Disrupted Tactile Acuity in People With Achilles Tendinopathy: A Preliminary Case-Control Investigation

Methods

Procedure

Prior to testing, both groups provided demographic information, and the participants with Achilles tendinopathy completed the VISA-A questionnaire,¹⁸ a reliable and valid measure of disability caused by pain in the Achilles tendon. An esthesiometer with precision of 1 mm was used to measure TPD over the Achilles tendon (Lafayette Instrument Company, Lafayette, IN). Prior to formal testing, familiarization trials were conducted on the participant's arm. During formal testing, participants were positioned in prone with the ankle in a neutral position (0° of dorsiflexion). For patients, the center point of pain over the painful tendon was marked, and a corresponding point was marked on the nonpainful side, by an independent researcher. This served as the central point for all testing. For healthy controls, the testing was centered on a point 4 cm above the Achilles tendon insertion, based on the average distance seen in the patient population. Patients and healthy controls were recruited at different sites, so testers were not blinded to clinical status. However, the tester assessing the clinical population was blinded to the side of pain, and the tester of the healthy controls was blinded to the results of the patient population.

The esthesiometer was applied parallel to the tendon with even pressure through both tips, until the first blanching of the skin (FIGURE). Participants were instructed to inform the tester whether they could feel 1 or 2 points. If participants perceived 2 points because of a temporal delay in the presentation of the 2 points, participants were asked to inform the researcher, and this application was repeated.

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Two ascending and 2 descending runs were performed for each leg tested, in random order. Ascending runs began with the points 0 mm apart, and the distance was increased by 5-mm increments. The distance at which the participant first perceived 2 distinct points was recorded as the threshold value. Descending runs began with the points 80 mm apart, followed by decrements of 5 mm. The distance at which the participant first perceived only 1 point was recorded as the threshold value. “Catch trials,” in which only 1 point was presented, were conducted to verify that participants were not guessing. A mean TPD value was obtained from the 4 threshold scores and used for subsequent analysis. In the patient population, both legs were tested in random order. In the healthy controls, only 1 side was tested, with the limb tested determined by random allocation. Good interrater (intraclass correlation coefficient model 2,1 = 0.78) and intrarater (intraclass correlation coefficient model 2,1 = 0.86) reliability at the foot using a similar device and protocol have been previously reported.⁴

Results

All participants completed all parts of the study. The VISA-A score for 1 patient was incomplete and was coded as missing; there were no other missing data. The mean ± SD age was 40.1 ± 15.6 years for healthy participants and 40.5 ± 8.9 years for the participants with Achilles tendinopathy. Participants were reasonably split between men (Achilles tendinopathy, n = 7; healthy, n = 6) and women (Achilles tendinopathy, n = 6; healthy, n = 7). The mean ± SD VISA-A score was 62.7 ± 24.1, suggesting a moderately affected group, and the average ± SD symptom duration was 14.6 ± 13.1 months.

All TPD values were normally distributed (all, P>.05). In the patient sample, mean ± SD TPD over the affected tendon was 45.2 ± 19.6 mm and was 33.4 ± 10.7 mm for the unaffected side. This difference was statistically significant (mean difference, 11.7 mm; 95% CI: 1.9, 21.5; P = .02), suggesting that people with Achilles tendinopathy have poorer tactile acuity over the Achilles tendon on the affected side.

The mean TPD value for the healthy controls was 32.1 ± 3.9 mm and, as mentioned, the mean TPD for the affected tendon was 45.2 ± 19.6 mm. This difference was statistically significant (mean difference, 13.1 mm; 95% CI: 1.6, 24.6; P = .03), suggesting that people with Achilles tendinopathy may have poorer tactile acuity over the painful tendon in comparison to healthy controls.

There was no significant difference in TPD values between the healthy controls and the unaffected side in people with Achilles tendinopathy (mean difference, 1.4 mm; 95% CI: −7.9, 5.1; P = .66), suggesting that the deficit in tactile acuity may be specific to the area of pain.

