A significant interaction between time and group was observed for all 3 psychological variables assessed (P < 0.001). Post hoc tests showed that pain self-efficacy and pain catastrophising significantly improved (ie, PSEQ increased and PCS decreased) in both LBP groups from baseline to 2 months (P < 0.001) and, in the persistent LBP group, further improvement was shown from 2 to 4 months (P = 0.043). However, the persistent LBP group had significantly lower levels of pain self-efficacy and higher levels of pain catastrophising compared with the recovered LBP at all time points (P < 0.047) (Fig. 2). Depression, anxiety and stress (DASS-21) scores were low and in the normal range in all 3 groups. Post hoc tests showed that DASS-21 scores significantly decreased in recovered LBP from baseline to 2 and 4 months (P < 0.004) and in persistent from baseline to 2 months (P = 0.011). A significant difference was observed between the LBP groups and the pain-free controls at baseline (P < 0.044), but no significant differences were observed between groups at 2 and 4 months.
Longitudinal data for QST variables at 3 time points and linear mixed-effect model analyses are reported in Table 4.
No significant interaction between time and group was found for WUR at both sites (P > 0.05). No significant main effects for time and for group were observed (P > 0.02) after removing the interaction term. The z-score plots (Fig. 3) illustrate that compared with the recovered LBP group, the persistent LBP group shows a trend towards an increase in WUR at the hand between baseline and 2 months, with a further increase at 4 months, then reaching a difference of 2 SDs from controls.
There was no significant interaction between time and group for the cold pressor test (P = 0.017). No significant main effects for time and for group were observed (P > 0.05) after removing the interaction term.
There was no significant interaction between time and group for the CPM response (P = 0.251). No significant main effects for time and for group were observed (P > 0.05) after removing the interaction term (Fig. 4).
This exploratory study is the first to report the time course of somatosensory function in an inception cohort of acute LBP followed up until 4 months. A comprehensive QST protocol encompassing static and dynamic tests was used, and longitudinal changes in pain-related psychological factors were concurrently evaluated.
The main finding of this study was that an increase in mechanical pain sensitivity was observed in the persistent LBP group, suggesting potential underlying changes in the nervous system sensitivity occurring in the subacute stage. Specifically, an increase in pressure pain sensitivity was seen between 2 and 4 months; and an earlier trend towards increased temporal summation was identified between baseline and 2 months, and 2 to 4 months, at which point it exceeded 2 SDs beyond the pain-free control reference value (although not reaching statistical significance). In addition to the temporal changes in mechanical sensitivity in the persistent LBP group, a gain in cold pain sensation was observed in the recovered LBP group from baseline to 2 months, which normalised from hypoesthetic to the pain-free values by 2 months.
At baseline, pressure pain tests were similar between groups, which aligns with results from a previous prospective study in acute LBP48 and other studies that reported no differences in PPT between acute LBP and healthy controls.38,39 When the z-score plots (Fig. 3B) are examined, it is evident that the pressure pain sensitivity of the 2 LBP groups diverges, with the persistent LBP group significantly increasing over time (particularly at the back). By 4 months, these differences between persistent and recovered groups are significant. A similar increase in pressure pain sensitivity at the back has been reported in cross-sectional studies in subacute LBP.10,11 Enhanced responses to localised pressure pain testing may reflect underlying sensitisation of primary afferent nociceptors through the release of neuromediators such as neurotrophins and cytokines18 as well as the recruitment of silent nociceptors after persisting stimulation.54 Reduced PPT has been associated with functional disturbances in lumbar spine muscle activity in people with LBP,9 which may contribute to ongoing pain.
A significant decrease in PPT was also detected at the remote site at the hand in the persistent LBP group, although this was within 1 SD of the healthy control values and the differences between the LBP groups were not statistically significant. It is possible that widespread changes in pressure pain sensitivity become more evident in people with longer LBP duration1,5,15,16,37 whereby increases in central nervous system excitability are more likely to have been established. However, it has been recently shown that generalised changes in pressure sensitivity do not occur uniformly in chronic LBP, but are selectively associated with LBP subgroups14,43,53 which, interestingly, report more disturbed clinical and psychological profiles.
Nonetheless, it is important to note the tendency for PPT to significantly decrease over time (ie, control values reduce from baseline to 2 months, P < 0.02). This phenomenon of a systematic decrease in PPT in pain-free controls has previously been reported, particularly between the first and the second measurements.24 This emphasises the importance of longitudinal comparative analyses with pain-free controls to identify potential clinically meaningful differences.
The increase in temporal summation (WUR) at the hand in the persistent LBP group during the 4-month period is noteworthy, given that it was 2 SDs higher than the mean control value. The failure to reach statistical significance may be due to the relatively large variance, particularly in the persistent LBP group.
To the best of our knowledge, only one published study has reported on a range of QST variables in acute LBP (≤4 weeks from onset) using a prospective study design48 with QST performed at baseline. These authors reported that generalised hyposensitivity to thermal (non-noxious) stimuli, as well as enhanced temporal summation at the hand (but not at the back) measured in acute LBP, differentiated people who had not recovered at 6 months from those who had. Unlike in the study by Starkweather et al.,48 we did not find any differences in temporal summation (WUR) between the LBP groups at baseline; however, we identified a trend towards an increase in WUR amplitude in the persistent LBP group at the subacute stage. Two other cross-sectional studies have shown early enhancement of temporal summation in people with acute LBP (<4 weeks duration) compared with healthy controls,31,49 demonstrating that, in some subgroups of people with LBP, central hyperexcitability may be detected in the very early stages of LBP.
