Arthrogenic Muscle Inhibition of the Knee: A Surgeon-Focused Narrative Review of Diagnosis and Management

Abstract

Arthrogenic muscle inhibition (AMI) is a reflexive suppression of quadriceps motor drive that arises from abnormal joint afferent signaling rather than structural failure. It is a common and underrecognized barrier to recovery after knee injury and surgery, reported in more than half of acute anterior cruciate ligament (ACL) injuries and in roughly one-third of patients early after total knee arthroplasty. Even when a reconstruction, repair, or arthroplasty is technically successful, persistent inhibition can limit voluntary quadriceps activation, terminal knee extension, gait, and functional strength. This narrative review synthesizes the current evidence with a surgeon-facing perspective, organized around three areas: the neurophysiology of AMI, its clinical assessment and diagnosis, and current management strategies. The pathophysiology is time-dependent: acute AMI is predominantly a spinal reflex phenomenon driven by effusion, pain, inflammation, and altered mechanoreceptor input, whereas chronic AMI reflects corticospinal and cortical reorganization that responds less reliably to joint-directed treatment alone. AMI has no diagnostic gold standard and is recognized clinically after structural causes are excluded, with the Sonnery-Cottet (SANTI) classification providing a practical bedside grade and quantitative measures such as the central activation ratio reserved for research settings. Among management options, neuromuscular electrical stimulation carries the strongest evidence, supported by meta-analyses of randomized trials after ACL reconstruction, with earlier initiation associated with greater quadriceps strength recovery. Targeted activation exercises and cryotherapy are widely used and supported by observational and experimental work, though the evidence behind them is less direct. We consolidate this evidence into graded summary tables and a proposed bedside clinical pathway. Early recognition of AMI, particularly in high-risk perioperative windows, allows the surgeon to distinguish neuromuscular inhibition from mechanical block, guide patient-specific counseling, and coordinate treatment before recovery is compromised.

Introduction

Arthrogenic muscle inhibition (AMI) is not a structural problem. Even when a reconstruction, repair, or arthroplasty is technically successful, patients may still have difficulty regaining quadriceps control, terminal knee extension, normal gait, and functional strength. AMI helps explain this disconnect between structural treatment and functional recovery. AMI has been reported after acute anterior cruciate ligament (ACL) injury, ACL reconstruction, and total knee arthroplasty (TKA), with recent studies showing AMI in 56.7% of acute ACL injuries (170 of 300 patients) and in 36% of patients (95% CI, 30–42) two weeks after knee arthroplasty.^1,2 Its clinical importance comes from its association with quadriceps weakness, extension deficits, altered gait mechanics, delayed rehabilitation, lower functional outcomes, and decreased satisfaction after surgery.³

AMI is best understood as a neural activation deficit rather than simple postoperative weakness. After joint injury or compromise, effusion, inflammation, pain, or surgery, altered sensory input from the joint can reduce the nervous system’s ability to fully activate the surrounding musculature. Around the knee, this most often presents as impaired quadriceps activation despite an intact extensor mechanism.⁴ This distinction matters because early strength loss after knee injury or surgery may reflect impaired motor drive secondary to AMI rather than muscle atrophy alone. Persistent quadriceps dysfunction has been described after ACL reconstruction, arthroscopic or open joint preservation procedures, and TKA, and may interfere with functional recovery when not recognized and treated as a distinct neuromuscular problem.³

Despite increasing recognition, AMI remains difficult to identify in routine orthopaedic practice. It can resemble or coexist with other causes of poor postoperative function, including pain-limited effort, deconditioning, arthrofibrosis, cyclops lesion, nerve injury, extensor mechanism disruption, or a mechanical block to motion, making it difficult to determine whether neural inhibition is the primary driver or one part of a broader problem.² A second challenge is the lack of a universally accepted diagnostic standard. Research tools such as the central activation ratio, interpolated twitch technique, Hoffmann reflex testing, transcranial magnetic stimulation, and electromyography can help measure neuromuscular inhibition, but they are not routinely available in most clinical settings, and may be confounded by patient pre-injury state.⁵ Clinical systems such as the SANTI classification offer a more practical bedside approach, but no widely adopted surgeon-facing algorithm for diagnosis and management yet exists.¹

