Neural excitability alterations after anterior cruciate ligament reconstruction.
Pietrosimone BG, Lepley AS, Ericksen HM, Clements A, Sohn DH, and Gribble PA. J Athl Training. 2015; 50(6) 665-674.
Take Home Message: Following anterior cruciate ligament (ACL) surgery, patients have changes in the excitability of pathways that go from the brain (primary motor cortex) and down the spinal cord when compared with an uninjured limb as well as healthy control participants.
Many patients experience neuromuscular deficits after ACL reconstruction (ACLR). These deficits may be caused by changes in spinal-reflex excitability or corticomotor excitability, which is the excitability of the brain (primary motor cortex) and the related descending pathways in the spinal cord. By understanding the neural changes that occur in patients after an ACLR, clinicians may be able to improve ACLR rehabilitation to improve knee function, reduce the risk of reinjury, and potentially protect long-term joint health. Therefore, Pietrosimone and colleagues completed a case-control study to determine whether corticomotor and spinal-reflex excitability differed between individuals with an ACLR and healthy controls. The authors included 57 individuals: 28 individuals with ACLR (time post-surgery ~ 48 months) and 29 control participants. All participants described their function and physical activity levels by completing the IKDC and Tegner activity scale, respectively. To assess corticomotor excitability the authors measured the active motor threshold by having a participant sit in a Biodex dynamometer and maintain a quadriceps contraction at 5% of their maximal voluntary isometric contraction. During the contraction, the authors applied transcranial magnetic stimulation. The active motor threshold was the lowest amount of stimulation required to elicit a notable change in vastus medialis muscle activity (via electromyography). The researchers assessed spinal-reflex excitability by having a participant lie supine with electrodes to measure muscle activity placed over the vastus medialis. A disc-stimulating electrode was positioned over the femoral nerve and the authors increased the stimulation until they could record the maximum Hoffmann reflex, which was then normalized to the maximal muscle activity that could be stimulated by the electrical stimulation. The authors also assessed the central activation ratio (maximal voluntary contraction divided by the maximal electrically stimulated contraction, the manuscript has a great figure showing this). Overall, the researchers found diminished corticomotor excitability for the injured limb of ACLR patients compared with their uninjured limb and the control group. There was some indication that participants with ACLR and low voluntary central activation had diminished corticomotor excitability than the control group. Furthermore, the participants with ACLR and high voluntary central activation may have greater spinal-reflex excitability than the control group, which the authors suggest could be a coping strategy that some patients adopt to maintain better voluntary activation.
Overall, the current study presents some useful data to clinicians because it highlights that neuromuscular function after an ACLR can be influenced by central factors in the brain and spinal cord. The primary finding was that ACLR patients require more activation energy at the brain (primary motor cortex) to contract the quadriceps. It is interesting that the diminished corticomotor excitability is present even though the average patient was tested 48 months after surgery. Further, the IKDC scores of ACLR patients was lower than controls, while Tegner activity scores were not different between groups. This demonstrates that ACLR patients, even several years after surgery, are attempting to keep activity levels comparable to healthy controls while their subjective and objective knee function are impaired. We need to wonder if this is safe for our patients. With this in mind, clinicians may wish to dedicate more time to neural training during the rehabilitation process. The authors suggest that we should consider developing therapeutic strategies to increase spinal-reflex excitability (e.g., cryotherapy or transcutaneous electrical stimulation) or corticomotor excitability (e.g., biofeedback). While more research is needed to test the benefits of these therapies for these goals they are unlikely to cause harm to a patient and therefore may be worth trying in the clinical setting.
Questions for Discussion: How much neural training to do you incorporate into your ACL rehabilitation programs? Do you think we should be doing a better job restoring neuromuscular function before a patient returns to play after an ACLR?
Written by: Kyle Harris
Reviewed by: Jeffrey Driban
ACL Graft Type May Not Matter When Attempting to Improve Patient-Reported Outcome 2-Years Post-Surgery