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Tactile acuity (dys)function in acute nociceptive low back pain: a double-blind experiment

Adamczyk, Wacław M.a,b,*; Saulicz, Oskarc; Saulicz, Edwarda; Luedtke, Kerstina,d

doi: 10.1097/j.pain.0000000000001110
Research Paper
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Research shows that chronic pain is related to cortical alterations that can be reflected in reduced tactile acuity, but whether acute pain perception influences tactile acuity has not been tested. Considering the biological role of nociception, it was hypothesized that nociceptive pain will lead to a rapid improvement in tactile acuity and that this effect is correlated with pain intensity and pain distribution. In this randomised double-blind controlled experiment (trial no. NCT03021278), healthy participants were exposed to 1 of 3 experimental conditions: acute, nociceptive low back pain induced by saline injection, a sham injection (without piercing the skin) potentially inducing nocebo pain, or no intervention. Tactile acuity was measured by a battery of tests, including two-point discrimination threshold (TPD), before, during the pain experience, and after it subsided. We found that TPD did not improve but deteriorated during pain induction in the experimental group compared with the control group (P < 0.001; η2 = 0.20) and changed from 56.94 mm (95% confidence interval: 53.43-60.44) at baseline to 64.22 mm (95% confidence interval: 60.42-68.02) during the pain experience. Maximum reported pain was a significant predictor (β = 0.55, P = 0.01) and accounted for 26% of the variance in TPD (P < 0.05). Other tests, point-to-point test and two-point estimation task, changed with a similar trend but did not reach significance. We concluded that acute, nociceptive pain does not improve but deteriorates tactile acuity linearly. The biological role of the observed phenomenon is unknown, and therefore, future studies should address this question.

Supplemental Digital Content is Available in the Text.Tactile acuity deteriorated under acute low back pain. The findings suggest that pain perception rather than cortical reorganisation play a crucial role in tactile acuity deterioration.

aDepartment of Kinesiotherapy and Special Methods in Physiotherapy, The Jerzy Kukuczka Academy of Physical Education, Katowice, Poland

bPain Research Group, Institute of Psychology, Jagiellonian University, Kraków, Poland

cRegional Specialised Hospital No. 4, Bytom, Poland

dDepartment of Orthopedics/Physiotherapy, University of Luebeck, Luebeck, Germany

Corresponding author. Address: The Jerzy Kukuczka Academy of Physical Education, ul. Mikołowska 72B, 40-065 Katowice, Poland. Tel.: (+48) 32 2075318. E-mail address: w.adamczyk@awf.katowice.pl (W. M. Adamczyk).

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.painjournalonline.com).

Received August 04, 2017

Received in revised form October 17, 2017

Accepted October 27, 2017

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1. Introduction

Available data support the view of chronic low back pain (CLBP) as a condition mediated by changes in the brain. Indeed, the body of evidence suggests that CLBP is associated with central nervous system (CNS) alterations occurring as a result of neuroplasticity.37,53,76 It has been shown that cortical reorganization includes shifted functional representation of the back in the somatosensory cortex,24 reduced gray5,65 and white matter8,9 volumes, enhanced responsiveness to tactile24 and noxious stimuli in the sensory cortex,26 decreased activation of pain-inhibitory pathways,25 and lower activation thresholds for spinal reflexes.73 Interestingly, some of these alterations seem to be related to clinically observable features such as reduced tactile acuity, typically measured as the two-point discrimination threshold (TPD).1,11,60,61

A recent systematic review and meta-analysis on tactile acuity in patients with low back pain and healthy controls1 resulted in 3 general conclusions: first, patients with CLBP had reduced tactile acuity compared with pain-free controls; patients needed an approximately 1 cm larger distance between 2 tactile stimuli to be able to perceive them as 2 separate points. Second, almost all studies defined their CLBP population as “nonspecific.” This implies that pain mechanisms underlying altered tactile acuity remain unknown. Third, the systematic search revealed a knowledge gap regarding tactile acuity in acute spinal pain. Interestingly, tactile acuity has never been investigated in any acute low back,1,11 acute neck,45 and—to the best of our knowledge—other pain states.