For orthopaedic surgeons, recognizing AMI is important because persistent quadriceps inhibition may limit recovery despite technically successful treatment. Earlier recognition may help surgeons identify patients at risk for delayed rehabilitation, rule out structural mimics when recovery is not progressing as expected, allow for improved patient-specific counseling, and coordinate targeted treatment with rehabilitation teams. Therefore, the purpose of this review is to summarize the current understanding of AMI after knee injury and surgery around three objectives. The first area concerns the neurophysiology underlying inhibition, the second pertains to clinical assessment and diagnosis, and the third focuses on current management. Each area is examined within high-risk contexts, such as anterior cruciate ligament injury, ACL reconstruction, and total knee arthroplasty. Whereas prior reviews have approached AMI primarily from a rehabilitation or neurophysiologic mechanism standpoint, this review frames AMI for the operating surgeon, organizing evaluation and management around perioperative decision points and consolidating the evidence into a proposed bedside pathway for early identification and treatment (Figure 1). Although recent reviews have examined the neurophysiology of inhibition, rehabilitation programming, and return-to-sport testing in detail, no comprehensive account has delineated the clinical pathway from a stalled postoperative knee through exclusion of structural mimics, bedside grading, and evidence-based treatment selection. The present review aims to address this gap.

Figure 1.

Proposed clinical pathway for the recognition and management of arthrogenic muscle inhibition (AMI). This pathway synthesizes current evidence and is intended as a clinical decision aid rather than a validated protocol. A patient presenting with quadriceps weakness, an extension deficit, or stalled rehabilitation first undergoes exclusion of structural mimics, since AMI is a diagnosis of exclusion. When a structural cause is identified, it is treated directly. When no structural cause is identified, bedside severity is graded with the SANTI classification. Management addresses effusion and pain with cryotherapy as a pre-rehabilitation adjunct, targeted activation exercises as a commonly used first-line measure, and neuromuscular electrical stimulation as the most strongly supported adjunct when activation failure persists. Chronic or refractory presentations reflect cortical reorganization and respond less reliably to joint-directed treatment alone. The preoperative arm flags patients with acute anterior cruciate ligament injury, persistent effusion, or poor voluntary activation as already inhibited before surgery. Box color denotes the type of step: assessment and diagnosis (blue), treatment (green), and caution or directed treatment (amber). Arrows indicate the direction of the clinical decision sequence.

Search Strategy and Selection Criteria

A structured search of PubMed/MEDLINE was performed for articles published through July 2026. Terms for arthrogenic muscle inhibition, including quadriceps inhibition and voluntary activation failure, were paired with knee terms such as anterior cruciate ligament injury, ligament reconstruction, total knee arthroplasty, joint effusion, and rehabilitation. Reference lists of relevant articles and prior reviews were hand-searched. Clinical studies in postoperative populations took priority. Where direct clinical evidence was unavailable, experimental effusion models and neurophysiologic studies were used and identified as such. Eligible sources included original studies, systematic reviews, meta-analyses, and consensus statements. This is a narrative rather than a systematic review, so selection favored clinical relevance to the operating surgeon over formal quantitative synthesis.

