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00005768-200906000-0000200005768_2009_41_1175_pietrosimone_transcutaneous_6article< 108_0_14_6 >Medicine & Science in Sports & Exercise©2009The American College of Sports MedicineVolume 41(6)June 2009pp 1175-1181Immediate Effects of Transcutaneous Electrical Nerve Stimulation and Focal Knee Joint Cooling on Quadriceps Activation[CLINICAL SCIENCES]PIETROSIMONE, BRIAN G.1; HART, JOSEPH M.2; SALIBA, SUSAN A.1; HERTEL, JAY1; INGERSOLL, CHRISTOPHER D.11Exercise and Sport Injury Laboratory, University of Virginia, Charlottesville, VA; and 2Department of Orthopaedic Surgery, University of Virginia, Charlottesville, VAAddress for correspondence: Christopher D. Ingersoll, Ph.D., A.T.C., F.A.C.S.M., F.N.A.T.A., 210 Emmet St South, PO Box 400407, Charlottesville, VA 22904-4407; E-mail: Ingersoll@virginia.edu.Submitted for publication September 2008.Accepted for publication December 2008.ABSTRACTPurpose: To determine whether transcutaneous electrical nerve stimulation (TENS) and focal knee joint cooling will affect the quadriceps central activation ratio (CAR) in patients with tibiofemoral osteoarthritis.Methods: Thirty-three participants with diagnosed tibiofemoral osteoarthritis were randomly allocated to the 45-min TENS treatment (six males and four females, 56 ± 10.1 yr, 174.11 ± 10.78 cm, 89.34 ± 21.3 kg), the 20-min focal knee joint cooling treatment (six males and five females, 58 ± 8.4 yr, 176.41 ± 8.29 cm, 83.18 ± 17.97 kg), or the control group (five males and seven females, 54 ± 9.9 yr, 166.37 ± 13.07 cm, 92.14 ± 25.37 kg). Volitional quadriceps activation, maximal voluntary isometric contraction, and subjective pain measurements were conducted at baseline and at 20, 30, and 45 min. The 20-min focal knee joint cooling intervention consisted of two 1.5-L ice bags to the anterior and posterior aspects of the knee. The TENS group received 45 min of a sensory, biphasic square wave stimulation (150-μs phase duration and 150 pps) from four 2 × 2-inch electrodes positioned around the patella.Results: TENS resulted in a significantly higher percent change in CAR scores compared with control at 20 min (6.4 ± 4.8 vs −3.5 ± 8, P = 0.006), 30 min (9.7 ± 10.16 vs −1 ± 7.9, P = 0.025), and 45 min (11.25 ± 6.96 vs 0.81 ± 9.4, P = 0.029). Focal knee joint cooling resulted in significantly higher percent change scores compared with the control group at 20 min (5.75 ± 7.25 vs −3.5 ± 8, P = 0.009) and trended to be higher at 45 min (9.06 ± 9.63 vs 0.81 ± 9.4, P = 0.098). No significant differences in percent change for CAR were found between the TENS and the focal knee joint cooling group.Conclusions: Both TENS and focal knee joint cooling increased the quadriceps CAR immediately after application in participants with tibiofemoral osteoarthritis.Tibiofemoral osteoarthritis has commonly been associated with decreased quadriceps voluntary activation, resulting in muscle weakness (3,4,17,20,27,28). Decreased volitional activation can be linked to arthrogenic muscle inhibition (AMI) (30), a clinical impairment characterized by a reflex inhibition of the motor neuron pool in uninjured muscles surrounding an injured joint (5,22,24-26). This reflex inhibition, modulated by both presynaptic and postsynaptic mechanisms (25,26), decreases the ability for the muscle to recruit motor neurons during a contraction (10,11), thus limiting its potential to generate force.AMI has been called a limiting factor in joint rehabilitation (5), which has lead authors (5,6,23) to suggest that reflex inhibition should be addressed before engaging in therapeutic exercise. Conventional rehabilitation does not focus on disinhibiting the quadriceps before strengthening the muscle and may not result in full restoration of function (10). It has been proposed that disinhibiting the muscle before performing therapeutic exercise may create a more optimal neural environment for normal motor patterns (5,6). Previous reports have suggested that quadriceps strength is not effective in preventing the progression of osteoarthritis (32). This suggests that optimal neural activation of the musculature may be a more important factor compared with strength in regaining a neuromuscular control strategy that may provide a protective shock absorbing quality to joints of the lower extremity (35).Both transcutaneous electrical nerve stimulation (TENS) and focal knee joint cooling have individually been reported to increase quadriceps motor neuron pool excitability in healthy subjects with experimentally effused