Discussion

The purpose of this study was to determine whether tactile acuity is altered in people with Achilles tendinopathy, and whether any alterations are specific to the site of pain. In keeping with our hypotheses, we found that tactile acuity is impaired over the affected tendon in comparison to the unaffected side and in comparison to healthy controls. Furthermore, we found no difference between controls and the unaffected side in the patient group, suggesting that the problem is specific to the area of symptoms.

These data add to a reasonably large body of evidence that suggests that tactile acuity may be diminished in people with chronic pain,³ and that this impairment is most noticeable at the painful area.³ This finding is important, as several lines of evidence suggest that tactile acuity is a reasonable clinical signature of reorganization within the somatosensory cortex. In healthy people, tactile acuity has been shown to be tightly coupled with primary somatosensory cortex representation (r = −0.47),⁶ and sensory training has been shown to simultaneously enhance tactile acuity and somatosensory cortex organization.¹⁴ Clinical populations have also shown a tight coupling between symptoms, tactile acuity, and somatosensory cortex representation. Studies in people with complex regional pain syndrome have shown that tactile acuity is strongly correlated with somatosensory cortex reorganization (r = −0.77)¹⁵ and that symptom improvement is paralleled by normalization of tactile acuity and somatosensory cortex map size.¹⁶ Furthermore, training of tactile precision in patients with phantom-limb pain has been shown to simultaneously improve tactile acuity and normalize cortical reorganization as well as reduce pain,⁷ and subsequent studies in individuals with low back pain have further supported the idea that this type of training reduces pain.²⁰ Other factors might have contributed to the altered tactile acuity seen in the current study, and further research is required to determine whether somatosensory cortex reorganization contributes to this impairment in people with Achilles tendinopathy.

If present, it is possible that disrupted cortical maps contribute to the clinical presentation of people with Achilles tendinopathy. Planning and coordination of movement require an intact representation of the body, and movement quality is likely to decline if stored body maps are degraded, an idea supported by the positive association between tactile acuity and performance on lumbar motor control tasks.¹⁰ In Achilles tendinopathy patients, suboptimal movement patterns might abnormally load the tendon and could contribute to nociceptive input. It has also been hypothesized that pain may arise as a result of incongruence between the predicted and actual sensory feedback associated with movement by virtue of disrupted cortical maps—the so-called sensorimotor incongruence hypothesis⁸—and this process could also contribute to the pain experience in Achilles tendinopathy. It is also plausible that local tissue sensitivity may be enhanced by distorted cortical maps and related changes in body perception. A change in body perception may make the area feel less safe and robust, and increased local sensitivity may emerge as a response to this perception. In support of this idea, data show that sensitivity to experimental pain is increased when body perception is altered by visual manipulation.¹³ Finally, though speculative, loss of sensory precision and decreased ability to accurately localize sensory input could enhance sensitivity by increasing the salience and threat value of any sensory information, noxious or otherwise, received from the affected area.

Consideration must be given to the limitations of this study. While the researcher testing the participants with Achilles tendinopathy was blinded to side, neither tester was blinded to clinical status. We attempted to control for this by having 2 different researchers assess the cases and controls, and each tester was unaware of the results of the other. The inclusion of 2 testers might have introduced some additional error to the measurements, though interrater reliability in healthy populations is good.⁴ Finally, it is feasible that the deficits observed in tactile acuity may result from peripheral abnormalities such as local reduction in cutaneous receptor field density secondary to local tissue events.

Conclusion

Participants with Achilles tendinopathy demonstrated reduced tactile acuity over their affected tendon when compared with their unaffected tendon and with healthy controls. Preliminary data support the use of sensory discrimination training strategies as a means of improving pain in other clinical conditions characterized by impaired tactile acuity. Research is needed to determine whether similar therapeutic strategies may be worth using in the management of Achilles tendinopathy. Further work is also required to explore the mechanisms that underpin tactile acuity changes in this population.