Low back pain associates with altered activity of the cerebral cortex prior to arm movements that require postural adjustment

Abstract

Objective: To determine whether low back pain (LBP) associates with altered postural stabilization and concomitant changes in cerebrocortical motor physiology.

Methods: Ten participants with LBP and 10 participants without LBP performed self-initiated, voluntary arm raises. Electromyographic onset latencies of the bilateral internal oblique and erector spinae muscles were analyzed relative to that of the deltoid muscle as measures of anticipatory postural adjustments (APAs). Amplitudes of alpha event-related desynchronization (ERD) and of Bereitschaftspotentials (BP) were calculated from scalp electroencephalography as measures of cerebrocortical motor physiology.

Results: The APA was first evident in the trunk muscles contralateral to the arm raise for both groups. Significant alpha ERD was evident bilaterally at the central and parietal electrodes for participants with LBP but only at the electrodes contralateral and midline to the arm raise for those without LBP. The BP amplitudes negatively correlated with APA onset latencies for participants with (but not for those without) LBP.

Conclusions: Cerebrocortical activity becomes altered prior to arm movements requiring APAs for individuals with chronic LBP.

Significance: These results support a theoretical model that altered central motor neurophysiology associates with LBP, thereby implying that rehabilitation strategies should address these neuromotor impairments.

Fig. 1

The relative timing of the selected dependent measures. Traces represent a representative participant's average traces, low-pass filtered to 15 Hz for illustration. The top trace represents an average EEG voltage signal from the Cz electrode, demonstrating the epochs in which mean alpha power and mean BP amplitudes were calculated. This trace is illustrated relative to the timing of activation onset for the deltoid (DELT), internal oblique (IO), and erector spinae (ESP) muscles. These muscle onset latencies appear similar only due to the lengthened time scale.

Fig. 2

Mean EMG onset latencies for each group. The left chart illustrates the EMG activation of the DELT, IO, and ESP muscles from an example trial of a participant without LBP. The solid, black vertical line denotes the onset of the DELT muscle. The right chart illustrates the group mean (± 95% CI) EMG onset latencies of the IO and ESP muscles contralateral (contra) and ipsilateral (ipsi) to the arm movement for the participants with LBP (gray bars) and those without LBP (open bars).

Fig. 3

Grand mean Bereitschaftspotentials (BPs) for each group and electrode location. The top panel illustrates the grand mean EEG waveforms for participants with LBP (thick, gray traces) and those without LBP (thin, black traces) at each analyzed electrode location, with the Fc and Cc electrodes contralateral to the arm movement and the Fi and Ci electrodes ipsilateral to the arm movement. The bottom, left chart expands the traces from the Cz electrode to better illustrate the BP potential from its location of maximal amplitude as well as to illustrate the final 100 ms prior to the onset of the contralateral IO muscle (gray bar) from which mean BP amplitudes were derived for each participant. The bottom, right chart illustrates the grand mean (± 95% CI) BP amplitudes from the Cz electrode for the participants with LBP (gray bar) and those without LBP (open bar).

Fig. 4

Associations among EMG onset latencies and BP amplitudes. The scatter plots illustrate the associations among the participants' IO and ESP muscle onset latencies with their mean BP amplitudes for those with LBP (left column) and those without LBP (right column). Circles denote values of individual participants and the solid lines denote the best-fit lines. The R-values represent the Spearman's correlation coefficients, and the P-values represent the Bonferroni-corrected levels of significance. Axes were kept constant to facilitate comparisons between the participant groups but differ for each muscle.

Fig. 5

Alpha event-related desynchronization (ERD) at central electrodes for each group. The 2-dimensional shaded graphs demonstrate each group's grand mean of morlet coefficients (lighter shades illustrate higher coefficients; darker shades, lower coefficients) across the morlet scales within the alpha frequencies of 8-13 Hz (vertical axis; which has been reversed to reflect the pseudo-frequencies of the morlet output rather than the scales of the morlet output) over the 2000 ms that preceded activation of the contralateral IO muscle (horizontal axis). Color scales are equal for both groups. The Cc electrode represents the electrode contralateral to the arm movement; the Ci electrode, ipsilateral to the arm movement. The line charts illustrate each group's mean (standard deviation) binned and baseline-normalized alpha coefficients across the three central electrodes and the four successive 500-ms intervals that preceded activation of the contralateral IO muscle. The lines have been horizontally offset to facilitate visualization of each line.