Repeated-measures ANOVAs for PTP results revealed no statistically significant main effects or interaction (“session” × “group”), indicating that acute pain or sham injection had no effect on the PTP score (Supplementary file 2, available online at http://links.lww.com/PAIN/A504). However, PTP increased in the experimental group from 31.46 mm (95% CI: 26.98-35.94.44) at baseline to 36.64 mm (95% CI: 31.02-42.21) during the second assessment (acute pain) with a trend for significance (F(1,54) = 3.19; P = 0.079; η2 = 0.06). No significant PTP change was observed in the sham-injection (F(1,54) = 0.46; P = 0.50; η2 = 0.01) and the control groups (F(1,54) = 0.10; P = 0.75; η2 = 0.01). Between-group planned comparisons did not reveal statistically significant differences (see Supplementary file 2, available online at http://links.lww.com/PAIN/A504 and Fig. 3).
Analysis of variance for TPE scores revealed a statistically significant effect of “session” (F(2,108) = 3.12; P < 0.05; η2 = 0.05). Within-group planned comparison tests did not reveal a significant difference between session 1 and 2 in the experimental group (F(1,54) = 0.06; P > 0.05; η2 = 0.00) and the sham-injection group (F(1,54) = 2.19; P > 0.05; η2 = 0.04). A significant decrease in TPE scores from 37.44 mm (95% CI: 25.91-48.97) at baseline to 27.24 mm (95% CI: 15.15-39.33) during the second assessment (acute pain) was noted only in the control group (F(1,54) = 5.37; P < 0.05; η2 = 0.09), indicating for a strong learning effect for the TPE task. The magnitude of this change was not significantly different from the magnitude observed in the experimental (F(1,54) = 2.14; P > 0.05; η2 = 0.04) and sham-injection groups (F(1,54) = 0.35; P > 0.05; η2 = 0.01) (Figures 3 and 4).
This study was aiming to address the hypothesis that the experience of pain leads to measurable change in tactile acuity within the primary hyperalgesic area. And indeed, the current data provide evidence that pain influences the precision of touch, yet the direction of this change was contrary to the stated hypothesis. Tactile acuity was not improved but deteriorated after the induction of acute, peripheral nociceptive low back pain. This effect, although significant only in the results of the TPD, was also noticeable in the additional, novel measures of tactile acuity. Reduced tactile acuity cannot be explained by repeated execution of TPD because it was absent in the control condition. Moreover, the effect size was significantly predicted by the perceived pain intensity according to the rule “the more severe the pain was, the more it impaired tactile acuity.” Interestingly, deterioration was not significant in the group exposed to the nocebo pain (sham-injection), although TPD results showed the same direction of change.
The current literature confirms that nociception and pain play a biological role in living organisms by triggering adaptive responses.10,52,54 Acute pain promotes healing and body protective behaviour. Lack of this protection, for example, in patients with congenital insensitivity to pain17,18 produces debilitating changes in homeostatic regulations and often leads to premature death. In humans, protection is ensured by motor,42 perceptual,70,71 hyperalgesic, and allodynic responses.10 As a consequence, non-noxious tactile stimuli delivered to an area of injury are perceived as painful, and objects related to noxious stimuli are perceived as being closer to the body than objects not associated with noxious stimulation.70,71 It was expected to observe a similar trend in other sensory functions, that is, tactile acuity. Intriguingly, these current results showed a seemingly contrary effect.
However, our results cannot be explained by peripheral mechanisms, only. In this study, a linear trend between experienced pain and the magnitude of tactile acuity change was elucidated. This is particularly interesting because all participants received the same volume of hypertonic saline solution, hence the same “amount” of nociception lead to a variety of subjective pain experiences. It is, therefore, concluded that peripheral nociception was not the exclusive mechanism to evoke tactile acuity changes. Instead, the perception of pain played a crucial role in that change. This perspective can be supported by 2 facts: first, the nocebo intervention (sham injection) triggered a similar pattern of tactile acuity changes as measured by the TPD test, the most popular measure of tactile acuity.1,11 It is possible that the trend would have become significant in a larger sample and with more convincing nocebo-like verbal suggestion, inducing long-lasting pain without damage. Second, TPD results returned toward normal when the pain had subsided (Fig. 3).