Pathophysiology/Neurophysiology

AMI is driven by aberrant afferent signaling from the injured joint that reflexively suppresses motor drive to the quadriceps at multiple levels of the nervous system. The knee is a densely innervated sensory organ: mechanoreceptors within the capsule, ligaments, menisci, and periarticular tissues continuously transmit information about joint position, pressure, and movement to the spinal cord and higher motor centers. After injury or surgery, the normal afferent traffic is disrupted by several stimuli, including effusion, pain, inflammation, and altered mechanoreceptor input. Effusion and hemarthrosis distend the capsule and increase pressure-sensitive afferent discharge. At the same time, ligament rupture removes or distorts the proprioceptive input normally provided by receptors on joint structures like the ACL. The result is abnormal sensory input to the central nervous system, which can activate inhibitory neural pathways and reduce quadriceps motor drive.^4,6

Joint effusion is the best characterized peripheral trigger. Classic experimental work demonstrated H-reflex depression of the vastus medialis at intra-articular volumes of approximately 20 to 30 mL, with inhibition of other quadriceps heads occurring at higher volumes.^4,7 Smaller effusions can also matter, with inhibition reported at intra-articular volumes as low as approximately 10 mL, since the relevant stimulus is capsular pressure rather than absolute volume and a stiff post-surgical capsule can generate high pressure from a modest effusion.⁸ These thresholds should be understood as evidence that modest effusion directly impairs quadriceps activation, not as fixed cutoffs, since intra-articular pressure rather than absolute volume is the stronger mechanistic driver.^4,7 Because this inhibition is a reflex rather than a conscious response to pain, AMI can be present in a patient who is minimally swollen and reports little discomfort. Pain and inflammation contribute in parallel. High-threshold nociceptive afferents, sensitized by mediators such as IL-1β, TNF-α, and substance P, can amplify inhibitory interneuron input at the spinal level. However, pain, inflammation, and effusion may not have strictly additive effects.^4,9

At the spinal level, abnormal afferent input converges on inhibitory interneuron pathways that suppress the quadriceps alpha motor neuron pool. Multiple circuits are implicated, including group I non-reciprocal inhibitory pathways, flexion-reflex circuitry, and gamma-loop dysfunction.^4,10 In practical terms, the injured joint sends abnormal sensory input that reduces the excitability of the quadriceps motor pathway, making full voluntary contraction difficult even with maximal patient effort. The net effect is decreased motor neuron pool excitability such that voluntary activation fails even when the muscle-tendon unit is structurally intact. Critically, this joint-afferent inhibition operates during voluntary contraction, not only at rest, which is why patients with AMI cannot simply overcome the deficit through greater effort.⁴ The magnitude of this activation deficit is clinically meaningful, as changes in voluntary quadriceps activation have been shown to predict changes in muscle strength and gait biomechanics after knee joint effusion.¹¹ Experimental effusion reduces the Hoffmann reflex and reflex activation history while leaving the muscle response unchanged, locating at least part of the inhibition at a presynaptic level rather than within the muscle itself.¹²

The supraspinal contribution to AMI is time-dependent. In acute experimental effusion models, cortical motor excitability is not reduced and may transiently increase, suggesting compensatory upregulation in the face of spinal inhibition.⁸ Chronic and post-surgical cohorts, by contrast, demonstrate persistent corticospinal deficits, altered sensorimotor cortical organization, and increased intracortical inhibition that accumulate over weeks to months following reconstruction.¹³ A longitudinal study tracking patients from before reconstruction through six months found that spinal-reflexive deficits dominated the early period and normalized by six months, while corticospinal threshold elevations were absent acutely and emerged only at six months.¹⁴ Meta-analytic data across 14 studies confirm elevated motor thresholds in both limbs after reconstruction, with involved-limb corticospinal output reduced further beyond two years.¹⁵ Acute AMI is therefore predominantly a spinal reflex phenomenon, while chronic AMI reflects central reorganization less amenable to peripheral intervention.

The mechanisms of AMI are self-reinforcing. Inhibition prevents full quadriceps loading, which reduces normal mechanoreceptive feedback and sustains aberrant afferent drive, perpetuating spinal motor neuron suppression. Disuse accelerates secondary atrophy, and over time, cortical reorganization consolidates the deficit. Persistent quadriceps inhibition, when accompanied by reflex hamstring overactivity and altered loading mechanics, sets the stage for extension loss, delayed rehabilitation, and postoperative stiffness if not recognized and addressed early.^2,10 These AMI-driving stimuli, their proposed neural mechanisms, and their clinical correlates are summarized in Table 1.