Investigating tactile acuity in an early phase of pain may lead to a better understanding of the development of CLBP and of the mechanism underlying tactile acuity alterations. Furthermore, it can answer the question whether long-lasting pain or pain per se is critical for the precision loss in the tactile sense. A previous attempt to identify a relationship between the duration of CLBP and tactile acuity failed,11 probably because only data from chronic pain populations were available at the time. Evoking non-neuropathic pain in a laboratory setting can also provide a deeper insight into the role of nociception in the processing of tactile acuity. If the pain itself produces changes in the structure and function of the CNS,29,62,63,68 it is reasonable to assume that tactile acuity is diminished even in acute pain. Biologically, however, it is unlikely that nociceptive input would produce such unfavorable changes within the brain.55 The pervading view of nociception assumes that it is an adaptive transmission of danger cues into the CNS10,52 exhibiting neuroplastic changes such as enlargement of receptive fields at the spinal level.56,77 Thus, tactile acuity should be improved not deteriorated in acute pain states. Such adaptation would enable a more precise localization and recognition of threat or danger.70,71

In this randomised controlled study, participants were exposed to 1 of 3 experimental conditions: acute, nociceptive pain induced by saline injection, a sham injection (without piercing the skin) potentially inducing nocebo pain, or no intervention. Tactile acuity was investigated before, during the pain experience, and after it subsided. It was hypothesized that nociceptive pain will lead to a rapid improvement in tactile acuity and that this effect is associated with pain-related variables such as pain intensity and pain distribution. It was also hypothesized that sham injections will have a similar but less pronounced effect.

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2. Methods

This study was performed at the Academy of Physical Education in Katowice. The design of the study was established a priori according to a preregistered protocol (NCT03021278). The study was conducted in accordance with the Declaration of Helsinki, and its protocol was approved by the local Bioethics Committee. Data were reported according to the CONSORT checklist.49

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2.1. Participants

Seventy healthy male participants (age between 18 and 35 years) were recruited for the purpose of this study. Participants were excluded if they were left-handed, reported pain at the time of examination, had any history of chronic pain, that is, pain lasting more than 3 months, reported back pain episode lasting more than 24 hours within a month before participation, reported comorbidities affecting the nervous system, cardiovascular diseases, psychiatric illnesses, any disease requiring systematic drug consumption, diagnosed scoliosis, or hypersensitive reaction to saline solution. To be included, participants had to have similar tactile detection thresholds at both sides of the spine (L3 level). Tactile threshold was measured only once by Semmes-Weinstein filaments (Touch Test, Sensory Evaluators) to confirm study eligibility. Inclusion criteria were adapted from previous tactile acuity studies on healthy subjects.4,12,13

Thirteen participants did not meet the criteria. Therefore, 57 participants (mean age = 24.46 ± 4.28) were randomly allocated to 1 of 3 groups: experimental (n = 19), sham injection (n = 19), or control group (n = 19). The included sample was recruited from the community of the Academy of Physical Education by verbal announcements and social-media advertisements published in academic groups. Included participants were asked to provide written informed consent for participation before the experimental procedure. They were informed that they could stop participating at any point during the study without providing a reason for their withdrawal. Participants were compensated with vouchers (value of 25 PLN each) for their participation, and all of them were fully debriefed at the end of the study.

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2.2. Sample size

Because no previous published studies investigated tactile acuity changes in acute low back pain, the sample size calculation was based on data from our own systematic review and meta-analysis1 and previous cross-sectional data in healthy controls.4 Based on the reported mean difference of 9.49 mm between patients with CLBP and healthy controls and a standard deviation of 9.90 mm, a total sample size of 57 participants (19 per group) was required to detect a significant effect. The between-group effect during the experience of pain was, therefore, regarded as the primary outcome. Further statistical analyses detailed below were conducted at an exploratory level. The power calculation was performed a priori for 2-sided comparisons detailed in the section on “statistical analysis” below. The calculation was performed in G*Power22 (G*Power 3.1.9.2 statistical software) with the alpha level set at α = 0.05 and 80% power.

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2.3. Research team, blinding, and randomisation

Two investigators performed the experiment: 1 physician and 1 physiotherapist (assessor). The physician was responsible for the randomisation, the blinding of the assessor, the experimental manipulation (pain induction), and the behavioural data collection. Randomisation was by drawing a card from the closed pool. The card included information on group assignment and was drawn by the physician after collecting baseline tactile acuity data (assessment 1). The mixed pool of randomisation cards assured that the randomisation sequence was not known by the physician. The assessor performed the tactile acuity assessments. The assessor was absent during the pain induction and randomisation procedures to maintain blinding toward the group allocation and the painful side. Participants were instructed to not reveal their pain experience during tactile acuity assessments, thereby ensuring assessor blinding. In addition, participants were naive to the experimental hypotheses.

