Research suggests light touch sensation in the foot and ankle may be negatively affected several years after anterior cruciate ligament (ACL) reconstruction—a finding consistent with studies that have reported decreased somatosensation in patients with other lower extremity conditions.
By Matthew Hoch, PhD, LAT; Steven Morrison, PhD; and Johanna Hoch, PhD, LAT
Injuries to the anterior cruciate ligament (ACL) are common in physically active populations. Although surgical reconstruction for this injury is frequently sought, patients may experience subsequent reinjury1 and long-term consequences such as diminished self-reported function2 and post-traumatic osteoarthritis (OA).3,4 In many cases, these negative consequences may be associated with biomechanical alterations during dynamic activity despite extensive rehabilitation.5
Neuromotor deficits associated with quadriceps activation,6 postural control,7 and joint position and movement sense8 have been identified in patients who have undergone ACL reconstruction (ACLR). These deficits may provide insight into sources of movement dysfunction in this population. The further examination of the impact of ACL injury on the somatosensory system may provide additional insights into the underlying causes of these impairments.
Many of the neuromotor deficits that occur after ACLR are thought to originate as a consequence of alterations in the function of the mechanoreceptors within the ligament itself.9 These mechanoreceptors are important for movement, as they provide information to the central nervous system (CNS) regarding joint movement and position.9 These mechanoreceptors also influence muscle spindle activity in the muscles that surround the knee, which can affect overall muscular stiffness.9 The overall result of ACL injury is therefore widespread, negatively impacting the ligamentous and musculotendinous components of the somatosensory system, which can alter neural feedback to the CNS—a consequence that has been proposed to contribute to CNS reorganization and alteration of the motor output.10 These alterations in ascending neural feedback, coupled with mechanical instability and abnormal joint movement, provide further justification for assessing the impact of ACL injury on somatosensory function.
While the ligamentous and musculotendinous components of the somatosensory system have been extensively investigated following ACL injury, less attention has been directed toward the third aspect of this system, the cutaneous mechanoreceptors. These mechanoreceptors are found in the skin and include Merkel, Ruffini, Meissner, and Pacinian corpuscles. These receptors respond to a range of mechanical stimuli in the form of pressure and vibration.11 The density of cutaneous mechanoreceptors varies throughout the body, but higher concentrations are found in the glabrous skin on the hands and feet.12,13
It is possible that cutaneous somatosensation may be disrupted in individuals who have undergone ACLR because of damage to cutaneous nerves during surgical procedures.14 However, diminished vibration perception and tactile acuity has been identified in lower extremity conditions unrelated to surgery, such as chronic ankle instability,15-17 patellofemoral pain,18 Achilles tendinopathy,19 femoroacetabular impingement,20 and hip and knee OA.21,22
Cutaneous mechanoreceptors are typically the only aspect of the somatosensory system in direct physical contact with the environment. Theoretically, diminished lower extremity cutaneous sensation, particularly in the feet, may increase the detection thresholds for recognizing perturbations and changes in terrain; this could ultimately increase the latency of motor responses evoked to compensate for any such perturbations. Any neural delays linked to ACL injury could lead to further neuromotor deficits, biomechanical alterations, and reinjury mechanisms.
The study of alterations in cutaneous sensitivity associated with orthopedic conditions is an emerging area of research. Further understanding of how ACL injury leads to sensory changes may help us cultivate novel approaches to movement dysfunction, rehabilitation, and the development of OA in this population.
We conducted a study23 to determine if differences in lower extremity cutaneous detection thresholds were present in post-ACLR patients compared with healthy controls. For this case-control study, 15 participants were included in each group. Individuals were included in the ACLR group if they were at least one year post-ACLR and cleared for physical activity, had self-reported participation in all activities considered meaningful to the patient, were at least moderately physically active, and aged between 18 and 35 years. The ACLR and healthy groups were matched for gender, limb, and age. The ACLR group had a median time from surgery of four years.