Among the thermal pain tests (cold and heat) including the cold pressor test, only the CPT showed a differential change over time (Fig. 3A) with CPT at the hand significantly increasing (return to normal) in the recovered LBP group from baseline to 2 months. However, although this change was statistically significant, the magnitude of CPT change (within 1 SD of pain-free controls) is unlikely to be clinically meaningful.
This study provides the first data on tactile acuity in acute LBP as well as serial measures over time, until the onset of chronic LBP. The results showed no differences in TPD threshold between the 2 LBP groups and the controls, suggesting that in this cohort tactile acuity was not impaired in the acute, subacute, or early chronic LBP phases. However, there was a small, but significant decrease in TPD threshold over time, indicating an improvement in tactile acuity, although these changes were within the measurement error range.4 The significance of this change is unclear, although a learning effect may have contributed. A previous systematic review has demonstrated a relatively consistent presence of altered tactile acuity in chronic LBP, particularly when measured at the area of greatest pain.3 Studies included in the review investigated people with longstanding chronic LBP (eg, from 30 to 108 months) and may reflect functional changes that develop over longer periods, compared with the maximum 4-month duration of LBP in our study. The lack of changes in tactile acuity in our study may also be due to the fact that the measurement was performed at a standardised site at the back (L3), rather than the most painful site, due to the need to maintain blinding of assessor.
Our result that those with acute LBP had a significant CPM effect that did not differ from pain-free controls adds to the limited literature on this topic. Two previous reports of CPM in acute LBP (<6 weeks' duration) also found no significant differences in CPM effect from controls.35,59 It has been suggested that ongoing persistent pain may impair the balance in descending spinal cord modulation reducing CPM inhibition and/or increasing facilitation.41 However, the literature reporting changes in CPM in chronic LBP is sparse and somewhat conflicting with some studies reporting altered pain inhibition5,42 and others showing no difference in CPM effect25,35,58 compared with controls. In other chronic pain conditions such a fibromyalgia or headache, CPM dysfunction has been more consistently documented.28 The current longitudinal analysis did not find changes in descending pain inhibition with LBP persistence, at least in the early months in this study sample. However, in light of the methodological variability of CPM testing,41 it is also not possible to exclude that the test was unable to detect changes if they did exist.
Of interest was that the only measures that differentiated the persistent from recovered LBP groups at baseline were psychological measures of self-efficacy (PSEQ) and pain catastrophising (PCS). Clinically significant lower self-efficacy scores were noted at baseline for the persistent LBP compared with the recovered LBP group (baseline PSEQ [SD] = 32.2 [5.8] mild impairment and 52.3 [3.0] minimal impairment, respectively [Electronic Persistent Pain Outcomes Collaboration, https://ahsri.uow.edu.au/eppoc/resources/index.html]). This would suggest that even mild PSEQ impairment may be noteworthy at baseline in acute LBP.
Psychological distress and pain-related cognitions both reduced over time in both LBP groups, although significant differences between the 2 groups were maintained at all time points. The improvements in pain-related psychological variables, particularly in the persistent LBP group align with the concurrent reduction of pain severity and disability levels (measured by RMDQ) observed at all 3 time points assessed (Table 3). This may reflect the fact that our sample was primarily community-based with relatively low initial levels of psychological distress and inherently greater capacity to cope with, and adapt to, pain over time.
The strengths of this study are that established protocols were used for multimodal QST testing by a single DFNS-trained assessor; that we were able to assemble and follow-up an inception cohort of people at as early as 3 weeks from onset of LBP; and that we reduced bias by blinding the investigator to participants' condition.
The following limitations of the study are acknowledged: first, the sample size was relatively small; so, we may have been underpowered to detect statistically significant differences between groups at different time points, particularly for some QST measures. Nonetheless, the results from this novel time series provide insights into longitudinal changes, which will be valuable for the design and conduct of future research. Second, although the recruitment strategy aimed to target both primary care clinics and the community, most of the people were recruited from the community. Therefore, these results are most relevant to people not seeking care for LBP.
The results of this exploratory study suggest that to understand the role of somatosensory changes in the development of acute to persistent LBP, mechanical pain tests (ie, PPT and temporal summation) are variables of potential significance to further investigate. The fact that higher levels of pain-related cognitions at baseline distinguish persistent LBP from the recovered LBP groups emphasizes the importance of concurrent evaluation of psychological contributors, in particular confidence to manage pain (self-efficacy) and pain-related worries (catastrophizing). In future studies of samples seeking care for LBP, psychological factors such as depression and anxiety (which were not observed at clinical levels in this community sample) would also be important to assess. Although changes in endogenous pain modulation continue to be of great interest, efforts need to first focus on the standardisation of a CPM protocol to improve the reliability and interpretability of the test.
The authors have no conflict of interest to declare.
The study was supported by a 2016 Macquarie University NHMRC Accelerate Safety Net Grant to J.M. Hush and by the Centre of Physical Health in the Department of Health Professions (Macquarie University). A. Marcuzzi was supported by a Macquarie University International Excellence Research Scholarship.
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