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2.4. Study design and overview

Details regarding the time frame of the study are presented in Figure 1. After the screening procedure and preparation phase, participants were informed that the study included 2 branches so they can either be assigned to the experimental group (with injection) or to the control group without injection. In fact, participants were randomly assigned to 1 of 3 groups: experimental, sham injection, or control. Groups differed only in terms of the specific manipulation. The experimental group was exposed to pain induced by intramuscular hypertonic saline injection. The sham-injection group was exposed to a sham injection not piercing the skin but provoking a needle-like sensation with a PinPrick device. No manipulation took place in the control group. Tactile acuity was assessed 3 times in each of the groups: before the manipulation, at the time when the experimental group perceived the maximum pain intensity, and at the time when the experimental groups' pain had subsided.

Figure 1

Figure 1

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2.4.1. Preparation

Participants were comfortably positioned in prone with their lower back exposed.13,75 The assessor palpated the L3 spinous process,14 shaved, and cleaned both sides of the spine to reduce between- and within-subject variability that might occur during tactile acuity assessment. A horizontal axis was drawn at the level of the L3 spinous process to determine the locations for tactile acuity assessment and pain induction (see Fig. 2 for details). Tactile acuity was measured at a 5-cm distance from the midline (Fig. 2). This standardisation was in line with the protocol described in our previous study.4

Figure 2

Figure 2

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2.4.2. Tactile acuity assessment

Tactile acuity was assessed in 3 sessions in each of the group. Sessions were separated by 6-minute intervals. The first session served as a baseline measure of tactile acuity. The second session was performed after experimental manipulation, when the pain induced by saline injection in the experimental group had not changed for a minimum of 30 seconds. Similarly to a previous study,72 this plateau phase was reached approximately 2:30 minutes after the injection (mean time: 2:29 ± 0:45). The plateau phase was identified by tracking the individual participants' pain ratings every 30 seconds. Starting the second tactile acuity measurements individually ensured standardisation of the procedure and ensured that tactile acuity assessments were completed while participants experienced maximum back pain. The final measurements were performed after the pain in the experimental group had subsided to explore if changes in tactile acuity were short- or long-lasting and if they were associated with the pain experience. During each session, tactile acuity was assessed on the left and right side of the spine. Each session included assessments consisting of 3 distinct tactile acuity tests: TPD,13 point-to-point (PTP) test,4 and the recently developed two-point estimation (TPE) task.2 Each test was performed in the previously marked area (Fig. 2) by using mechanical sliding callipers (Powerfix, digital calliper: Z22855) with a precision of 0.01 mm. The order of the tests and the first side of measurement (left or right) were randomised. At the end of each measurement, the subject's back was cleaned with alcohol to create similar conditions for subsequent sessions.

The two-point discrimination test was assessed along the horizontal line at L3 level (1L or 1R) according to a previously published protocol4 (Fig. 2). In brief, the callipers were applied to the premarked line until the very first blanching of the skin.48 Testing commenced with 0 mm between the 2 calliper's tips. The distance was gradually increased until participants were able to verbally report that 2 points had been touched instead of 1.51 Subsequently, the descending sequence was applied until the perception of 1 point. This procedure was repeated twice so that the TPD score was based on the mean of 4 staircases, 2 ascending and 2 descending. Lower values indicate greater tactile acuity. Two-point discrimination threshold performed at the lumbar area is characterised by good reliability.4,20,46

Point-to-point test was performed according to a previously published protocol.4 In brief, the examiner lightly stimulated 1 of the points (“1L” or “1R”). The participants were instructed to indicate the stimulated point by using a pen. The assessor measured the distance between the stimulated and the indicated point. Mean values of 3 repeated trials served as PTP scores that were used in the data analysis. Lower PTP values indicate greater tactile acuity. Intrarater reliability of PTP is generally acceptable.4,30

Two-point estimation test was used as a novel tactile acuity tool. The test measures the precision of tactile perception and can also be used to reflect body image distortions,2 frequently observed in patients with CLBP.51,57 For the TPE test, 2 callipers were used, 1 by the assessor and 1 by the participant. The assessor applied 1 tactile stimulus along the horizontal line, with a 120-mm horizontal separation between the callipers' tips.2 The aim of this stimulus was to evoke a tactile sensation perceived clearly as 2 distinct points by all participants. Subsequently, participants were asked to manually indicate with their callipers the distance they perceived (TPE score). Patients held the callipers that they could only see the backside of the callipers and not the display. Three repeated measurements were performed, and mean values were used in the analysis. Participants were unaware that the same distance was used for each measurement but instructed to make a decision based on their subjective perception. For analysis, the TPE score was calculated according to the following formula: TPE score = 120 mm − x, where “x” refers to the value (distance) indicated by the given participant. Lower TPE values indicate greater tactile acuity. Intrarater reliability of TPE is excellent if performed at the lumbar area.3