Table 1.

AMI-Driving Stimuli: Dominant Neural Mechanisms and Clinical Correlates

Stimulus	Dominant Neural Mechanism	Clinical Correlates
Joint effusion	Elevated intra-articular pressure activates Group II–IV capsular afferents; pre- and post-synaptic spinal inhibition of quadriceps alpha motor neurons	Inhibition of the VM is detectable at ~20-30 mL and is independent of pain; pressure is a stronger predictor than absolute volume4,7
Pain/nociception	High-threshold Group III/IV afferents reinforce flexor facilitation and extensor inhibition via dorsal-horn circuits and descending pathways	Pain and effusion are parallel rather than strictly additive drivers; combined effect varies by phenotype and timing9
Inflammation/synovitis	IL-1β, TNF-α, bradykinin, and substance P sensitize articular afferents, lowering thresholds and sustaining discharge after gross swelling resolves	AMI can persist after visible effusion is gone; subclinical synovitis maintains afferent drive4
Mechanoreceptor loss/gamma-loop dysfunction	ACL disruption removes normal Ia proprioceptive input; impaired fusimotor drive degrades spindle sensitivity and alpha motor neuron excitability	Bilateral gamma-loop abnormalities persist after ACLR; contributes to lasting activation asymmetry9
Chronic central adaptation	Sustained afferent barrage drives maladaptive spinal interneuron plasticity and cortical motor map reorganization; increased intracortical inhibition accumulates over weeks to months	Corticomotor asymmetry documented months to years post-ACLR; less reversible with peripheral interventions alone13

Abbreviations: VM, Vastus Medialis; ACLR, anterior cruciate ligament reconstruction; IL-1β, interleukin-1 beta; TNF-α, tumor necrosis factor alpha. Superscripts refer to references below.

Clinical Presentation and Consequences

AMI can delay return to activity and reduce performance after knee surgery, so recognizing its clinical manifestations early is vital for recovery.4 The primary presentation of AMI is marked weakness of the quadriceps muscle group.3,4 This may further manifest secondarily as either a functional or structural flexion contracture, pain, swelling, joint laxity, altered gait mechanics, delayed rehabilitation progress, and poor functional outcomes.7,13 Presentation of AMI can also vary depending on the injury and/or postoperative timeline. Inhibition has been reported to be most pronounced in the early postoperative period, with the magnitude of activation failure decreasing thereafter as effusion and pain subside.4 This may hinder a clinician’s identification of AMI in the early postoperative stages, as many surgeries require some period of knee immobilization or activity limitation that obscures AMI when it is most severe.

Evaluation and Diagnosis

AMI is primarily recognized clinically, with neurophysiologic testing reserved mainly in research or specialized settings. Currently, there is no universally accepted gold standard test, so identifying and treating AMI requires comprehensive history and physical examination. For patients with high suspicion of AMI, ruling out other potential pathologies that may result in similar presentations is crucial. These include mechanical causes such as arthrofibrosis, extensor mechanism injuries, and neurogenic causes. The initial step to rule out structural causes typically includes radiographic and MRI imaging. Imaging is not used to diagnose AMI directly, but radiographs or MRI may be used when structural causes of weakness or motion loss are suspected.⁵ Therefore, imaging may support the diagnosis by helping exclude structural mimics, but it should not be considered a direct diagnostic test for AMI.

