Effect of Experimental Anterior Knee Pain on Measures of Static and Dynamic Postural Control

http://www.healio.com/orthopedics/journals/atshc/%7B423d8efa-8b24-469e-ae50-3eb389df06de%7D/effect-of-experimental-anterior-knee-pain-on-measures-of-static-and-dynamic-postural-control

http://www.healio.com/~/media/Journals/ATSHC/2014/1_January/10_3928_19425864_20140103_03/10_3928_19425864_20140103_03.pdf

Emily Elizabeth Falk, MS, ATC; Matthew K. Seeley, PhD, ATC; Iain Hunter, PhD; Jihong Park, PhD, ATC, CSCS; J. Ty Hopkins, PhD, ATC
  • Athletic Training and Sports Health Care
  • January/February 2014 – Volume 6 · Issue 1: 7-14
  • DOI: 10.3928/19425864-20140103-03

Abstract 

The neuromechanical influence of anterior knee pain on sensorimotor function, independent of other knee pathology factors, is unclear. The purpose of this study was to determine whether experimental anterior knee pain independently alters static and dynamic postural control. Fifteen healthy participants performed single-leg quiet stance, landing, and walking tasks under 3 experimental conditions (pain, sham, control), at 3 different times (preinjection, injection, and postinjection) for each experimental condition.The dependent variables were (1) participant-perceived pain, (2) anterior–posterior and medial–lateral center of pressure velocity during single-leg quiet stance, (3) anterior–posterior, medial–lateral, and vertical time to stabilization during landing, (4) and medial–lateral center of pressure position during the stance phase of walking. Participant-perceived pain was influenced by time and experimental condition (P < .05); however, the other dependent variables were not significantly influenced by time or experimental condition, indicating that anterior knee pain does not independently affect static and dynamic postural control. [Athletic Training & Sports Health Care. 2014;6(1):7–14.]
Ms Falk is from the Department of Athletics, Mt. Hood Community College, Gresham, Oregon; Dr Seeley, Dr Hunter, and Dr Hopkins are from the Department of Exercise Sciences, Brigham Young University, Provo, Utah; and Dr Park is from the Department of Sports Medicine, Kyun Hee University, Youngin, Korea.
The authors have disclosed no potential conflicts of interest, financial or otherwise.
Address correspondence to Matthew K. Seeley, PhD, ATC, Department of Exercise Sciences, 106 SFH, Brigham Young University, Provo, UT 84602; e-mail: matthewkseeley@gmail.com.
Received: January 29, 2013
Accepted: November 06, 2013
Posted Online: January 03, 2014
Joint pain is a common ailment. Some common causes of joint pain are impingement,1 effusion,2 instability,3,4 inflexibility,4 and overuse.5 Joint pain is a chief symptom for many musculoskeletal diseases (eg, osteoarthritis6). Of all the weight-bearing joints, the knee is most commonly affected by osteoarthritis.7,8 Knee pain is also a chief symptom for patellar disorders that affect 25% of young adults and more than 25% of athletes.9
Related to knee osteoarthritis, patellar disorders, and various other knee joint pathologies, joint pain impairs muscle strength,8,10,11 overall performance,8,12,13 and static and dynamic postural control.10,13 Dynamic postural control is defined as the ability to control body position to maintain whole-body stability and orientation.14,15 Because postural control requires integration of sensory inputs10 and sensory inputs affect motor components such as muscle strength, muscle activation, and contraction patterns,16 knee pain can theoretically alter postural control independently.3,17 Anterior knee pain, for example, independently interferes with nociceptor and mechanoreceptor signals at central processing, delaying returning efferent messages and altering proprioception3; these modifications, due to anterior knee pain, likely alter the body’s base of support during static and dynamic movement and consequently alter stability and postural control.3,18–20
The independent effects of anterior knee pain on postural control are difficult to study because of confounding variables such as inflammatory factors, joint degeneration, and associated muscle weakness. These confounding variables make it difficult to isolate anterior knee pain as a cause of altered postural control. Various models that involve experimental muscle pain, produced via intramuscular hypertonic saline injections,21,22 and delayed-onset muscle soreness23,24 have been used in attempts to study the effects of pain on posture; however, these models are limited in that muscle is sometimes not the source of musculoskeletal pain25 (eg, patellofemoral pain disorder). An experimental anterior knee pain model that can isolate anterior knee pain could potentially eliminate the aforementioned confounding variables and increase understanding of the effects of anterior knee pain on postural control.
Injection of hypertonic saline into the infrapatellar fat pad is an effective way to represent clinical anterior knee pain.12 The infrapatellar fat pad is a source of anterior knee pain26,27 that contains nociceptors that are sensitive to substance P.28 Group III and IV nociceptive afferents found within the infrapatellar fat pad are stimulated by hypertonic saline, which also indicates that the pathways elicited by a hypertonic saline injection are consistent with those of musculoskeletal pain.29,30 Although previous researchers17,18 have injected hypertonic saline into various parts of the knee to answer various research questions related to posture, to our knowledge no study has yet injected hypertonic saline into the infrapatellar fat pad to study the independent effects of anterior knee pain on posture in a group of young, able-bodied participants.
The purpose of this study was to answer the following research question: does experimental anterior knee pain influence static and dynamic postural control?We hypothesized that, relative to a pain-free condition, experimental anterior knee pain would alter 3 mechanical quantities that previously have been associated with decreased postural control: (1) center of pressure (COP) velocity during single-leg quiet stance,31,32 (2) time to stabilization during a landing task,33–35 and (3) COP position during walking.31

