Deficit in Quadriceps Voluntary Activation After Anterior Cruciate Ligament Reconstruction: Roles of the "Learned Non-use" Paradigm and the Interhemispheric Inhibition

Deficit in Quadriceps Voluntary Activation After Anterior Cruciate Ligament Reconstruction: Roles of the "Learned Non-use" Paradigm and the Interhemispheric Inhibition

Anterior cruciate ligament (ACL) tear is mainly caused by sport injuries. 40% of injuries are attributed to noncontact mechanisms involving pivoting. Regaining quadriceps strength is a primary focus of patients pursuing a rehabilitation program after ACL reconstruction (ACLR). Unfortunately, despite rehabilitation programs aimed at reversing this muscle weakness, quadriceps strength deficits may persist for years. Moreover, this deficit leads to increased risk of sustaining another knee injury, and increased risk for developing posttraumatic osteoarthritis. At present, neither the optimal rehabilitative program nor the clinical and instrumental parameters to take into account at the time of return to activity have reached a consensus among clinicians.

The investigators hypothesize that:

• a persistent deficit in voluntary activation, that is an inability to achieve complete activation of a muscle, is present after ACLR.
• this deficit in voluntary activation is associated with a phenomenon of "learned/acquired non-use" both in balance and during gait. This phenomenon will be demonstrated by investigating asymmetries in the recruitment of the injured lower limb in balance tests and during gait.
• the "learned/acquired non-use" paradigm is associated to asymmetries in the hemispheric cortical activity. This phenomenon will be investigated through transcranial magnetic stimulation.

The primary endpoint is the demonstration that the quadriceps muscle weakness after ACLR may represent a case of "learned non-use". This behaviour looks automatic and unconscious, so that the adjective "acquired" seems preferable to "learned". It consists of the under recruitment of the impaired side, once healed, as a form of unconscious protection, which is adopted when the contralateral side may carry out the function.

The secondary outcome is the investigation of the correlation among the deficits in voluntary activation, in balance tests, during gait, and in the neurophysiologic trials, with the clinical conditions of the patients.

It is expected that the injured lower limb show a deficit in the activation of the quadriceps muscle with respect to the contralateral one and with respect to normative data. The impaired limb will present lower recruitment in balance tests and a deficit in power production during gait.

The contralesional hemisphere will demonstrate higher interhemispheric inhibition, lower short-interval intracortical inhibition (SICI) and higher short-interval intracortical facilitation (SICF) with respect to the ipsilesional hemisphere.

The evidence for an asymmetry between the two lower limbs would support the hypothesis that the "acquired non-use" paradigm has a role in the deficits following ACL lesions and that it is unspecific across asymmetric impairments, and independent of the underlying disease.

Results from the present study will allow:

• the identification of clinical and instrumental criteria to guide the return-to-sport decision following ACLR.
• the estimate of the sample size for future experimental protocols and new rehabilitative programs.

Inclusion Criteria:

• anterior cruciate ligament tear with arthroscopic reconstruction, between 6 and 18 months before the tests;
• Tegner activity level > 5;
• Body Mass Index between 18 and 25;
• voluntary knee extension of at least 70°;
• ability to understand the instructions;
• ability to wittingly sign the informed consent form.

Exclusion Criteria:

• other previous knee injuries or surgical interventions;
• major procedures associated with the anterior cruciate ligament reconstruction: osteotomy, other ligaments reconstruction;
• meniscectomy, with surgical removal of more than 30% of the meniscal volume or removal of the meniscal root;
• comorbidities, such as: rheumatic diseases; other congenital or acquired neuromuscular pathologies; diabetes mellitus; osteoporosis; cancer; heart disease; history of epilepsy, endocranial hypertension;
• first degree relatives affected by epilepsy;
• current treatment with oral anticoagulant or antiplatelet therapy;
• drug therapy, which could induce epileptic crisis;
• history of high alcohol consumption;
• implanted electro-sensitive devices;
• implanted intracranial or intraocular metallic devices;
• history of retinal detachment;
• presence of cochlear implant.