The Sonnery-Cottet (SANTI) classification is a clinical classification system used to help diagnose and evaluate AMI clinically.¹⁶ This classification system is primarily based on muscle testing and ranges from grade 0 to grade 3, depending on the severity of muscle inhibition, with grade 0 being normal vastus medialis oblique (VMO) contraction and grade 3 being a chronic, irreducible, passive extension deficit requiring extensive posterior arthrolysis.⁶ The SANTI classification and the reported response to targeted activation exercises derive largely from a single research group, so both are best regarded as a practical clinical grading approach awaiting independent replication rather than an established diagnostic standard. This classification can help to identify and quantify the level of AMI before further testing. Although advanced testing is less common in clinical practice, several neurophysiological methods can help quantify AMI by measuring voluntary activation deficits, often through force or torque testing combined with electrical stimulation or EMG. More accessible bedside approaches have also been described, and a supine isometric physical examination has been shown to detect quadriceps inhibition as confirmed by electromyography.¹⁷

The central activation ratio (CAR) is a force-based measure used to quantify voluntary activation failure in AMI. CAR is the ratio of force produced during a maximal voluntary isometric contraction to the force produced when that contraction is superimposed with an electrical stimulus.¹⁸ The superimposed stimulus is delivered percutaneously to the femoral nerve or directly over the quadriceps, and the distinction matters when comparing studies. A lower CAR value indicates greater voluntary activation failure. Another testing measure is using the twitch interpolation technique, which similarly relies on providing electrical stimulus during maximal voluntary contraction, and additional force generation indicates incomplete activation. These diagnostic modalities, what each measures, and their key limitations are summarized in Table 2.¹⁹

Table 2.

Diagnostic Modalities for Arthrogenic Muscle Inhibition

Modality	What it Measures	Setting	Key Limitation
SANTI classification16	Bedside severity of quadriceps inhibition and reducibility, grade 0 to 3	Clinical	Qualitative; grades a presentation rather than quantifying activation deficit
Central activation ratio18	Voluntary activation failure from superimposed stimulation during MVIC	Research	Requires force or torque instrumentation; no standardized threshold
Twitch interpolation19	Incomplete voluntary activation from added force on superimposed stimulus	Research	Equipment-dependent; not scalable to routine practice
H-reflex7	Spinal motor neuron pool excitability	Research	Indirect measure; sensitive to testing conditions
TMS13	Corticospinal excitability	Research	Specialized equipment; investigational for diagnosis
EMG17	Muscle electrical activity during contraction	Research	Does not directly quantify voluntary activation deficit
Radiographs/MRI5	Structural joint pathology	Clinical	Excludes mimics only; not a direct test for AMI

Notes: No modality serves as a diagnostic gold standard; AMI is recognized clinically after exclusion of structural pathology. Superscripts refer to references below.

Abbreviations: MVIC, maximal voluntary isometric contraction; TMS, transcranial magnetic stimulation; EMG, electromyography.

Although multiple techniques exist to quantify AMI, these tools are not widely used in clinical practice due to limited availability and the lack of standardized diagnostic thresholds.^5,19 Therefore, AMI is most recognized clinically through quadriceps dysfunction after the exclusion of any structural pathology. Identification of AMI early in the pre-operative setting may help identify patients at risk for poor post-operative recovery and functional limitations.

Preoperative and Postoperative Considerations

Preoperative and postoperative recognition of AMI is clinically important because quadriceps inhibition may be present before surgery and may persist during recovery despite technically successful treatment.^4,6 Patients with acute ACL injury, persistent effusion, poor voluntary quadriceps activation, or limited terminal extension may already demonstrate AMI preoperatively, which can complicate rehabilitation and delay restoration of gait, strength, and motion and can be a cause of secondary surgery if not addressed early. Reported factors associated with AMI include the presence of effusion, concomitant injuries, and high pain scores after ACL injury, while in the arthroplasty population high pain (OR, 13.57; P<0.001), early flexion-contracture posturing (OR, 5.89; P<0.001), and female sex (OR, 2.81; P<0.002) were independently associated with AMI at two weeks.^1,2 In ACL reconstruction cohorts, preoperative effusion (OR, 8.97), bucket-handle meniscal tear (OR, 5.24), and reduced flexion range of motion have been identified as preoperative predictors. Furthermore, preoperative arthrogenic muscle inhibition predicts postoperative inhibition (OR, 3.56).²⁰ Preexisting inhibition is among the most consistent predictors of persistence across populations, with preoperative AMI predicting inhibition at 30 days after arthroplasty (OR, 6.08) and 30-day inhibition predicting persistence at 60 days (OR, 15.6), in addition to obesity, longer symptom duration, older age, and higher postoperative opioid requirements.²¹ In the postoperative setting, AMI should be considered in patients who are not progressing as expected, particularly when quadriceps activation remains poor or terminal extension is difficult to regain despite otherwise unremarkable surgical findings.^5,16 AMI should not be diagnosed in isolation without first excluding structural and neurologic causes of persistent dysfunction, including arthrofibrosis, cyclops lesion, extensor mechanism disruption, nerve injury, or other mechanical blocks to motion.^5,6 For surgeons, early recognition helps identify high-risk patients, differentiate AMI from structural postoperative complications, and coordinate rehabilitation targeting effusion control and activation training.^4,16