Method 

Experimental Design 

We used a crossover design to evaluate the effect of experimental condition (pain, sham, and control) and time (preinjection, injection, postinjection) on participant-perceived pain level and several mechanical variables: (1) anterior–posterior and medial–lateral COP velocity during single-leg quiet stance, (2) anterior–posterior, medial–lateral, and vertical time-to-stabilization during a landing task, and (3) medial–lateral COP position during walking. Each experimental condition was separated by 2 to 4 days and was performed in a counterbalanced order. The pain, sham, and control condition involved a hypertonic (5% NaCl) saline injection, isotonic (0.9% NaCl) saline injection, and no injection, respectively. For each experimental condition, participants performed single-leg quiet stance, landing, and walking at 3 different times: (1) preinjection, (2) injection (immediately following the saline injection), and (3) postinjection (20 minutes after the saline injection). Quiet stance, landing, and walking were consistently performed in the aforementioned order for every experimental condition and time, to facilitate between-condition comparisons for each task. For the pain and sham conditions, we measured participant-perceived pain immediately before and after the injection; 90 seconds after the injection (immediately prior to quiet stance); immediately before the landing trials; immediately before and after the walking trials; and 5, 10, 15, and 20 minutes after the walking trials (Figure 1). Participant-perceived pain was also measured at corresponding times for the control condition.

Participant-perceived pain significantly increased between some of the times during the pain condition (asterisks indicate statistical differences; P < .05). There were no between-time changes for the sham or control conditions. Error bars define standard deviation.

Figure 1.
Participant-perceived pain significantly increased between some of the times during the pain condition (asterisks indicate statistical differences; P.05). There were no between-time changes for the sham or control conditions. Error bars define standard deviation.

Participants 

Fifteen participants were included in the study (8 women, 7 men; age = 23 ± 2 years; height = 1.71 ± 0.10 m; mass = 73.4 ± 17.3 kg). The dominant leg (kicking leg) was consistently used for testing. All participants were physically active (exercising a minimum of 3 times per week for 30 minutes) and had no current lower-extremity pathology, muscle pain, joint pain, or history of dominant-leg surgery. The appropriate human subjects protection committee approved this project before data collection. All participants provided informed consent before participating.

Instruments 

We used one force platform (200 Hz; AMTI Inc, Watertown, Massachusetts), embedded in the laboratory floor, to measure COP position during single-leg quiet stance and a landing task. COP anterior–posterior and medial–lateral velocity was derived from the COP position data using a finite central differences approach for the single-leg quiet stance trials. Anterior–posterior, medial–lateral, and vertical times to stabilization were determined from the COP position data for the landing trials. We used pressure-sensing insoles (100 Hz; Tekscan Inc, Boston, Massachusetts) to measure medial–lateral COP position during walking on a treadmill (Quinton Instrument Co, Bothell, Washington). We measured participant-perceived pain with a 10-cm visual analogue scale.36

