Arthrogenic Muscle Inhibition Following Anterior Cruciate Ligament Injury

Abstract

Arthrogenic muscle inhibition (AMI) is a common impairment in individuals who sustain an anterior cruciate ligament (ACL) injury. The AMI causes decreased muscle activation, which impairs muscle strength, leading to aberrant movement biomechanics. The AMI is often resistant to traditional rehabilitation techniques, which leads to persistent neuromuscular deficits following ACL reconstruction. To better treat AMI following ACL injury and ACL reconstruction, it is important to understand the specific neural pathways involved in AMI pathogenesis, as well as the changes in muscle function that may impact movement biomechanics and long-term structural alterations to joint tissue. Overall, AMI is a critical factor that limits optimal rehabilitation outcomes following ACL injury and ACL reconstruction. This review discusses the current understanding of the: (1) neural pathways involved in the AMI pathogenesis following ACL injury; (2) consequence of AMI on muscle function, joint biomechanics, and patient function; and (3) development of posttraumatic osteoarthritis. Finally, the authors review the evidence for interventions specifically used to target AMI following ACL injury.

Arthrogenic muscle inhibition after anterior cruciate ligament injury: Injured and uninjured limb recovery over time

“…Interestingly, this trend is also observed in the injured limb at the 12-month post-ACLR timepoint for both quadriceps and hamstrings musculature, where quadriceps AvgFR returns to near pre-surgery levels further away from the control level and hamstrings AvgFR increases away from the control level. Previous studies have similarly demonstrated altered neural activation and motor control deficits at 12 months post-ACLR and beyond, via different methodologies ( 12 , 14 , 15 ). The findings of this study, in combination with previous investigations that have identified altered motor control, may suggest that rehabilitation should be extended until motor control, both central and specifically of the thigh musculature, returns and is more similar to motor control of healthy subjects ( 26 , 42 ).…”

“…It is well established that AMI persists after ACL injury and during rehabilitation after ACLR; however, different mechanisms that contribute to AMI and their effects continue to be explored. It is well known that deficits exist and persist in central neural activation after ACLR and beyond RTS ( 8 , 12 ). Previous studies have demonstrated acute and long-term changes in both central and peripheral mechanisms of inhibition, including altered electrocortical brain activity, increased excitability of the spinal-reflex pathways and reduced excitability of corticospinal pathways ( 13 – 15 ), and central activation failure ( 14 , 15 ).…”

“…Previous studies have demonstrated acute and long-term changes in both central and peripheral mechanisms of inhibition, including altered electrocortical brain activity, increased excitability of the spinal-reflex pathways and reduced excitability of corticospinal pathways ( 13 – 15 ), and central activation failure ( 14 , 15 ). Further, with the hypothesized presynaptic reflex inhibition of the thigh musculature and known central activation alterations post ACL-injury, it would follow that changes of motor control are evident in analysis of the electrical activity of the thigh muscles ( 12 ). These neural deficits may contribute to aberrant motor patterns that could contribute to future ACL injury risk, even though patients are expected to achieve 85%–90% limb symmetry on functional tasks necessary to return to sport.…”

Conduction Velocity of Spinal Reflex in Patients with Acute Lateral Ankle Sprain

“…Only three studies have described reflexive excitability characteristics among patients with ALAS, with Hall et al [ 9 ] failing to find differences between involved and uninvolved limbs, Klykken et al [ 10 ] observing muscle-specific facilitation and inhibition between involved and uninvolved limbs, and Kim et al [ 11 ] reporting bilateral soleus inhibition between injured and uninjured groups. It has been hypothesized that arthrogenic muscle inhibition resulting from pain and swelling effectively diminishes the excitability of the alpha motor neuron pool and makes it more difficult to activate muscles, a factor that can potentially predispose these individuals to subsequent injury [ 12 ]. Interestingly, many of these changes have been observed independent of symptom severity (e.g., swelling, pain), suggesting that any degree of pain and swelling may yield inhibitory changes [ 9 , 11 ].…”

Arthrogenic Muscle Inhibition: 20 Years On

“…We have learned a great deal since those educated guesses were made. In this special section, we hope to provide a summary of what we have learned: an update on the mechanisms that drive AMI, 2 how joint pain influences and complicates AMI, 3 the relationship of Gamma loop dysfunction to AMI, 4 the AMI patterns associated with specific joint injuries, [5][6][7] and a clinical perspective of the implications of AMI. 8,9 We will also introduce a few original research pieces with AMI as the central theme.…”