Management Strategies

Management is multimodal, addressing the underlying triggers of pain and inflammation, the inhibition itself, and its functional consequences. The primary goal is to reverse reflexive inhibition of the quadriceps motoneuron pool and restore voluntary activation. Neuromuscular electrical stimulation carries the strongest supporting evidence, while targeted exercises and cryotherapy rest largely on observational and experimental work. Evidence across modalities relies on different endpoints. Some studies measure physiological disinhibition or motoneuron pool excitability, while others assess voluntary activation, quadriceps strength, or patient-reported function. These endpoints are not equivalent, and a modality shown to disinhibit the motoneuron pool has not necessarily been shown to improve strength or clinical outcomes. Most of this evidence comes from acute ACL injury, ACL reconstruction, and experimental effusion models, with comparatively little from total knee arthroplasty or other knee procedures, so treatment selection outside ACL populations rests on weaker ground. In a prospective study of 300 acute ACL injuries by Sonnery-Cottet et al,² simple targeted knee exercises during a single session resolved AMI in 79% of affected patients (135 of 170), with patients showing AMI also demonstrating significantly worse Lysholm, IKDC, Simple Knee Value, and KOOS scores than those without (P<0.0001). In a case series of 30 patients by Dos Anjos et al,²² a single session of neuromotor reprogramming therapy in patients with AMI following knee injury or surgery increased VMO activation by a mean of 45% (P<0.01) and reduced the knee extension deficit from 4.03 to 1.93 cm (P<0.01). Management modalities and their strength of evidence are summarized in Table 3.

Table 3.

Management Modalities for Arthrogenic Muscle Inhibition by Strength of Evidence

Intervention	Proposed Mechanism	Evidence Strength	Level of Evidence	Setting
NMES23–27	Bypasses the inhibited pathway through direct involuntary contraction	Strong; meta-analyses of randomized trials after ACL reconstruction, pooled SMD 0.53 (95% CI, 0.27–0.79) to 0.73 (95% CI, 0.29–1.16)	I	Supported adjunct
Cryotherapy28–30	Disinhibits the quadriceps motor neuron pool; transiently raises excitability	Moderate; experimental effusion models showing short-term disinhibition	II	Pre-rehabilitation adjunct
TENS31–33	Facilitates motor neuron pool via cutaneous and joint afferents	Limited; experimental disinhibition, no demonstrated post-surgical clinical benefit	II	Investigational
Targeted activation exercises2,22	Reverses reflexive motor neuron pool inhibition; restores voluntary drive	Moderate; single large observational cohort, not independently replicated	III	Commonly used first-line
TMS13	Enhances motor cortex excitability to address corticospinal deficit	Limited	V	Investigational
Blood flow restriction/vibration	Proposed disinhibitory and strengthening effects	Limited	V	Investigational

Notes: Level of Evidence reflects the highest-quality study supporting each modality. Evidence strength is a separate judgment that additionally accounts for study design, consistency across studies, directness of the outcome measured, and applicability to postoperative patients, so a modality supported by a single higher-level study may still be graded as moderate. Rows are listed in decreasing order of Level of Evidence. Superscripts refer to references below.