Data Collection 

Because walking speed affects walking mechanics, the walking speed for all experimental conditions for each participant was standardized to leg length (anterior–superior iliac crest to medial malleolus). This standardized walking speed is dimensionless and equaled 1 for all participants and conditions. The rationale and methods related to this standardization process have been described previously.37 A standardized athletic shoe was used for all tests (T-Lite VIII; Nike Inc, Beaverton, Oregon). The insoles were removed and replaced with a custom fit, calibrated, pressure-sensing insole. Only once, at the beginning of each experimental condition, participants warmed up by walking on the treadmill for 5 minutes at the standardized speed. Immediately after this warm-up, participants performed the preinjection, single-leg quiet stance, landing, and walking trials.
Single-Leg Quiet Stance Trials. Three 30-second trials of single-leg quiet stance were performed on the force platform, with 15 seconds between each trial.During these trials, participants had their hands on their hips, eyes open, looking straight ahead, with the nondominant leg lifted off the ground via knee flexion. If the participant touched the ground during the trial with the nondominant leg, the trial was discarded and repeated. Participants were allowed to practice the quiet stance before the 5-minute warm-up.
Landing Trials. Next, participants performed 3 landing trials, with 15 seconds between each trial. For each landing trial, participants landed with the dominant leg onto the force platform, from a height of 0.31 meter.38 Just prior to each landing trial, participants had their hands on their hips, with their eyes open, looking straight ahead. Participants left the 0.31-meter height while standing on one leg. They were not allowed to gradually lower their center of mass until contacting the force platform, or jumping from the 0.31-meter height (these requirements were subjectively evaluated throughout the study by the same researcher). Participants practiced this landing task before the 5-minute warm-up.33 Participants were directed to stabilize as quickly as possible after landing and remain standing for 6 seconds.38 If the nondominant leg touched the force platform, the trial was discarded and repeated.
Walking Trials. Next, participants walked on the treadmill at the standardized walking speed for 15 seconds while plantar pressures were recorded.
For all experimental conditions, following the preinjection trials, participants lay supine on a treatment table. For the pain or sham conditions, 0.75 mL of hypertonic or isotonic saline, respectively, was injected laterally to a 10-mm depth into the participant’s dominant-leg infrapatellar fat pad, using a 25-gauge needle at a 20° angle in a superior–lateral direction.3,39 To spread the solution throughout the infrapatellar fat pad, the needle was moved around at several angles inside the fat pad during the injection. The participants and researchers were not masked regarding which injection the participants received. After the injection, to avoid a vasovagal reaction, participants remained supine for 30 seconds, sat up for 30 seconds, and then stood for 30 seconds. For the control condition, no injection was given; however, participants were still required to lay supine for 30 seconds, sit up for 30 seconds, and stand for 30 seconds. After the 90 seconds of familiarization time for all experimental conditions, participants performed the injection trials (single-leg quiet stance, landing, and walking trials). After the injection trials, for all experimental conditions participants sat for 20 minutes so that pain could resolve for the pain condition. After these 20 minutes, postinjection trials were performed in the same manner as the preinjection and injection trials (ie, standing, landing, and then walking).

Data Reduction 

We averaged instantaneous COP anterior–posterior and medial–lateral velocities across the entirety of each 30-second single-leg quiet stance trial.These averages were then averaged across 3 trials for each experimental condition and time. Anterior–posterior, medial–lateral, and vertical times to stabilization were calculated for the landing trials using previously described methods.40 For walking, 3 stance phases were manually determined from the pressure data: initial pressure applied to the heel indicated heel strike and terminal pressure applied to the forefoot indicated toeoff. Then, COP medial–lateral position throughout stance was determined by first establishing a reference line from the heel to the medial border of the big toe (determined using the pressure data). The perpendicular distance from the reference line to the COP was determined for each data point throughout stance (Figure 2).These perpendicular distances were plotted against time.

A depiction of how medial–lateral center of pressure position was calculated. First, a reference line was constructed from the point of foot–ground contact during heel strike to the point of foot–ground contact during toe-off. Second, for each percentage of the stance phase, the perpendicular distance from the reference line to the center of pressure position (dashed line) was measured. Third, this perpendicular distance was plotted across the entire stance phase of walking.

Figure 2.
A depiction of how medial–lateral center of pressure position was calculated. First, a reference line was constructed from the point of foot–ground contact during heel strike to the point of foot–ground contact during toe-off. Second, for each percentage of the stance phase, the perpendicular distance from the reference line to the center of pressure position (dashed line) was measured. Third, this perpendicular distance was plotted across the entire stance phase of walking.