knee joints (6). A 20-min focal knee joint cooling treatment has increased knee extension torque production (9) and quadriceps motor neuron pool excitability above preeffusion levels for up to 40 min after ice bag removal (6), whereas a 30-min TENS treatment returned quadriceps motor neuron pool excitability to preeffusion levels, which immediately decreased after TENS removal (6). It has been hypothesized that these two disinhibitory interventions may increase excitatory afferent stimuli sent to the spinal cord, thus overriding the inhibitory signals arising from an injured or a distended joint (6).Although focal knee joint cooling and TENS have been previously reported to immediately increase quadriceps motor neuron pool excitability in healthy, artificially effused knee joints (6), it remains unknown how these modalities will affect the ability to activate the quadriceps muscle in a clinically inhibited population, such as tibiofemoral osteoarthritis. The ability for these modalities to immediately increase quadriceps muscle activation in patients with tibiofemoral osteoarthritis may have significant clinical benefits, primarily allowing for disinhibition prior therapeutic exercise.Therefore, the purpose of the current study was to separately compare the immediate effects of focal knee joint cooling and TENS on volitional quadriceps activation in patients with tibiofemoral osteoarthritis. We hypothesized that both focal knee joint cooling and TENS would individually increase quadriceps activation compared with the control group, whereas focal knee joint cooling would increase quadriceps volitional activation more than TENS due to previous reports (6) of higher levels of motor neuron excitability after joint cooling compared with TENS.METHODSThe current study was a single-blinded randomized-controlled trial with two independent variables including time (baseline and 20, 30, and 45 min after intervention application) and treatment group (20 min of focal knee joint cooling, 45 min of TENS, and a control). The main outcome measure was quadriceps volitional activation expressed as a central activation ratio (CAR). Secondary outcome measures included quadriceps knee extension torque and pain during knee extension. Concealed, random allocation was used to assign participant treatment group after baseline measurements. The investigator evaluating all outcome measures remained blinded to group assignment throughout the trial. A separate experienced investigator, also blinded to group assignment, processed all data used for analysis.SubjectsThirty-nine participants initially volunteered for the study. Subjects were recruited from a variety of local clinics specializing in orthopedic clinics and physical therapy and from responses to recruitment advertisements throughout the community. Medical records for all subjects were obtained and indicated a previous history of tibiofemoral osteoarthritis diagnosed via plain radiographs, magnetic resonance imaging, or arthroscopy by an orthopedic surgeon or radiologist. Due to the variability in the length of time between diagnostic images and baseline measurements and the multitude of methods used to grade the presence of osteoarthritis, we were unable to characterize an accurate and uniformed grade of osteoarthritis for all participants at the time of the study. Participants were excluded if they had a history of rheumatoid arthritis, lower extremity orthopedic surgery, or acute knee injury in the past 6 months. Participants did not take any analgesics or anti-inflammatory medication 6 h before testing.Three subjects were excluded from the study after baseline measurements because they were fully activated and had no measurable activation deficits (CAR >99%). Two additional subjects were excluded after data collection because that they were not able to sustain a maximal quadriceps contraction during the burst superimposition technique. An additional participant was excluded from the TENS group because the treatment was inadvertently terminated prematurely; therefore, this participant did not receive the full dosage of the TENS treatment. Thirty-three subjects were included in the final analysis, and demographics are presented in Table 1. If participants had a history of bilateral tibiofemoral osteoarthritis, the leg with the highest level of pain on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) score was determined before the baseline measurements. This study was approved by our institutional review board (HSR-13215) before subject enrollment, and