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2.4.3. Experimental manipulation

In the experimental group, acute, nociceptive low back pain was induced using 1.0 mL of hypertonic (5% NaCl) saline bolus injection, which is a commonly used model of acute low back pain.31,32,66 Saline solution was injected into the lumbar longissimus dorsi muscle 50 mm lateral to the L3 spinous process just above (5 mm) the previously marked point “1L” or “1R” (Fig. 2). Injections were performed by a trained physician under ultrasound imaging guidance to ensure that each single injection was equally placed at a depth of 30 mm.72 The side (left or right) of pain induction was randomised and counterbalanced across subjects. The needle insertion mark and the corresponding point on the opposite side of the body were covered by placing a small piece of adhesive plaster. This procedure ensured assessor blinding because he was unaware which body side was painful.

In the sham-injection group, a real needle was shown in full view to the participants to imitate and enhance the anticipation of nocebo pain. During ultrasound examination, a pinprick sensation was produced by a weighted stimulus (flat contact area, 0.25 mm in diameter; PinPrick; MRC Systems GmbH, Germany) applied perpendicularly to the skin just above (5 mm) the point “1L” or “1R” without piercing the skin. A stimulus of 512 mN was used because it has been validated as the force activating cutaneous nociceptors.28 Single stimulation of nociceptors was used to create a valid assertion of injection serving as the group with nocebo-like pain. Adhesive tapes covering stimulation and corresponding opposite point were also provided. Blinding of the sham-injection condition allowed for the comparison between tactile acuity change in the nociceptive condition (injection) and non-nociceptive condition (sham injection).

The control group was only screened by ultrasound imaging but was not exposed to any intervention. Adhesive tapes were placed in the same way as in the previous 2 groups. Participants were instructed to rest between tactile acuity assessments (Fig. 1). Results of the control group enabled us to control for confounding factors such as the learning effect.

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2.5. Pain and fear measure

Pain and fear of pain were measured behaviourally on a Numerical Rating Scale. The scale for pain intensity ratings ranged from 0 = “no pain” to 10 = “the worst pain imaginable.” Fear of pain was measured only once before the group allocation. It was rated on a scale ranging from 0 = “not at all” to 10 = “very much.” Pain intensity was measured individually just after saline or sham injection and monitored every 30 seconds until reaching a plateau. If pain was still present after the second tactile acuity assessment, the measurements were continued until full recovery. In addition, participants were asked to indicate the distribution of the experienced pain by estimating the diameter of the circle every 30 seconds.72 Greater circle (diameter in centimeter units) referred to the greater distribution of pain (larger body area affected). For better characterisation of the included sample, participants were asked to complete a set of questionnaires: the Pain Catastrophizing Scale and the Fear of Pain Questionnaire.

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2.6. Manipulation check questions

To check whether the sham injection was detected by participants, a questionnaire was handed out at the end of experiment. Participants had to decide to which group they had been allocated. If they picked the “group with injection,” they had to decide if they received a real saline solution injection (yes or no). The latter question was used to control for successful manipulation. A similar procedure has been used in other sham-controlled experiments.35,41 Participants from the experimental and sham-injection groups were also asked to answer the question whether their pain was maintained during the second tactile acuity assessment (yes or no).

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2.7. Statistical analysis

Baseline differences in descriptive statistics were analysed by 1-way analysis of variance (ANOVA) with “group” as a between-subject factor. The main analysis was performed using a repeated-measures ANOVA design, with “group” (experimental, sham injection, and control) as a between-subject factor and “session” (assessment 1-3) as a within-subject factor. To test the hypothesis on tactile acuity improvement during pain induction, F-tests were followed by planned comparisons on tactile acuity data from assessment 1 vs assessment 2 in each of the group. To determine whether the magnitude of tactile acuity improvement differed between the groups, planned comparisons were performed on the difference in tactile acuity (assessment 1 vs assessment 2) between experimental and control group and between sham-injection and control group. Exploratory comparisons were performed to check if the tactile acuity change normalised after the experimental pain had subsided.

Although data from both sides (left or right) of the spine were collected, statistical analyses were performed using the data representing the side which was randomly exposed to pain. In the control group, there was no pain, but still the side for analysis was chosen randomly. Collecting the data from the other side served only as a procedural requirement to maintain blinding of the assessor.