Light touch detection thresholds were assessed at four locations on the foot and ankle: the head of the first metatarsal and base of the fifth metatarsal, medial malleolus, and lateral malleolus. Participants were positioned prone on a plinth with noise-reducing headphones. Cutaneous sensation was assessed using a 20-piece Semmes-Weinstein monofilament (SWM) kit. These monofilaments were selected for this study because they provide a method of assessing light touch sensitivity commonly used in clinical practice. Monofilaments were applied perpendicular to the skin with enough force to bend the monofilament into a “C” shape. The participants were blinded to monofilament application and instructed to state “yes” when a monofilament was perceived. A stepping algorithm24 was used to determine detection thresholds. Based on the patient’s responses, the monofilament weight was decreased or increased until a detection threshold was identified. We recorded the lightest weight monofilament that could be detected in at least 50% of applications.
Participants in the ACLR group had higher detection thresholds at the head of the first metatarsal and medial malleolus than the healthy controls. However, no differences in detection thresholds were identified at the base of the fifth metatarsal or lateral malleolus. At the head of the first metatarsal, 80% of the ACLR participants had detection thresholds of 3.84 or greater, which would be classified25 as “diminished protective sensation,” while 87% of the healthy participants had detection thresholds of 3.61 or lower, which would be classified as “normal sensation.” These findings suggest physically active individuals with a history of ACLR exhibit cutaneous sensation deficits at the foot and ankle.23
Cutaneous somatosensation and the knee
Until recently, investigations examining cutaneous sensation after ACLR have been primarily focused on sensory deficits related to surgery. For example, involvement of the saphenous nerve has been documented following ACLR using a hamstring or patellar tendon autograft.14,26-31 In our study,23 decreased sensation over the medial malleolus could have been related to surgical involvement. However, we also observed decreased sensation over the head of the first metatarsal, which is associated with tibial nerve distribution and is not commonly impaired following surgery. Therefore, we hypothesize the sensory deficits identified in our study are related to sensory reweighting rather than surgical intervention.
Additionally, Thorlund and colleagues32 examined the vibrotactile detection threshold of the medial malleolus and medial femoral condyle in individuals who were at least 10 weeks post-ACL injury or at least 16 weeks post-ACLR, compared with controls. Interestingly, this study determined the ACL/ACLR group demonstrated greater sensitivity than controls at the medial mallelus; however, their was no difference at the medial femoral condyle. Although the results of this study contradict our findings, a primary difference between the two studies is the time since surgery. Patients in our study were at least one year post-ACLR, and the median time from surgery was four years; by comparison, patients averaged 14 months since surgery in the study by Thorlund et al.32
Prospectively monitoring somatosensory changes after ACL injury and subsequent reconstruction may provide insight into the natural course of sensory alterations that occur. The initial response to injury or surgery may be to heighten sensation as a protective mechanism, followed by an inhibition of sensation in the later stages of recovery.
The hypothesis that sensory inhibition may be experienced over time is supported by studies that have looked at cutaneous sensitivity in patients with knee OA without total knee replacement.21 In patients with knee OA, vibratory detection thresholds were increased at the first metatarsal, medial malleolus, lateral malleolus, and medial and lateral femoral condyles, compared with healthy controls.21 The authors concluded these sensory deficits may be associated with the neuromechanical pathophysiology of knee OA; however, whether sensory deficits preceded OA development has not been determined.21
Similar findings have also been identified in hip OA patients.22 However, these patients also exhibited decreased sensation over the radial head. This suggests somatosensory deficits may be generalized throughout the body; however, this concept has not yet been explored in any other patient populations.