written informed consent was obtained for before any participation.TABLE 1. No significant differences were found between groups for any of the participant demographics.InstrumentsIsometric force signal was recorded from a dynamometer (Biodex System 3; Biodex Medical Systems, Shirley, NY) and was exported through a remote access port via a custom-built coaxial cable to a 16-bit analog/digital converter (MP150; BIOPAC Systems, Inc, Goleta, CA) where it was digitized (200 Hz) (29). A square-wave stimulator (S88; GRASS Telefactor, West Warwick, RI) in conjunction with a stimulation isolation unit (SIU8T) produced a 100-ms train of 10 stimuli, at 100 pps, with a pulse duration of 0.6 ms and a 0.01-ms pulse delay. With the low switch engaged on the stimulation isolation unit and an estimated 3000Ω load, each subject was stimulated with approximately 125 V. Highly conductive multipurpose Signa gel (Parker Laboratory Inc., Fairfield, NJ) was used as a coupling agent and applied to two separate 8 × 14-cm carbon-impregnated electrodes (Bloomex International Inc, Elmwood Park, NJ) used to deliver the stimulus to the quadriceps for the burst superimposition procedure (29). The stimulating electrodes were secured to the quadriceps with an elastic bandage (Hartmann-Conco Inc, Rock Hill, SC) to prevent movement of the electrodes during testing.The TENS 210(T) (Mettler Electronics Corp, Anaheim, CA) was used to create a continuous, biphasic pulsatile current (150 Hz, 150 μs). Four separate 2 × 2-inch self-adhesive electrodes (Re-ply reusable electrodes; Uni-Patch, Wabasha, MN) were used to deliver the TENS stimulation to the knee joint of participants.The WOMAC score was used to assess the subjective dysfunction, pain, and stiffness of participants with osteoarthritis before muscle activation testing. A 100-mm visual analog scale (VAS) was used to determine subjective knee pain during a knee extension maximal voluntary isometric contraction (MVIC). Either side of the 100-mm line was bordered by boxes stating "absolutely no pain" and "worst pain imaginable."ProcedureCentral activation ratioParticipants were secured to the dynamometer (Biodex System 3 Pro; Biodex Medical Systems) unit with hips flexed to 85° and 70° of knee flexion (29). All landmarks were aligned according to Biodex manufacturer's specifications and were previously reported in the literature (29). The cathode was positioned over the distal vastus medialis, whereas the anode was positioned over the proximal vastus lateralis and an elastic bandage was used to secure the electrodes to the thigh.A graded warm-up was conducted to assure that subjects were able to exert maximal effort during the test and were accustomed to the stimulus. A series of submaximal contractions at 25%, 50%, and 75% of their perceived maximal voluntary isometric contraction (MVIC) were paired with submaximal stimuli at 25%, 50%, and 75% of the maximum testing voltage of 125 V. In addition to submaximal trials, participants performed three to five practice MVIC until the investigator was confident that each subject was able to exert maximal effort.The exogenous stimulus was applied to the quadriceps when the test administrator observed that a maximal force plateau had been reached. Two to three trials, separated by a 60-s rest period, were performed to ensure that two acceptable trials could be averaged at each time interval (baseline and 20, 30, 45 min after) for data analysis.VAS pain scoresAt the beginning of each time interval, an MVIC without an augmented electrical stimulation was performed. Each participant was asked to rate the pain felt in the knee during an MVIC on a 100-mm line.InterventionsRandom allocation to the intervention group, using a concealed envelope, was performed immediately after baseline testing by a clinician separate from the investigator who was assessing voluntary quadriceps activation. All clinicians applying the treatments were experienced certified athletic trainers who had been instructed on intervention placement and procedures before testing. Visual aides were available for reference during setup for all clinicians to ensure a systematic setup of the interventions throughout the study. Participants were instructed by the clinicians not to divulge or to ask any questions about the interventions to the investigator. The blinded investigator, assessing the muscle activation, left the laboratory before group allocation and was called back in approximately 20 min after the treatment was initiated. This allowed for the ice bags to be secured and