Forward, stepwise multiple regression was performed as a secondary analysis to determine the degree to which tactile acuity change measured by for example, TPD ([INCREMENT]TPD = assessment 2 − assessment 1) is predicted by maximal and average pain intensity and maximal and average pain distribution. Independent variables were chosen based on the findings from previous studies, showing that a change in tactile acuity is correlated with severity of reported pain. All the analyses were conducted using the STATISTICA data analysis software, version 12 (StatSoft Inc, Tulsa, OK), and the data were screened for normality assumptions before the inferential analysis. The level of significance was set at P < 0.05.

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3. Results

3.1. Baseline differences

Table 1 shows the characteristics of the participants by experimental group. There were no significant differences across groups for age (F(2,54) = 1.23; P > 0.05; η2 = 0.04), body mass (F(2,54) = 0.80; P > 0.05; η2 = 0.03), height (F(2,54) = 0.44; P > 0.05; η2 = 0.02), fear of pain (trait) (F(2,54) = 0.91; P > 0.05; η2 = 0.03), pain catastrophizing (F(2,54) = 1.14; P > 0.05; η2 = 0.04), and fear of pain (state) (F(2,54) = 0.45; P > 0.05; η2 = 0.02). In addition, groups did not differ in baseline tactile acuity: there were no significant differences for TPD threshold (F(2,54) = 0.69; P > 0.05; η2 = 0.02), PTP test (F(2,54) = 0.22; P > 0.05; η2 = 0.01), and TPE task (F(2,54) = 0.05; P > 0.05; η2 = 0.00). Table 2 shows mean and SDs of tactile acuity tests across groups and sessions (Table 2).

Table 1

Table 1

Table 2

Table 2

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3.2. Manipulation check

The main assumption of this experiment was that tactile acuity tests are performed during acute nociceptive pain in the experimental group. Seventeen of 19 participants (89.5%) reported that they felt pain during the second tactile acuity assessment. In 5 participants (26%), pain outlasted the second tactile acuity assessment. In the sham-injection group, 11 participants (57%) reported pain after “injection,” but only 2 reported that they felt pain during the second tactile acuity assessment. No pain was reported by the control group. Analysis of variance confirmed a statistically significant main effect of “group” for the outcomes pain intensity (F(2,54) = 71.04; P < 0.001; η2 = 0.72), pain distribution (F(2,54) = 26.75; P < 0.001; η2 = 0.50), and (estimated) pain duration (F (2,54) = 872.79; P < 0.001; η2 = 0.97). Post hoc Tukey test results revealed that the experimental group experienced a significantly higher mean pain intensity (P < 0.001), lasting for a longer time period (P < 0.001), and reported their pain at a larger body area (P < 0.001) compared with the sham-injection group and control group (Table 3). Eleven of 19 (58%) participants from the sham-injection group indicated that they received real saline injection. Pain ratings and times of reaching the plateau phase in individual subjects are reported in the Supplementary file 1 (available online at http://links.lww.com/PAIN/A504).

Table 3

Table 3

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3.3. Tactile acuity perception across groups

Repeated-measures ANOVA for TPD revealed a statistically significant main effect of “session” (F(2,108) = 4.32; P < 0.05; η2 = 0.07) and a marginally nonsignificant “session” × “group” interaction (F(2,108) = 2.38; P = 0.056; η2 = 0.08), indicating that participants had different TPD results in respect to the session, and that the size of this effect varied among examined groups. Within-group planned comparison tests revealed a statistically significant difference between assessment 1 and 2 in the experimental group (F(1,54) = 12.64; P < 0.001; η2 = 0.19), indicating that acute low back pain increased the mean TPD threshold (Fig. 3) from 56.94 mm (95% confidence interval [CI]: 53.43-60.44) at baseline to 64.22 mm (95% CI: 60.42-68.02) during the second assessment (acute pain). Furthermore, TPD thresholds normalised after the experimental pain had subsided: the difference between assessment 1 and 3 was not statistically significant (Table 2) and dropped from 64.22 mm (95% CI: 60.42-68.02) during the second assessment (acute pain) to 60.80 mm (95% CI: 57.50-64.10) at the third assessment.

Figure 3

Figure 3

The difference between assessment 1 and 2 was not significant in the sham-injection group (F(1,54) = 1.08; P > 0.05; η2 = 0.02), but mean TPD thresholds showed the same direction of change (Fig. 3). No significant change was observed in the control group (F(1,54) = 0.03; P > 0.05; η2 = 0.00).