Our study is the first to show that nociceptive pain itself is the cause of altered tactile acuity. The results are robust. First, the required sample size was estimated for testing the main hypothesis by TPD test established as a primary outcome. As a result, experimental manipulation led to a statistically significant and strong effect (η2 ∼ 0.20). The effect cannot be attributed to the fact that the test was repeated over time, as the control group showed—although not significant—a trend toward a learning effect, which has been described in other studies utilizing TPD.23,47 Second, the experimental manipulation was successfully applied. Most participants experienced pain during the tactile acuity assessment. Third, the experimental procedure was performed with extreme caution and in a double-blinded manner: patients were not informed about the hypotheses tested, whereas the examiner was not informed about group allocation and the side affected by pain. Blinding was not used in prior case-control studies43,57,69,75; therefore, the effect in chronic pain populations, similar in magnitude (∼10 mm) to the effect observed in this study (7 mm), could have been overestimated. Fourth, a novel control (sham injection) paradigm was designed for the purpose of the current experiment. The hypothesis that tactile acuity can be changed even in the total absence of nociception is tempting. In the group exposed to sham injection, a small subgroup revealed a strong pain experience. It is highly likely, that, if the nocebo condition would be enhanced, for example, by adding verbal suggestion of strong hyperalgesia, the same significant change in tactile acuity as observed in the experimental group could be reached. Future studies need to address these issues and replicate current findings. Finally, the primary outcome was measured by reliable tools, especially by the TPD test. Hitherto, 4 independent studies confirmed high intrarater reliability of TPD test performed at the lumbar area around L3 or L5 spinal level.4,13,20,46
Based on these current findings, some implications for pain science and clinical practice should be acknowledged. Enhanced protection during acute pain is not reflected by improving tactile acuity, and future studies should account for the biological role of tactile acuity changes. Furthermore, sensory discrimination training, a therapy aiming to restore cortical maps, should be applied with caution until establishing a clear relationship between pain, tactile acuity, and cortical changes in CLBP and other chronic conditions; current findings question the mechanisms underlying cortical restoration as a mechanism leading to pain reduction in CLBP.74 Alternatively, if sensory discrimination training indeed reduces pain, it should be verified in acute as well as in chronic pain. Certainly, future studies should investigate tactile acuity not only in the experimental setting but also in clinical populations to enhance the generalizability of our results. In addition, the effect of the experimental procedure on tactile perception should be examined in a variety of pain models. For example, we only monitored changes located at the area of primary hyperalgesia. To complement this study, capsaicin-based models of widespread pain could be performed and tactile acuity should be monitored over time for longer time, in areas of referred pain as well as in the hyperalgesic area. Last, the observed difference in tactile acuity was relatively small probably due to the body part exposed to tactile acuity measurement and pain. Tactile acuity scores at the lumbar region are much higher than for other body locations, for example, hand or mouth.1,11 Therefore, it is more likely to observe a more pronounced effect in locations with relatively greater acuity at baseline.
The authors have no conflicts of interest to declare.
The authors would like to express special thanks to Professor Andrzej Małecki and Mrs Danuta Smykla from the Academy of Physical Education. Their help and support in purchasing the equipment (PinPrick device; MRC Systems GmbH, Germany), and realizing the whole project was outstanding and invaluable. Kindly thanks to the research group at the Laboratory of Movement Analysis (Academy of Physical Education) for help with laboratory equipment and special thanks to Tomasz Adamczyk (Logotech AA) for important intellectual contribution to the project and support during all stages of the study. This research did not receive specific funding, although it was performed as a part of a project funded by the Statutory Research Program for Young Researchers and PhD Students at The Jerzy Kukuczka Academy of Physical Education (grant No. AN-510-FMN-1/2016). Wacław Adamczyk is supported by a scholarship awarded within the grant 2014/14/E/HS6/00415 from the National Science Centre in Poland.
Supplemental digital content
Supplemental digital content associated with this article can be found online at http://links.lww.com/PAIN/A504.
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