Experimentally induced LBP elicited altered postural coordination during and after the experience of pain, and this altered coordination associated with CNV amplitudes. Specifically, the Pain condition elicited smaller peak forces, longer movement times, and altered hip motion during the sit-to-stand movement, similar to previous reports on people with chronic, recurrent LBP (Gioftsos and Grieve 1996
; Simmonds et al. 1998
; Shum et al. 2005a
). These movement modifications exhibited in the Pain condition concomitantly occurred with increased self-reported anxiety to perform the sit-to-stand movement. A post-hoc exploratory analysis revealed that amplitudes of CNV potentials at the C4 electrode increased during the Pain condition compared to the NoPain1 condition, but no significant effects of condition on CNV amplitudes were evident when analyzed by the omnibus statistic. As expected, the group exhibited high inter-individual variability in both motor and neurophysiologic responses to the induced LBP. Amidst the high inter-individual variability that prevented a significant pain-related change in the CNV response across the group, however, the participants’ CNV amplitudes in the Pain condition exhibited moderate to very high coefficients of determination with multiple pain-related changes in movement parameters. The CNV amplitudes exhibited in the Pain condition also moderately associated with the extent that movement parameters were modified from before to after the pain experience. The CNV potential, therefore, provides a neurophysiologic correlate for changes in postural coordination associated with an acute LBP experience.
The pain-related increase in CNV amplitude at the C4 electrode (located on the dorsolateral convexity overlying the sensory-motor and premotor cortex) was not as we predicted; we predicted changes to occur at the Cz electrode, where the CNV potential exhibited its maximal amplitude and is somatotopically localized over the task-relevant leg and trunk region of the sensory-motor cortex. Asymmetric pain-related increases in CNV amplitude, however, have been previously reported at the C4 electrode, but the previous study examined a model of induced pain and motor responses at the finger (Babiloni et al. 2004
), rendering it unclear whether the lateral asymmetry reflected the motor characteristics of the task and the somatotopic organization of the sensory-motor cortex rather than somatotopically non-specific pain-associated activity. The increase at the C4 electrode in this study, however, would not likely reflect activation of the arm or hand region, or be asymmetric, because this study’s sit-to-stand task primarily involved bilateral function of the legs and trunk and utilized a bilateral pain stimulus to the low back.
Although speculative and requiring further study for confirmation, the pain-related increase at C4 may reflect activity similar to other reports of right-hemisphere lateralized cortical activity, such as (1) non-motoric right-hemisphere lateralizations of the CNV potential that represent covert shifts in attention (Van ’t Ent and Apkarian 1998
), (2) right-hemisphere cerebral hemodynamic responses to induced pain stimuli that depend on the individual’s attention to the painful stimulus (Peyron et al. 1999
), and/or (3) the right-hemisphere cerebral hemodynamic responses of the lateral premotor and dorsolateral prefrontal cortex during the inter-stimulus interval between a warning cue and a pain stimulus (similar to a CNV paradigm; López-Solà et al. 2010
). In addition, the pain-related changes in pre-movement EMG activity or movement patterns associated with CNV amplitudes may also function to alter the perception of pain during the sit-to-stand movement (Le Pera et al. 2007
). Whether this study’s observed changes in CNV potentials at the C4 electrode during the Pain condition reflect these mechanisms, however, remains uncertain.
It is important to recognize that the C4 electrode’s increased CNV amplitudes during the Pain condition were identified by a post-hoc paired-t test and not by the omnibus statistic. This result must, therefore, be considered exploratory due to the increased chance of a Type I error. Because, however, the pain-related changes in sit-to-stand behavior predicted these CNV amplitudes to a coefficient of determination equal to 0.95, we believe it is unlikely that the pain-related increase in CNV amplitudes at the C4 electrode represent a chance phenomenon.
As noted in the introduction, the CNV potential relates to the anticipation of the stimuli and motor task, sensory-motor status prior to the imperative stimulus, and motor preparation for the response (Kok 1978
; Haagh and Brunia 1985
; van Boxtel and Brunia 1994
; Pfeuty et al. 2008
), representing activation of a widespread cortical network (Lamarche et al. 1995
; Hamano et al. 1997
; Bares et al. 2007
). The stepwise regression analyses identified both pre-movement changes in muscle activation as well as sit-to-stand kinematic and kinetic response characteristics as significant independent predictors of CNV amplitudes, suggesting any or all functional aspects of the CNV potential may have been affected in the Pain condition. Thus, further research is warranted to disentangle the functional role of the CNV potential in relation to the modification of movement patterns associated with acute LBP.
To account for methodological considerations, it is possible the changes in CNV amplitudes in the Pain condition simply reflect the slowed velocity of the sit-to-stand movements, rather than the more complex motor modifications known to accompany LBP. We believe it is highly unlikely the pain-related changes in CNV amplitudes solely reflect a slower pace of movement, however, because: (1) previous comparisons of CNV amplitudes between movement conditions of slow and fast velocity demonstrated decreased CNV amplitudes with decreased velocity (Grünewald et al. 1979
), whereas this study demonstrated increased CNV amplitudes in the Pain condition that elicited longer movement times, and (2) only one of the stepwise regression models identified movement time as a significant predictor of CNV amplitudes and all models included other variables of force output or joint motion as significant predictors of CNV amplitudes independent of movement time.
In addition, the generalizability of this study’s results should be tempered on the basis that electrocutaneous stimulations might not accurately model the pain experience of chronic, recurrent LBP. We argue, however, that this model of painful electrocutaneous stimulation to the low back has previously elicited changes in postural coordination that parallel those demonstrated by people with chronic, recurrent LBP (Hodges and Richardson 1999
; Moseley and Hodges 2005
; Moseley and Hodges 2006
; Jacobs et al. 2009
), and this study’s results likewise elicited changes in coordination during the sit-to-stand task exhibited by people with a history of chronic, recurrent LBP (Gioftsos and Grieve 1996
; Simmonds et al. 1998
; Shum et al. 2005a
). In addition, experimentally induced LBP and clinical pain populations exhibit changes in cerebral activation within many shared regions (Peyron et al. 2000
). Despite these arguments, some differences appear to exist between the cerebral hemodynamic responses associated with the experience of spontaneous pain in a chronic LBP population and those associated with experimentally induced LBP (Baliki et al. 2006
). Further, although induced pain elicits changes in CNV amplitudes prior to movement (Stude et al. 2003
; Babiloni et al. 2004
; Babiloni et al. 2005
), people with chronic LBP do not exhibit consistent differences in pre-movement cortical potentials such as the CNV or bereitschaftspotential (although, similar to this study, inter-individual differences in the bereitschaftspotential correlated with differences in postural coordination) (Tandon and Kumar 1996
; Jacobs et al. 2010
). Nevertheless, the results provide insight into how an acute LBP experience could elicit changes in movement patterns that are also exhibited by people with a history of chronic, recurrent LBP.
In summary, the present study demonstrates that acute, experimentally induced LBP elicits modifications in sit-to-stand movement patterns similar to those reported for people with chronic, recurrent LBP, thereby further supporting the face validity of this induced-pain model for study on LBP. In addition, this study identified the CNV potential as a neurophysiologic correlate for modified sit-to-stand behavior associated with acutely induced LBP. Thus, future studies investigating the effects of acute LBP on the CNV potential and motor coordination have promise to improve our understanding of the neurophysiologic mechanisms that govern the long-term behavioral changes in movement patterns associated with LBP.