Cutaneous sensitivity has also been examined in patients with a history of meniscectomy and in patients with active patellofemoral pain. Vibratory detection thresholds in patients who were on average four years since meniscectomy did not differ from those of controls at the medial malleolus or the medial femoral condyle.32 In contrast, patellofemoral pain patients did exhibit light touch sensory deficits around painful areas of the patella compared with controls.18 However, the average duration of patellofemoral symptoms was six years, with a range from one to 21 years. These studies indicate additional research regarding sensory deficits in different patient populations is warranted, and specific consideration should be given to time since surgery, type of surgery, the presence of pain, and duration of symptoms.
Few studies have examined how decreased cutaneous sensitivity can influence functional movement performance or biomechanics. However, ACLR patients with diminished vibratory detection thresholds have also scored poorly on functional testing.33 Further, women with decreased sensation at the first metatarsal and medial malleolus exhibited diminished movement quality during stair descent and the forward lunge, as indicated by an increased medialization of the knee position relative to the foot position during these tasks.33 These sets of findings clearly suggest there is a need for further understanding of the implications of decreased sensation over the foot and ankle in ACLR patients, specifically in identifying the impact these deficits may have with regard to biomechanics and reinjury mechanisms.
Currently, there is a lack of understanding as to the origin of cutaneous sensory deficits. As previously mentioned, damage to the saphenous nerve can be a consequence of surgical intervention after ACL injury. However, we believe these deficits are not completely linked to surgery. A recent neurophysiological model to explain the neuromuscular deficits after peripheral joint injury proposed a loss of ascending afferent information as one of the main factors contributing to CNS reorganization and motor control deficits.10 This theory is supported by a growing body of evidence suggesting changes in the CNS after joint injury, supported by neurophysiologic measures of somatosensory dysfunction, motor system excitability, and plasticity of neural networks.34-36
Identifying the origin of cutaneous sensory deficits may be useful when developing relevant rehabilitation strategies. For example, purposeful stimulation of the somatosensory system may increase muscle activation following ACL injury. Modalities including transcutaneous electrical nerve stimulation and cryotherapy have been associated with increased quadriceps motoneuron pool excitability when applied to artificially induced knee effusions and patients with acute and chronic knee conditions.37-40 Similarly, interventions focused on mechanical deformation of the skin and muscle tissues—such as whole body vibration, local muscle vibration, and massage—have also enhanced components of motor output.41-43 Collectively, these studies highlight that increased emphasis on purposively stimulating the somatosensory system during rehabilitation may be a necessary component for complete neuromotor restoration. Considerably more research is needed to identify the most effective treatment strategies and their ability to improve patient outcomes.
Lastly, we believe these findings may have implications for long-term health. In addition to patients who have undergone ACLR, those with knee OA also exhibit decreased cutaneous sensation in the foot and ankle.44 At this point it is not clear if there is a direct association between somatosensory impairment after ACLR and OA development. It is possible these are coincidental findings, because both groups have a history of intraarticular knee pathology.
Also, diminished foot and ankle sensation is a risk factor for falls in aging populations.45 While somatosensory function degrades with normal aging,46 it is unknown if this process is accelerated or exacerbated in people who sustained an ACL injury as an adolescent or young adult.
Investigating the role of somatosensory deficits as a contributing factor to OA development and fall risk are important, because these conditions may have more profound health implications than the original condition triggering the somatosensory effects. Furthermore, interventions may need to be developed that target somatosensory function throughout the lifespan to mitigate these conditions.
Patients who have undergone ACLR have demonstrated deficits in light touch sensation at the first metatarsal and medial malleolus compared with healthy persons. These findings suggest the somatosensory system may be affected several years after reconstruction, which is in line with recent research that has identified decreased cutaneous sensation in other lower extremity conditions. Continued research is needed to understand the role of somatosensory deficits with regard to reinjury mechanisms, CNS reorganization, and health issues experienced later in life, such as OA and falls.
Matthew Hoch, PhD, LAT, is an assistant professor; Steven Morrison, PhD, is a professor; and Johanna Hoch, PhD, LAT, is an assistant professor in the School of Physical Therapy and Athletic Training at Old Dominion University in Norfolk, VA.
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