Seventy to 85 percent of people experience low back pain (LBP) and yearly expenses due to LBP are estimated to total 100 billion dollars in the United States (Andersson, 1999
; Katz, 2006
). Although estimates vary based on the population sampled, up to 85% of people with LBP experience chronic, recurrent symptoms (Andersson, 1999
), demonstrating ineffective treatment for a large number of patients. Thus, we require a better understanding of the mechanisms that contribute to LBP in order to develop more effective rehabilitation strategies and improve treatment outcomes (Ebenbichler et al., 2001
LBP has been traditionally referred to in terms of mechanical changes to the spine and its surrounding tissues (Adams, 2004
). Alternatively, a ‘kinesiopathologic’ or ‘functional pathology’ model has recently been proposed, asserting that altered neural control of movement represents one possible mechanism for the development or persistence of chronic, recurrent LBP (Sahrmann, 2002
; Adams, 2004
; Langevin and Sherman, 2007
). This model theorizes that repeated movements and prolonged postures during everyday activities contribute to low back symptoms and pathology because these repeated movement patterns continually expose lumbopelvic musculoskeletal tissue to low-magnitude loading in the same manner, thereby accelerating either deconditioning through under-utilization or cumulative tissue stress and microtrauma through over-utilization. This pain-inducing trauma is then suggested to affect central sensory processing, which in turn, continues a cycle of aberrant movement patterns.
With regard to the altered neural functions hypothesized by the kinesiopathologic model, altered cerebrocortical processing of sensory input has been demonstrated, such that people with LBP exhibit an altered amplitude and spatial topography of cerebrocortical somatosensory-evoked potentials to painful or non-painful stimuli (Flor et al., 1997
; Wiech et al., 2000
; Schneider et al., 2004
; Siddall et al., 2006
; Diers et al., 2007
). Somatosensory-evoked potentials in response to pain stimuli are also modified by background muscle activation in participants with LBP, but not in participants without LBP, suggesting a change with LBP in the neural interactions of pain perception and motor output (Knost et al., 1999
). Changes associated with LBP in cerebrocortical motor physiology during self-initiated movements, however, remain unidentified.
In support of the kinesiopathologic model's assertion of altered motor control with LBP, patients with LBP exhibit altered patterns of postural coordination during voluntary movements (Hodges and Richardson, 1999
; Kuriyama and Ito, 2005
; Shum et al., 2005a, 2005b; Kiesel et al., 2007
; Mok et al., 2007
), and behavioral modification of a patient's coordination patterns often decreases or eliminates that patient's symptoms of LBP compared to when performing the movements with self-selected coordination patterns (Van Dillen et al., 2007
). In addition, people with LBP exhibit postural instability during challenging tasks of stance posture (Mok et al., 2004
; Cacciatore et al., 2005
; Leitner et al., 2007
; Popa et al., 2007
) and in response to externally induced perturbations to posture (Henry et al., 2006
). The timing of muscle responses to postural perturbations has also been shown to predict future low back injury (Cholewicki et al., 2005
). Despite this evidence to support the kinesiopathologic model, we are not aware of any studies that directly recorded changes in cerebrocortical motor physiology due to LBP during self-initiated voluntary movement. Thus, it remains necessary to determine whether changes in movement coordination associated with LBP also associate with changes in central motor neurophysiology in order to further validate the kinesiopathologic model.
Hodges and Richardson (1996
reported that patients with LBP exhibit delayed anticipatory postural adjustments (APAs) of the abdominal muscles during cued voluntary arm raises. APAs are defined as muscle activations within supporting body segments to stabilize and facilitate a voluntary limb movement against the anticipated perturbing forces resulting from the limb movement. The study of APAs provides unique insight into the central neural control of posture because APAs arise prior to when the perturbing forces resulting from the impending movement actually occur, thereby suggesting that APAs are pre-programmed by the central nervous system (Massion, 1992
). Specific regions of the central nervous system involved in generating APAs include the supplementary and primary motor cortex (Viallet et al., 1992
). Thus, delayed APA activity during movement in patients with LBP provides indirect support for the kinesiopathologic model's assertion that altered cerebrocortical motor physiology contributes to LBP.
Additional studies investigating the APAs of people with LBP demonstrated that their delayed APAs represent changes in coordination strategies rather than pain interference (Moseley and Hodges, 2005
) or delayed neural transmission (Hodges, 2001
). Further, people with LBP exhibit decreased anticipatory lumbopelvic movement in preparation for arm raises, which associates with increased spinal displacement during the arm raise (Mok et al., 2007
). Therefore, in support of the kinesiopathologic model, chronic LBP associates with delays in the timing of APAs that are centrally generated and changes in preparatory lumbopelvic coordination that result in increased spinal displacements that would presumably accelerate cumulative tissue stress and microtrauma with repetition (Langevin and Sherman, 2007
Pre-activation of the abdominal muscles during arm raises, however, is not always evident in people without a history of LBP, thereby causing uncertainty regarding the functional relevance of delayed APAs with LBP (Allison and Henry, 2002
; Marshall and Murphy, 2003
); could abdominal activation after movement onset in people without a history of LBP predispose those individuals to future LBP, or does it suggest a lack of necessity for pre-movement abdominal activation in order to maintain a life without LBP? Although inter-individual and inter-trial variability in APA onset latencies represent hallmarks of the behavior for people without a history of LBP, it should be noted that inter-trial variability decreases with both a history of chronic LBP and in response to experimentally induced LBP (Moseley and Hodges, 2006
; Jacobs et al., 2009
). In addition, the timing of the abdominal activation related to the APA correlates with the extent to which the area of that muscle's representation within the motor cortex becomes remodeled in people with LBP (Tsao et al., 2008
). Thus, the change in APA onset latency appears to represent a functionally relevant change in central motor control related to the experience of LBP. This study, therefore, seeks to provide a correlation analysis in order to understand the mechanisms of the inter-individual variability that remain so enigmatic yet potentially important to our understanding of chronic LBP.