Statistical Analysis 

We used repeated measures analyses of variance to evaluate the influence of experimental condition and time on perceived pain and dependent variables: (1) average anterior–posterior and medial–lateral COP velocity during single-leg quiet stance, and (2) average anterior–posterior, medial–lateral, and vertical times to stabilization during landing. For these dependent variables, when experimental condition × time interactions existed, Tukey’s post hoc tests were used to compare potential between-time differences for each experimental condition. Differently, the authors used a functional analysis to evaluate the effect of experimental condition and time on medial–lateral position of the COP during the stance phase of walking. All data points describing medial–lateral COP position were used in this statistical analysis, allowing for a comparison of treatment effects (polynomial functions) over the entire stance phase, rather than univariate or multivariate (discrete values) effects.41,42 This functional analysis approach allows for (1) detection of treatment effects between 2 groups and (2) insight regarding what time during the stance phase those effects exist.For all statistical analyses, the authors set the alpha level at 0.05.

Results 

The only dependent variable that was significantly affected by experimental condition over time was participant-perceived pain (Figure 1; Interaction:F18,406 = 14.13; P < .001). Participant-perceived pain immediately following the hypertonic saline injection was significantly greater than prior to the hypertonic saline injection; this increase lasted until 10 minutes after the walking and injection trials were completed (P < .001; Figure 1). Means and standard deviations for the mechanical variables are presented in the Table.None of the mechanical variables were significantly affected by experimental condition or time. Anterior–posterior (P = .445) and medial–lateral (P = .697) COP velocity during quiet-leg stance did not change between experimental conditions or across times. Anterior–posterior (P = .960), medial–lateral (P =.816), and vertical (P = .899) time to stabilization during the landing task were not affected by experimental condition or time. Similarly, medial–lateral COP position for every percentage of the stance phase of walking was not significantly influenced by experimental condition or time (Figure 3).

Means and Standard Deviations for the Mechanical Variables That Were Observed in the Current Studya

Table:
Means and Standard Deviations for the Mechanical Variables That Were Observed in the Current Study

Results from the functional analysis used to compare medial–lateral center of pressure position during walking between the control and pain conditions. The bolded black function line indicates mean difference in medial–lateral center of pressure position, for each percentage of the stance phase of gait. The vertical black lines represent corresponding 95% confidence intervals for each percentage of the stance phase of gait. The confidence intervals overlapped the zero line at every percentage of the stance phase of gait; this indicates no statistical difference between the control and pain conditions for medial–lateral center of pressure position at any percentage of the stance phase of gait.

Figure 3.
Results from the functional analysis used to compare medial–lateral center of pressure position during walking between the control and pain conditions. The bolded black function line indicates mean difference in medial–lateral center of pressure position, for each percentage of the stance phase of gait. The vertical black lines represent corresponding 95% confidence intervals for each percentage of the stance phase of gait. The confidence intervals overlapped the zero line at every percentage of the stance phase of gait; this indicates no statistical difference between the control and pain conditions for medial–lateral center of pressure position at any percentage of the stance phase of gait.

