Return to Play After an Anterior Cruciate Ligament Injury: Prioritizing Neurological and Psychological Factors of the Decision-Making Algorithm

CENTRAL NERVOUS SYSTEM NEUROPLASTICITY

Despite the vast amount of attention and research focused on the ACL, the re-injury rate still remains quite high. It has been reported that rehabilitation programs that employ traditional neuromotor training produce a re-injury rate as high as 30% after the athlete returns to sport.^25-28 The overall rate of sustaining a second ACL injury is 15%11 in all patient populations. For the general population <25 years of age, the re-injury rate is 21%, and for athletes <25 years of age, the re-injury rate rises to 23%.¹¹ With re-injury rates at this level, it is certainly fair to consider and be critical of the current rehabilitation methods being used with this population. One opportunity for improvement lies in the general approach used to rehabilitate ACL-injured patients. Therapy for this injury is protocol-driven, and the fact remains that most protocols prioritize restoration of peripheral systems, with minimal thought given to the cortical control necessary to manage those systems.^29,30 When neural factors are considered, it is usually within the context of increasing strength, balance, power, and biomechanical control,^31-34 which are certainly important but peripheral factors nonetheless. The missing element in many ACL protocols may be how to best manage the central neural components and cognitive factors associated with this injury.

If the CNS were to receive more consideration in ACL protocols, the opportunity for improved outcomes could be substantial because the CNS has been proven to be a very malleable system, as long as it receives the correct input. The CNS demonstrates neuroplasticity,³⁵ which means that it is capable of reorganization, based on the stimuli that it receives, whether internal or external.³⁶

This is an important consideration in ACL rehabilitation because the ACL graft, while restoring the biomechanical properties to the knee, is not fully capable of producing the same neurosensory properties of the original ACL.^37-42This is an important concept to understand because an ACL tear does indeed cause deafferentation in the ascending pathways to the brain.^37-40,42-46 This can lead to CNS reorganization and subsequent alterations in efferent output to the periphery.^37-40,42-46 Therefore, if a protocol with traditional musculoskeletal principles was used, then the mechanical function of the knee may certainly be remediated, but the neurosensory function will remain in a maladaptive state,^47-50 potentially leading to aberrant, non-protective movement strategies and a higher risk of re-injury.

The process of CNS reorganization may begin with the initial ACL injury. A peripheral musculoskeletal injury creates an inflammatory response that results in the arrival of chemical mediators such as histamine, substance P, calcitonin, and calcitonin gene-related peptide at the site of injury.⁵¹ As edema accumulates in the joint, tension is applied to the capsule, which may adversely affect proprioception from the receptors located within.⁴⁵ The interruption of consistent input from the peripheral mechanoreceptors may lead to long-term differentiation of the ascending pathways.⁵² This information is synthesized at 3 different levels of the CNS (spinal cord, brain stem, and motor cortex) to produce motor output.^53-56 Differentiation in the ascending circuitry can cause inhibition of motor neurons at the spinal cord.⁴⁵Animal research has shown that this differentiation can cause a breakdown in the cuneate nucleus of the brainstem,⁵⁷which provides sensory information from the upper body, while the gracile nucleus does the same for the lower body. These structures transfer proprioceptive input to the ventral posterior lateral nucleus in the thalamus, where it is then sent to the primary somatosensory cortex.⁵⁷ In general, the somatosensory, visual, and vestibular systems interpret afferent inputs to control movement, balance, and stability.^58,59 In a sport like soccer, where the movement tasks are dynamic and unpredictable, it is easy to see why even a slight deficit in somatosensory processing could disrupt a movement. Valeriani and colleagues^42,46 showed that somatosensory-evoked potentials were indeed altered in a cohort of ACL reconstruction (ACLR) subjects, indicating reorganization within the CNS.  Additionally, the deafferentation could not be changed by other afferent input coming from the knee or by the new ACL graft placed in the knee.^42,46The primary motor cortex has been found to have a substantial network of connectivity with the primary somatosensory cortex, which supports the theory that the motor cortex has a very strong linkage with the peripheral receptors in the joint.⁶⁰  The ligaments in the joint contain Ruffini, Pacinian, and Golgi receptors, all of which react to changes in the collagen fibers and send information regarding tension, length, speed, acceleration, position, and movement back to the CNS.^61-64 Unfortunately, the ascending pathway deafferentation can cause reorganization within the CNS, which makes the feedback provided from the periphery less effective in motor planning.

Ward and colleagues⁶⁵ have reported that reorganization within the motor cortex is the primary cause of chronic neuromuscular movement deficits in peripheral joint injuries. Researchers have used functional magnetic resonance imaging, transcranial magnetic stimulation, and electroencephalography in ACL patients to demonstrate changes in cortical activity and subsequent CNS reorganization.⁶⁵ Kapreli and colleagues⁴¹ reported that subjects with an ACL injury demonstrated higher cortical activation in the pre-supplementary motor area (pre-SMA). This is a region that is responsible for more complex motor planning.^66,67 This area becomes active before the primary motor cortex and is responsible for preparing the final movement pattern that the motor cortex executes.⁴¹ As the task becomes more complex, activity in the pre-SMA will increase.⁴¹ Additionally, they found that the posterior secondary somatosensory area and posterior inferior temporal gyrus showed increased cortical activity compared with controls.⁴¹ Visual planning is processed in the posterior inferior temporal gyrus, and so, it appears that the difficulty in processing somatosensory information due to ascending pathway deafferentation places an increased reliance on the visual system for movement planning.^68-70 This was observed while ACL-injured subjects performed a simple knee flexion-extension movement encompassing 40°, indicating the need to incorporate higher central levels of planning for a very simple movement pattern.⁴¹ Baumeister and colleagues^37,38 also showed that subjects with ACLR had higher levels of cortical activation in the areas of the brain that require attention and that process sensory input. They theorized that this occurred because of reduced efficiency of neural processing at lower levels in the CNS. Despite the higher levels of cortical activity observed, they found that subjects with an ACLR demonstrated proprioceptive testing that was deficient compared with that of controls. Heroux and Tremblay⁷¹ also demonstrated that subjects with an ACLR had increased resting motor cortex activity. They believed that this occurred as the motor cortex attempted to maintain neuromotor output to the periphery in the face of diminished afferent input.

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