removed after a focal joint cooling intervention, without divulging the group assignment to the blinded investigator. A screen was positioned in front of the participant, allowing the blinded investigator to see only the face of the participants without being able to determine whether the individual was wearing an active TENS unit, had received 20 min of focal joint cooling, or was in the control group. During all the interventions, participants remained seated in the dynamometer and were instructed to refrain from moving their legs.The skin of the participants in the TENS group was appropriately shaved if needed and was cleaned with an alcohol wipe to ensure proper electrode adherence. Four 2 × 2, self-adhesive square electrodes were applied on the medial and the lateral superior as well as the medial and the lateral inferior borders of the patella as previously reported (6) (Fig. 1). Care was taken not to place TENS electrodes on the quadriceps muscles or muscles of the anterior leg. The two TENS currents were crossed to encompass the most surface area under stimulation. TENS intensity was increased to the highest tolerable sensory stimulation that remained comfortable for the individual without causing a muscle contraction. The stimulator was clipped to the lap belt of the dynamometer, and participants were instructed on how to increase the intensity of the stimulation in the presence of accommodation. The TENS stimulation remained on the participant for 45 min and was not removed during posttesting.FIGURE 1. TENS electrode placement: TENS electrodes were positioned on the skin around the patella. Two separate currents were crossed (1 and 2) to increase the surface area under stimulation.The focal knee joint cooling intervention consisted of two 1.5-L bags of crushed ice secured to the anterior and the poster aspects of the knee joint with an elastic bandage as previously reported (6). Caution was taken by clinicians to ensure that the majority of the ice bag was over the knee joint and as little as possible was in contact with the various musculature surrounding the knee. The ice bags remained secured for 20 min and then were removed.During the control intervention, the participants were instructed to sit quietly for 20 min before posttesting.Data analysisCAR was calculated by dividing the force measurements of the maximal voluntary contraction (FMVIC) by that of the force produced by the superimposed burst (FSIB) plus the maximal voluntary contraction (FMVIC; equation 1) as previously performed (29,33).Equation (Uncited)The peak force (FSIB + FMVIC) value and the maximal voluntary contraction value (FMVIC) were calculated from the mean of the two best separate trials at each time in the series, when the superimposed burst was applied. FMVIC was calculated from a 0.1-s time epoch immediately before the administration of the exogenous electrical stimulus. All MVIC were normalized to subject body mass. The mean value of the voluntary force plateau was divided by the peak value of the force produced by the superimposed burst. Pain scores were calculated by measuring the distance of the mark made by the participant from the end marked "absolutely no pain." VAS scores were presented in millimeters with higher scores representing higher levels of pain.Statistical analysisAll statistical analyses were performed with the Statistical Package for the Social Sciences for Windows (version 15.1; SPSS Inc., Chicago, IL). Means and SD were calculated for CAR, MVIC, and VAS scores for all three groups. Three separate 3 × 3 ANOVA with repeated measures on time were used to compare percent change of CAR, MVIC, and VAS from baseline between conditions over time. A one-way ANOVA with multiple comparisons was performed post hoc to determine differences between groups. Pearson product moments were calculated for changes in VAS and CAR and were squared to examine the amount of variance in the change in quadriceps activation that could be explained by variance in changes in pain. Squared Pearson product moments were calculated for changes in CAR and MVIC post hoc to determine the amount of variance in the change in quadriceps activation that could be explained by variance in the change in MVIC. A priori alpha levels were set at P < 0.05. Standardized effect sizes were calculated for percent changes in CAR for the TENS and the focal knee joint cooling groups at all three posttests. Effect sizes were calculated by separately subtracting the mean CAR of the experimental groups from the control mean and divided by