Abbreviations: NMES, neuromuscular electrical stimulation; TENS, transcutaneous electrical nerve stimulation; TMS, transcranial magnetic stimulation.

Cryotherapy reverses neural inhibition in AMI and serves as a pre-rehabilitation strategy for strength gains after ACL reconstruction. Using knee effusion models, Hopkins et al²⁸ showed that cryotherapy disinhibits the quadriceps motoneuron pool. In the same study, cryotherapy also produced greater motoneuron recruitment above baseline.²⁸ In this experimental effusion model of 30 healthy volunteers, motoneuron pool facilitation in the cryotherapy group remained above baseline through the final measurement at 60 minutes, suggesting a clinical role for cryotherapy immediately prior to strengthening sessions. This concept has since been supported in additional work.^29,30 Thus, the application of cryotherapy immediately prior to quadriceps strengthening allows for greater activation of the quadriceps while reversing the neurophysiological inhibition of AMI. In the reported protocols cryotherapy is applied to the knee for roughly 20 minutes immediately before exercise, and the disinhibition is attributed to cold-induced modulation of joint afferent discharge rather than to analgesia alone.

Several other modalities have been investigated for their motoneuron disinhibitory properties in AMI, albeit with varying degrees of supporting evidence. These include Transcutaneous electrical nerve stimulation (TENS), Neuromuscular electrical stimulation (NMES), Transcranial magnetic stimulation (TMS), blood flow restriction, and vibration therapy.

TENS has traditionally been used clinically for pain modulation via cutaneous stimulation of sensory nerve fibers. Multiple models, however, have shown TENS to exert a disinhibitory effect in AMI.^28,31,32 One proposed mechanism suggests that stimulation of cutaneous and joint afferents via TENS facilitates activation of the quadriceps α-motoneuron pool independent of the γ-loop, potentially through a long-latency spinal reflex or supraspinal mechanism.³¹ However, no clinical trial has demonstrated a significant quantitative benefit of TENS as a disinhibitory modality for AMI following knee surgery.³³

NMES has been widely studied for treating strength deficits following ACL reconstruction and is a promising intervention for counteracting AMI-associated quadriceps weakness.^23–25 However, rather than disinhibiting the voluntary activation pathway directly, NMES circumvents the inhibited α-motoneuron pool by producing involuntary muscle contraction through direct stimulation of motor neurons. This provides the beneficial effect of providing a stimulus to muscle fibers that would otherwise not be received in the setting of AMI. Current evidence supports the use of NMES as an adjunct to standard rehabilitation protocols following knee surgery. Two meta-analyses report superior quadriceps strength recovery when NMES is combined with standard physical therapy after ACL surgery compared with standard rehabilitation alone, with one pooling 11 trials (N = 202) and finding a standardized mean difference of 0.53 (95% CI, 0.27–0.79) at six weeks or less and 0.59 (95% CI, 0.18–0.99) beyond six weeks (P<0.001), and another reporting a short-term effect of 0.73 (95% CI, 0.29–1.16) at 4 to 12 weeks. The effect was largest when NMES was started within the first postoperative week (SMD, 1.48; 95% CI, 0.80–2.17).^23–27

TMS is an emerging intervention for AMI that focuses on addressing the corticospinal excitability deficits that have been shown to contribute to AMI. With recent evidence demonstrating structural brain changes in ACL-injured patients associated with reduced corticospinal drive, TMS is proposed to reverse quadriceps inhibition by directly enhancing motor cortex excitability.¹³ TMS as a therapeutic modality for AMI remains investigational at this time, with limited current evidence supporting its therapeutic efficacy. The key studies underpinning these management recommendations, with their designs and levels of evidence, are summarized in Table 4.

Table 4.