Discussion 

The purpose of this study was to evaluate the independent effects of anterior knee pain on static and dynamic postural control using an experimental anterior knee pain model. Although the current model effectively produced anterior knee pain, the experimental anterior knee pain did not affect any of the mechanical measures related to quiet standing, landing, or walking. The authors believe that the results indicate that anterior knee pain does not independently influence static or dynamic postural control.
Using a single 0.75-mL hypertonic saline injection, the experimental pain model effectively caused anterior knee pain. The participants reported an average peak pain level of 2.9 cm on a 10-cm visual analog scale, with 10 being the highest score. Also, all participants were pain free within 20 minutes after the injection. Single injections of 0.25 mL,3,12,18,39 0.75 mL,43 and 1.0 mL44of hypertonic saline have also previously been used to induce experimental knee pain. Bennell et al39 and Hodges et al12 used single injections of 0.25 mL hypertonic saline solution to induce experimental anterior knee pain and reported that pain level peaked 2 to 3 minutes after the injection. The current data are comparable to previously reported experimentally induced anterior knee pain levels43,44 of 2.6 and 3.2 cm on a 10-cm visual analog scale, with 10 being the highest score. Furthermore, Henriksen et al43 reported that this pain level altered walking mechanics, indicating that the pain level in the current study should have been great enough to alter walking mechanics. However, the current data were not as comparable to those reported by Bennell et al,18,39who reported pain averages of 5.8 and 6.2 using an 11-point numerical rating scale, with 11 being the highest score. It is uncertain what is responsible for the differences in perceived pain levels in the aforementioned studies. In addition to the visual analog scale used to quantify perceived pain, the current study could have been strengthened if a functional questionnaire and a perceived exertion questionnaire to further qualify effects of the experimental anterior knee pain had been included.
Increased COP velocity during single-leg quiet stance is believed to suggest decreased postural control,31 and we found that experimental anterior knee pain does not influence anterior–posterior or medial–lateral COP velocity during single-leg quiet stance. Our COP velocity values were comparable to previously reported anterior–posterior (2.02 ± 0.26 cm/s) and medial–lateral (1.84 ± 0.17 cm/s) COP velocity values.45 Furthermore, our findings are somewhat consistent with a previous report that demonstrated that experimental knee pain does not influence bilateral COP in healthy older adults.18 However, in this previous report, the authors suggested that (1) COP was not influenced by pain because of compensation from the uninvolved leg and (2) pain does influence postural control; the current data do not support these ideas. If experimental knee pain does influence postural control during quiet single-leg stance, then perhaps average anterior–posterior and medial–lateral COP velocity are not sensitive enough to reveal differences in static postural control due to the effects of pain. Although perhaps not more sensitive, other relevant measures could have provided additional insight into this issue, including lower-extremity joint mechanics (kinematics and kinetics) and electromyography.
Increased time to stabilization during a landing task indicates stability,33 and the current data showed that experimental anterior knee pain does not influence dynamic postural control. The authors believe that they are the first to use time to stabilization as a measure of dynamic postural control in an experimental knee pain model. The time to stabilization values used in the current study are comparable to previously reported time to stabilization values (anterior–posterior = 1.34 ± 0.16 seconds; medial–lateral = 2.51 ± 0.93 seconds; vertical = 0.65 ± 0.24 seconds).33,46 Time to stabilization has been described as a sensitive and effective measurement of dynamic postural control for various samples,33,45,47 and we expect that time to stabilization was a valid method to measure effects of pain on dynamic postural control in the current context.However, center of pressure position and velocity theoretically may not have reflected altered lower-extremity neuromuscular strategies resulting from knee pain, due to potential compensatory mechanics. For example, it is possible that our participants modified hip and ankle mechanics in an attempt to compensate for altered knee mechanics. These simultaneous mechanical alterations at multiple lower-extremity joints could theoretically mask one another and not be reflected in center of pressure measurements. This idea could be relevant to the standing and walking tasks performed during this study. Hip, knee, and ankle joint mechanics, as well as electromyography data, could elucidate this idea. In support of this speculation, Henriksen et al43 showed that lower-extremity joint mechanics are altered as a result of experimental knee pain during walking. Similarly, experimental anterior knee pain did not appear to affect dynamic postural control during walking, as measured by medial–lateral COP excursion during the stance phase of walking. Henriksen et al43 observed a variety of mechanical alterations for the lower-extremity during walking while using the current pain model.43
The independent effects of anterior knee pain on postural control are difficult to study due to other confounding variables that are also related to knee joint pathology. Consequently, an experimental pain model has been created to eliminate these confounding variables. We believe that the current experimental pain model is a good representation of clinical anterior knee pain.The infrapatellar fat pad contains nociceptors that are spread throughout the fat pad and facilitate fat pad sensitivity to pain.48 Also, nerve fibers in the infrapatellar fat pad contain substance P, a protein that triggers nociceptors, which is consistent with musculoskeletal nociception.27,28,39 When hypertonic saline solution is injected into the infrapatellar fat pad, substance P is released and chemically irritates the nociceptors.49 In addition, animal experiments have shown group III and IV nociceptive afferents are stimulated by hypertonic saline; this also indicates that the pathways elicited by the pain model are consistent with those of musculoskeletal pain.29,30 Although experimental pain may be similar to anterior knee pain and osteoarthritis pain, differences exist in the quality of pain. Using this model, perceived pain exists for a relatively short duration (approximately 12 minutes in this study).Perhaps, if pain had remained longer, changes in the center of pressure would have been observed. Bennell et al18 hypothesized that the infrapatellar fat pad nociceptors may need longer stimulation to make changes to postural control.

Implications for Clinical Practice 

Experimental anterior knee pain, caused by one 0.75-mL hypertonic saline injection, does not affect static or dynamic postural control. It is plausible that neuromechanical changes resulted from the current experimental anterior knee pain; however, the measures related to the center of pressure did not reflect these changes. If neuromechanical changes occur as a result of independent anterior knee pain, compensation also occurs and masks the existing neuromechanical changes. Anterior knee pain probably does not independently alter an individual’s capacity to control whole-body center of mass position during the functional tasks observed during the current study (quiet single-leg standing, landing from a relatively low height, and walking at a preferred speed).

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