the pooled SD at each of the three posttest intervals.RESULTSNo differences were found between groups among the demographics listed in Table 1. No significant differences were found between groups for baseline CAR measurements (F2,32 = 1.11, P = 0.342). All mean CAR, MVIC, and VAS values are listed in Table 2. There was a significant difference between treatment groups (F2,30 = 6.205, P = 0.006) and over time (F2,60 = 6.85, P = 0.002, 1 − β = 0.908) for CAR percent change scores. Significant differences were found between treatment groups at 20 min (F2,32 = 7.39, P = 0.002), 30 min (F2,32 = 4.16, P = 0.025), and 45 min (F2,32 = 4.4, P = 0.021). TENS had significantly higher percent change in CAR scores compared with control at 20 min (P = 0.006), 30 min (P = 0.025), and 45 min (P = 0.029; Table 2, Fig. 2). The focal knee joint cooling group had significantly higher percent change scores compared with the control group at 20 min (P = 0.009) and trended to be higher at 45 min (P = 0.098; Table 2, Fig. 2). No significant differences in percent change for CAR were found between the TENS and the focal knee joint cooling group.TABLE 2. No caption available.FIGURE 2. Percent change in CAR from baseline: Both TENS and focal knee joint cooling increase immediately after the intervention. Error bars represent SD. The asterisks (*) indicate that the intervention groups have CAR significantly greater than the control group at those posttests. P ≤ 0.05.No significant differences were found for percent change scores in MVIC between groups (F2,60 = 2.96, P = 0.06, 1 − β = 0.55) and over time (F2,60 = 2.96, P = 0.067, 1 − β = 0.53). There were no significant changes in VAS between groups (F2,30 = 0.501, P = 0.484, 1 − β = 0.105) or over time (F2,60 = 0.291, P = 0.749, 1 − β = 0.094). Changes in MVIC explained a significant amount of change in CAR at 20 min (r2 = 0.81, P < 0.001), 30 min (r2 = 0.74, P < 0.001), and 45 min (r2 = 0.72, P < 0.001). Changes in pain were not related to changes in CAR for the TENS group, the focal joint cooling group, or the control group at any of the time intervals (Table 2). Effect sizes for CAR were strong at all time points for the TENS group as well as at 20 and 45 min posttests in the focal knee joint cooling group. A moderate effect size was found at the 30-min posttest in the focal knee joint cooling group (Fig. 3).FIGURE 3. CAR effect sizes with 95% confidence intervals: Diamonds with solid error bars represent focal knee joint cooling effect size point estimates and 95% confidence intervals, whereas circles with broken lines represent TENS effect size point estimates and 95% confidence intervals. All point measures and confidence intervals on the right of the vertical solid line represents beneficial effects whereas the left of the line represents nonbeneficial effects.DISCUSSIONThis study provides evidence that patients diagnosed with tibiofemoral osteoarthritis are immediately able to increase voluntary quadriceps activation after the applications of either TENS or focal knee joint cooling. In addition, changes in pain did not significantly explain changes in CAR, suggesting that these two modalities, often used for pain management, improved muscle activation independent of pain modulation pathways. Our results agree with previous reports (6) that motor neuron pool excitability increases immediately after the application of TENS and focal knee joint cooling. Although changes in CAR can be altered by both motor unit recruitment and firing frequency (13,34), previous work (6) reporting that TENS and focal joint cooling increase motor neuron pool excitability suggests that increased recruitment is most likely the cause of the higher CAR found in this study. Recently, because variance in motor unit firing rate was reported to explain 34% of the variance in CAR (14), it is possible that a portion of the remaining 66% of the variance in CAR is explained by variance in motor unit recruitment. If the number motor neurons available for recruitment is increased by application of these modalities, it is plausible that the motor system may immediately be able to recruit the corresponding motor units for a maximal contraction.AMI, which causes voluntary activation deficits in patients with knee injury (17,19,28,31,33), is due to decreased motor neuron pool excitability, modulated by both pre- and postsynaptic spinal reflex mechanisms (25,26). Disinhibitory modalities such as TENS and focal knee joint cooling have been theorized to affect these inhibitory reflex mechanisms, resulting