21/10/2024
Hot off the press 🔥
🦵 Knee joint pathology and efferent pathway dysfunction: Mapping muscle inhibition from motor cortex to muscle force
👫 Individuals with knee joint injury, particularly those with anterior cruciate ligament (ACL) injury, anterior knee pain (AKP), or knee osteoarthritis (OA), commonly present with quadriceps weakness that persists despite rehabilitation (https://pubmed.ncbi.nlm.nih.gov/39389762/, https://pubmed.ncbi.nlm.nih.gov/20064053/; https://pubmed.ncbi.nlm.nih.gov/38015817/; https://journals.sagepub.com/doi/10.1177/1941738118822739; https://pubmed.ncbi.nlm.nih.gov/33591346/).
🦵 This weakness is a major contributor to structural and functional decline over time functional decline (https://pubmed.ncbi.nlm.nih.gov/14872454/, https://pubmed.ncbi.nlm.nih.gov/34916210/, https://pubmed.ncbi.nlm.nih.gov/37884728/), knee OA development (https://pubmed.ncbi.nlm.nih.gov/36455966/) and risk of re-injury (https://pubmed.ncbi.nlm.nih.gov/27162233/). Despite rehabilitation efforts, this weakness often persists.
🦵 Due to the knee joint's role in generating proprioceptive information (https://pubmed.ncbi.nlm.nih.gov/2060205/, https://pubmed.ncbi.nlm.nih.gov/20870506/), injuries are increasingly viewed as complex insults to the sensorimotor system (https://pubmed.ncbi.nlm.nih.gov/28005191/; https://pubmed.ncbi.nlm.nih.gov/25561075/). Sensory nerve fibers and mechanoreceptors make up approximately 3% of knee ligament and joint capsule tissue volume (https://pubmed.ncbi.nlm.nih.gov/2060205/; https://pubmed.ncbi.nlm.nih.gov/20870506) and respond to nociception, changes in tissue length, or pressure to inform proprioception (https://pubmed.ncbi.nlm.nih.gov/6897495/). Knee joint pathologies result in persistent, undesirable activation or destruction of these sensory organs, forming the basis for a sensory origin of motor impairments: arthrogenic muscle inhibition and associated central nervous system plasticity (https://pubmed.ncbi.nlm.nih.gov/10348160/).
📘 In a brand-new paper by Sherman and colleagues (2024, https://pubmed.ncbi.nlm.nih.gov/39426249/) provide a comprehensive review of efferent pathway dysfunction following knee joint pathology, particularly focusing on motor cortex and muscle function impairments. The authors synthesize studies involving neuroimaging and neurophysiologic techniques to highlight how changes in motor systems contribute to muscle dysfunction, particularly in the quadriceps and hamstrings.
📊 The key findings are described subsequently
👉 Efferent Pathway Dysfunction:
After knee joint injuries, especially ACL injury, AKP, and OA, motor pathway disruptions are common. These include altered motor cortex excitability, reduced motor unit recruitment, and diminished voluntary muscle activation, primarily affecting the quadriceps. The deficits arise from a combination of reduced excitability in the motor cortex, alterations in the corticospinal tract, and impaired motoneuron pool activation, which leads to reduced muscle force generation and coordination.
🧠 Motor Cortex and Corticospinal Tract:
Changes in the motor cortex, including reduced activation and altered motor planning, are evident in individuals with ACL injury. ACL reconstruction (ACLR) patients show increased supplementary motor area activation and decreased pre-motor area activity. There is also evidence of reorganization in the primary motor cortex (M1), particularly a shift in the activation centroid, and reduced corticospinal excitability. These changes lead to decreased voluntary muscle contractions.
💪 Motoneuron Pool and Muscle Inhibition:
The knee joint provides proprioceptive feedback to the central nervous system, but knee injuries disrupt this, leading to "arthrogenic muscle inhibition" (AMI), which limits motor neuron recruitment and muscle contraction. The Hoffmann reflex (H-reflex) studies indicate altered motoneuron pool excitability post-injury. Early post-ACL injury stages show suppressed motoneuron excitability, which improves over time but can still exhibit long-term changes.
⬇️ Sensory-Motor Integration and Plasticity:
Knee joint injuries, particularly ACL injuries, result in deafferentation due to ligament tears, leading to a decrease in proprioceptive input. This contributes to long-term motor impairments through structural changes in the sensorimotor system. These sensory deficits disrupt proper motor unit recruitment, impairing muscle strength, force steadiness, and rate of force development (RFD).
🦵 Peripheral and Structural Changes:
Beyond neuromuscular deficits, knee injuries also cause peripheral structural adaptations in muscle, such as fiber type shifts (from Type I to Type IIa), muscle atrophy, and increased intramuscular fat, which further contribute to muscle weakness, reduced rate of force development and muscle dysfunction.
🏋️♀️ Clinical Implications and Rehabilitation:
These results highlight the need for treatments that specifically address efferent pathway dysfunction to improve outcomes. Strategies like eccentric-based exercise, neuromuscular electrical stimulation (NMES) and high intensity cross-education can help restore muscle function by enhancing neural drive and motor unit recruitment. Neuromodulatory interventions such as full body or local muscle vibration and visual biofeedback may also increase efferent drive. A lack of validated clinical diagnostics for efferent pathway dysfunction is noted, which limits the ability to tailor rehabilitation interventions effectively.
📷 The figure below shows sensorimotor adaptions present in ACL injury and reconstruction with emphasis on efferent pathways. Abbreviations: fMRI, functional magnetic resonance imaging; M1, motor cortex; EEG, electroencephalography; TMS, transcranial magnetic stimulation; DTI, diffusor tensor imaging; EMG, electromyography; dEMG, decomposition EMG. (https://pubmed.ncbi.nlm.nih.gov/39426249/)