Although observations of delayed, less-variable APAs and related changes in motor neuroanatomy provide indirect evidence for an altered central neural control of movement with chronic LBP, no direct measures of central neurophysiology have been recorded to confirm the hypothesis that LBP associates with altered central motor control during self-initiated voluntary movement. The Bereitschaftspotential (BP) – a pre-movement electroencephalographic (EEG) potential characterized by a negative shift in the EEG signal before voluntary movements – represents a measure of cerebrocortical motor physiology related to movement preparation (Kornhuber and Deecke, 1964
; Shibasaki and Hallett, 2006
). In addition, the neural generators of the BP include the supplementary and primary motor cortex (Shibasaki and Hallett, 2006
), thereby implicating the supplementary and primary motor cortex in the generation of both the BP and the APA. In support of this overlapping neurophysiology of the BP and the APA, the amplitude of the BP increases at electrodes overlying the supplementary and primary motor cortex when (1) the EEG signal is time-locked to the onset of the APA rather than to the prime movement (Saitou et al., 1996
), and (2) the BP is compared between a movement that requires an APA to a movement that does not require an APA (Yoshida et al., 2008
). In addition, transcranial magnetic stimulation of the primary motor cortex just prior to the onset of an APA (that is, when a BP would have presumably been evident) selectively facilitates the motor evoked potentials of a muscle used as part of the APA, but not of a muscle used as part of the goal-directed limb movement (MacKinnon et al., 2007
). Thus, cerebrocortical motor preparation and, therefore, components of the BP likely relate specifically to the preparation of the APA. The BP would, therefore, provide insight into whether the delayed APAs that are evident with LBP associate with changes in central motor neurophysiology.
In addition to the BP, event-related desynchronization (ERD) of EEG signals within alpha (8- to 13-Hz) frequencies provides another measure of movement-related cortical activation. Alpha ERD is defined by a decrease in alpha power just prior to movement onset (Neuper et al., 2006
). Alpha ERD is coincident with increased cortico-cortical and cortico-spinal excitation of sensory-motor cortex (Rau et al., 2003
), suggesting that alpha ERD represents cerebrocortical activation. When defined by the upper frequencies within the alpha band, alpha ERD exhibits a spatial topography that is specific to the somatotopic representation of cortex relevant to the movement task (Pfurtscheller et al., 2000
). The BP and alpha ERD, however, exhibit different spatio-temporal characteristics, suggesting they are not two measures of the same underlying motor process (Babiloni et al., 1999
; Shibasaki and Hallett, 2006
). Although we are unaware of any studies examining alpha ERD in patients with chronic LBP, alpha ERD has been shown to increase when a movement is expected to correspond with an experimentally-induced painful stimulus, and alpha ERD amplitudes predict a participant's subsequent evaluation of the stimulus-induced pain intensity (Babiloni et al., 2005
). Therefore, in addition to investigating changes in the BP in people with chronic LBP, analyzing the alpha ERD may also provide insight into potential LBP-related changes in cerebrocortical motor neurophysiology.
The kinesiopathologic model of LBP remains untested regarding whether altered movement patterns represent a pre-existing condition for the development of LBP or if such changes in motor control simply contribute to the persistence or recurrence of LBP after an initial injury. The latter contribution, however, remains important for discerning why some individuals develop chronic LBP while others do not, and is supported by observations that (1) normalizing the altered movement patterns performed by people with chronic LBP decreases or resolves the movement-induced LBP (Van Dillen et al., 2007
), and (2) altered motor patterns remain evident from people with a history of LBP who do not exhibit pain at the time of testing (Hodges and Richardson, 1999
; Jacobs et al., 2009
) as well as when people without a history of LBP perform several trials after the cessation of acute, experimentally induced LBP (Moseley and Hodges, 2005
). Thus, the kinesiopathologic model would support the hypothesis that people with chronic LBP exhibit altered cerebrocortical motor neurophysiology consequent to long-term changes in postural coordination that persist independent of pain state but which contribute to the persistence or recurrence of pain.
To test the hypothesis that chronic LBP associates with altered cerebrocortical motor neurophysiology, we recorded the BPs, alpha ERD, and APAs of participants with and without LBP during voluntary, self-initiated arm raises. We predicted that participants with LBP would exhibit delayed APAs (Hodges and Richardson, 1996
), altered BP amplitudes, and significant alpha ERD at electrodes overlying not only sensory-motor cortex of muscles activated for the arm movement, but also at those overlying the muscles activated for the APA. We further predicted these changes would be independent of the participants' pain state, as these changes in motor control likely represent long-term adaptive changes in motor strategy, as opposed to a temporary modification in response to current pain. Identifying changes in cerebrocortical motor physiology in people with LBP would validate a potential paradigm shift in the assessment and management of LBP to focus on aspects of motor control impairments in addition to the impairments of the lumbopelvic musculoskeletal structures. Such a paradigm shift would stimulate further study to investigate the effects of targeted movement re-education in order to improve treatment outcomes.