 1, 4, 5 and 6 are the tests that the Kinetic Control process would normally identify as a flexion control impairment of the lumbar spine. Tests 2 and 3 are tests that would normally be used to identify and extension control impairment (rather than flexion MCI).
Tests 4, 5 and 6 were not statistically related to predicting subjects who had back pain based on EMG co-contraction. However, it would have been really useful to know if during these tests the subjects failed to adequately prevent or control lumbar flexion occurring. Then there would have been decrease in posterior muscle EMG activity when the spine lost the ability to control or prevent lumbar flexion during the test movement.
In the Kinetic Control process, a flexion control impairment is identified or diagnosed by the failure to cognitively prevent or control the loss of a neutral position into uncontrolled flexion during the challenge of a movement control test. Objective measurement of movement kinematics to determine if recruitment co-contraction was linked to increased effort in order to maintain neutral during the challenge of a flexion control test or if failure of the ability to maintain neutral position resulted in a lack co-contraction.
If subjects demonstrated a flexion movement control impairment based on the Kinetic Control process, they would difficulty performing the tests in the study to the benchmark standards described. This would appear to be a point of confusion and possible conflict.
However, the positive message from this paper appears to be that patients with non-specific chronic low back pain demonstrate aberrant or excessive trunk muscle co-contraction in the attempt to maintain neutral spine alignment during the performance of a challenging movement of the limbs, or trunk. Also, significant asymmetry in recruitment patterns of the abdominal muscles appears to predict subjects who have non-specific chronic low back pain.
Thanks to Mark Comerford for his review