Between-group planned comparison tests for the difference between assessment 1 and 2 ([INCREMENT]TPD) revealed that the magnitude of this difference was significantly (F(1,54) = 6.90; P ≤ 0.01; η2 = 0.11) larger in the experimental group 7.29 (95% CI: 3.47-11.10) compared with the control group −0.33 (95% CI: −3.71 to 3.05). No significant difference between sham-injection and control group was found (Fig. 4 and Supplementary file 2; available online at http://links.lww.com/PAIN/A504). Regression analysis revealed that the variable “maximum reported pain” was a significant predictor (β = 0.55, P < 0.01) for the [INCREMENT]TPD (dependent variable) in the first and final step of the regression model (Fig. 5). Maximum reported pain accounted for a significant proportion of the variance in the [INCREMENT]TPD, that is, in the tactile acuity alteration (COR R 2 = 0.26, P < 0.05).

Figure 4

Figure 4

Figure 5

Figure 5

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).

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4. Discussion

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.

One explanation of the current results is a hypoesthetic effect.40 Pain triggered by hypertonic saline injection is based on a mechanical as well as a chemical enhancement of the sensitivity to mechanical stimuli. Excitation of muscle nociceptors is induced by mechanical damage of the muscle tissue itself and by cell shrinkage caused by an increase in extracellular osmolarity.27 These processes may lead to a secretion of chemical substances such as prostaglandin E2 or bradykinin and activation of Aδ and C fibres.39 It has been shown in an experimental setting that these cascades result in higher tactile, warm, and cold thresholds in the referred pain area.40 This tactile hypoesthesia has been linked to altered tactile acuity in a variety of clinical populations with neuropathic16,21,58,64,67 but not nociceptive pain.2,51,75 Another peripherally driven effect accounting for tactile acuity deterioration is the “touch-gate” phenomenon. As an analogy to the gate-control theory of pain, it has been reported that vibrotactile thresholds are increased when thermal stimuli are delivered either below or above pain thresholds regardless of attentional or arousal biases.6 Gating tactile stimuli by activation of the nociceptive system might delay the former and thus be a reason for lower discriminating abilities.

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).

To the best of our knowledge, tactile acuity has not been addressed in the context of acute pain states in any previous studies despite a body of literature focusing on chronic pain populations.19,34,38,50,51,60,64,69,75 Our findings suggest that the pain itself might be more important than cortical reorganisation, a phenomenon previously thought to be the main cause for altered tactile acuity in for example, CLBP. Reduced tactile acuity was not only reported for patients with CLBP1,2,11 but also for chronic neck pain,15,38,50 complex regional pain syndrome,44,59,60 osteoarthritis,7,69 rheumatoid arthritis,36 and recently in achilles tendinopathy.19 Our results are in line with the literature on chronic pain states and, therefore, undermine the supposed relationship between chronic pain, tactile acuity, and cortical reorganisation. Although the latter was not directly investigated in this study, it seems to be likely that even acute experimental pain produces some form of cortical reorganisation.68 According to this hypothesis, altered tactile acuity rather seems to be an epiphenomenon coexisting physiologically with nociceptive CLBP and adaptive brain changes. Some previous tactile acuity studies were conducted in populations with neuropathic syndromes characterized by “negative signs and symptoms.” It is well documented that neuropathies are related to larger TPD scores, for example, in patients with diabetes mellitus,21 carpal tunnel syndrome,33 median neuropathy,16 postherpetic neuralgia,58 and lumbosacral radiculopathy.64 The current results, showing that a significant deterioration in tactile acuity can be induced by peripheral nociceptive pain, contradict the hypothesis that a dysfunction in tactile function requires the injury within the peripheral nervous system resulting in neuropathic pain.

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.

To conclude, our study shows that altered tactile acuity is not only observed in chronic but also in acute nociceptive low back pain. Deterioration occurs immediately after the pain induction and is related to the intensity of the pain perception, which questions the causal role of cortical reorganisation in the formation of chronic pain. Moreover, tactile acuity alteration previously observed in neuropathic pain syndromes is associated with a nociceptive mechanism. The biological role of the observed deterioration is unknown, and therefore, future experimental studies should address this question.

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Conflict of interest statement

The authors have no conflicts of interest to declare.

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Acknowledgements

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.

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Keywords:

Tactile acuity; Two-point discrimination; Sensory dissociation; Sensory discrimination training; Low back pain; Pain mechanisms

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