in excitation of the previously inhibited motor neurons. TENS has previously been reported to decrease the presynaptic inhibition (12), and authors (6) have hypothesized that an increase in afferent signals interpreted as excitatory stimuli may override afferent inhibitory signals, thus allowing for an increased motor response. It has also been hypothesized that focal joint cooling and TENS may trigger mechanism that are spinally mediated or descending from higher brain centers that cause inhibition of Ib interneurons, effectively causing higher levels of muscle activation (6).Previously, 20 min of focal joint cooling reportedly facilitated motor neuron pool excitability above baseline levels and exceeded the capabilities of TENS. We did not find a difference between change scores in the TENS group compared with the focal knee joint cooling group. Although we hypothesized a similar result, we found that participants using TENS incurred a significantly larger increase in voluntary activation at all three posttests compared with the control group. CAR percent change scores trended to increase at all posttest time intervals for the focal knee joint cooling group, but the only significant changes were immediately after ice bag removal at the 20-min posttest. Previous studies (6,15) have reported that motor neuron pool excitability continues to increase after removal of the ice bags, which has been attributed to the excitatory afferent information to the interneurons at the spinal cord during the rewarming of cutaneous structures. Past studies have tested focal joint cooling interventions on motor neuron pool excitability in healthy subjects during static conditions (8,15), so it remains possible that the active nature of the CAR testing caused the extremity to rewarm at a faster rate, and a cooling intervention longer than 20 min may be necessary to see increased activation during exercise. Although no statistical difference in baseline CAR was found between groups, patients in the focal knee joint cooling group had slightly higher baseline CAR, which would allow for less room for improvement, possibly making large differences in activation more difficult to evaluate.Percent change of CAR in the TENS group tended to increase over time and was significantly greater than the control group at all posttest intervals. Hopkins et al. (6) removed the TENS after a 30-min intervention and reported decreases in motor neuron pool excitability back to baseline levels upon removal. In contrast, motor neuron pool excitability remained facilitated after the removal of the focal joint cooling intervention (6), which was likely due to continued afferent activity during the rewarming period. We chose not discontinue the TENS until after posttesting, allowing for participants to perform the CAR testing in a disinhibited environment, which we believe allows for a more fair comparison between TENS and focal knee joint cooling at the 30- and the 45-min posttests. We believe that a sustained 45-min TENS treatment more closely represents a clinical treatment, which would also not be removed during exercise. Although joint cooling was thought to be superior disinhibitory modality compared with TENS before this study, a longer TENS intervention may be more beneficial. Electrical stimulation can be administered throughout periods of exercise, allowing patients to move more freely, which would not be possible if an ice bag was secured to a joint. TENS compared with joint cooling provides the ability for easy regulation of individualized intensity for each participant, and independent adjustments can be made for accommodation throughout a desired time interval. These inherent benefits may make TENS a more desirable disinhibitory modality for many clinicians.Previous research (2) has reported that the use of TENS, in conjunction with therapeutic exercise, increased quadriceps strength by 26% in patients with knee osteoarthritis after a 20-session intervention. In addition, researchers have reported improvements in functional activities (16) as well as alterations in gait (2) after TENS therapy in patients with osteoarthritis. These improvements found in previous studies may partially be explained by the increased muscle activation caused by the TENS intervention found in this study. Although quadriceps activation was not assessed in either of these studies (2,16), it can be hypothesized that increased muscle activation may play a role in increased torque production through activation of additional motor units. Increased muscle