Summary of Key Studies on the Management of Arthrogenic Muscle Inhibition

Study	Design	LoE	Key Findings	Take-Home Message
Li et al, 202523	Meta-analysis of 11 RCTs (N = 202)	I	NMES with standard PT improved quadriceps strength vs PT alone (SMD 0.53 [95% CI, 0.27–0.79] at ≤6 wk, 0.59 [95% CI, 0.18–0.99] at >6 wk); earliest use ≤1 wk strongest (SMD 1.48 [95% CI, 0.80–2.17])	NMES is an effective strength adjunct, most so when started early
Hauger et al, 201824	Meta-analysis of 11 RCTs (6 pooled)	I	Short-term NMES benefit at 4–12 wk (SMD 0.73 [95% CI, 0.29–1.16]) with improved physical function	Adjunctive NMES improves early quadriceps recovery after ACL surgery
Hopkins et al, 200228	Controlled experimental effusion model (N = 30)	II	Cryotherapy raised motoneuron pool excitability through 60 min; TENS disinhibited early but failed by 30 min	Cryotherapy is an effective pre-rehabilitation disinhibitor; TENS effect is not durable
Konishi et al, 201731	Crossover experimental (vibration model)	II	Brief TENS (25–30 s) restored quadriceps MVC and EMG after vibration-induced weakness vs no-TENS	TENS can acutely restore activation even when the gamma-loop is disrupted
Son et al, 201632	Crossover experimental (N = 30, saline pain model)	II	Sensory TENS restored quadriceps MVC and central activation ratio vs placebo under experimental knee pain (P<0.05)	TENS acutely disinhibits the quadriceps in experimental pain, though post-surgical trial evidence is lacking
Sonnery-Cottet et al, 20242	Case-control (N = 300)	III	AMI in 56.7%; 79% resolved after a single session of simple targeted exercises	Simple activation exercises reverse most acute AMI at the bedside
Lepley et al, 201426	Parallel longitudinal study (N = 36)	III	Eccentric exercise, alone or with NMES, restored quadriceps activation and strength to healthy levels better than NMES alone	Eccentric exercise is a potent activation and strength strategy after ACLR
Dos Anjos et al, 202322	Case series (N = 30)	IV	A single neuromotor reprogramming session raised VMO activation 45% and cut extension deficit from 4.03 to 1.93 cm	Neuromotor reprogramming can acutely improve activation and extension

Notes: Studies are listed in decreasing order of Level of Evidence.

Abbreviations: LoE, Level of Evidence; NMES, neuromuscular electrical stimulation; TENS, transcutaneous electrical nerve stimulation; PT, physical therapy; VMO, vastus medialis oblique; RCT, randomized controlled trial; MVC, maximum voluntary contraction; CAR, central activation ratio; EMG, electromyography.

Conclusion

Arthrogenic muscle inhibition is a clinically important but often underrecognized barrier to recovery after knee injury and surgery. By limiting voluntary quadriceps activation despite an intact extensor mechanism, AMI may contribute to persistent weakness, motion loss, delayed rehabilitation, functional deficits, and even secondary surgery when structural treatment has been technically successful.⁴ For orthopaedic surgeons, early recognition of AMI is important both to identify patients at risk for poor progression and to distinguish neuromuscular inhibition from structural causes of postoperative dysfunction. The pathway summarized in Figure 1 is intended to facilitate practical bedside recognition, guiding clinicians from initial presentation through exclusion of structural causes to graded treatment selection. Greater integration of perioperative surveillance, targeted rehabilitation, and evidence-based management strategies may improve recovery, although further work is needed to standardize diagnosis and define practical treatment algorithms for routine clinical use. These findings should not be extrapolated across all knee surgery without qualification. The proposed pathway has not been prospectively validated, and the supporting evidence varies substantially across interventions and patient populations. Prospective work is needed to validate practical diagnostic criteria and management algorithms across ACL injury, ACL reconstruction, and arthroplasty.

Funding Statement

This research received no external funding.

Data Sharing Statement

Data sharing is not applicable to this article as no new data were created or analyzed in this narrative review.

Ethics Approval

Ethics approval was not required for this narrative review, as it did not involve human participants, human data, or animals.

Author Contributions

All authors made a significant contribution to the work reported, whether in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.