activation may allow for altering motor recruitment strategies, which may in turn alter function.Although focal knee joint cooling failed to produce significantly higher CAR at 30 and 45 min posttests, moderate and strong effect sizes were found at 30 and 45 min, respectively (Fig. 3). Confidence intervals for the CAR effect sizes after joint cooling at 30 and 45 min crossed zero, making it difficult to definitively suggest that a relevant increase in CAR was found at these time intervals. TENS produced large effect sizes at all posttests, and none of confidence intervals crossed zero, which allows us to suggest that a relevant increase in CAR was found at all posttests after TENS (Fig. 3). Moderate to strong effect sizes, in combination with most confidence intervals that do not cross zero, may provide enough evidence to warrant additional studies with higher sample sizes to determine the adequacy of focal joint cooling as a disinhibitory treatment.Normalized MVIC tended to increase in both the TENS and the focal knee joint cooling group yet did not reach a statistically significant difference between groups at any of the posttest time intervals. It should be noted that the variance in the change in MVIC explained a significant amount of the variance in the change in CAR at all posttests, suggesting that increases or decreases in activation percentage is linked to changes in MVIC. VAS scores during the MVIC decreased slightly for both treatment groups but also failed to reach a statistically significant difference compared with the control group. The statistically insignificant findings for both of these secondary outcome measures were likely due to low statistical power to detect differences in those measures. Mean pain scores were all less than 21 on a 100-point scale, suggesting that maximally extending the knee at 70° of knee flexion did not adequately provoke enough pain to see a clinically significant reduction. It remains interesting that changes in pain did not explain changes in CAR, further suggesting that disinhibitory modalities affect AMI on pathways independent of pain in both knee pathologies and artificial effusion (7,18,19,21,25,27). Therefore, AMI can manifest itself in the absence of pain, and these disinhibitory modalities may be affecting similar nonnoxious mechanoreceptor pathways.Although this study provides evidence that these modalities may be useful for increasing activation in many knee joint pathologies, we can only generalize our results to patients with diagnosed tibiofemoral osteoarthritis. Other limitations include our inability to accurately stratify groups by radiographic grade of osteoarthritis. Although we were not able to stratify groups by osteoarthritis severity, randomization techniques did provide statistically equivalent groups based on WOMAC score, which were similar to previous studies (18,21,27) that have used the WOMAC to quantify dysfunction in patients with tibiofemoral knee osteoarthritis.The ability to increase muscle activation in patients with tibiofemoral osteoarthritis with a modality such as joint cooling or TENS may have significant effects on decreasing the detrimental effects of AMI. Disinhibition is not a replacement to therapeutic exercise but rather an adjunct, possibly allowing patients to access motor neurons that may otherwise be unattainable in an inhibited state. AMI affecting the quadriceps has been reported to detrimentally alter gait kinematics (36) and to effect shock attenuation during landing (22). In addition, quadriceps dysfunction has been hypothesized to contribute to the onset of osteoarthritis after acute knee injury (1). Although we have reported that patients with tibiofemoral osteoarthritis were able to increase volitional quadriceps activation after TENS and focal knee joint cooling, it remains unknown to what extent these modalities will affect functional strength gains in the long term as well as patient satisfaction.The authors would like to thank Lindsay K. Drewes, M.Ed., A.T.C., and Kate R. Jackson, M.Ed., A.T.C., for their assistance in data collection. This study was partially funded by a grant from the Eastern Athletic Trainers' Association, Inc. The results of the present study do not constitute endorsement by the American College of Sports Medicine.REFERENCES1. Becker R, Berth A, Nehring M, Awiszus F. Neuromuscular quadriceps dysfunction prior to osteoarthritis of the knee. J Orthop Res. 2004;22:768-73. [CrossRef] [Medline Link] [Context Link]2. 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