scholarly journals Promising Effect of Visually-Assisted Motor Imagery Against Arthrogenic Muscle Inhibition – A Human Experimental Pain Study

2021 ◽  
Vol Volume 14 ◽  
pp. 285-295
Author(s):  
Shota Oda ◽  
Masashi Izumi ◽  
Shogo Takaya ◽  
Nobuaki Tadokoro ◽  
Koji Aso ◽  
...  
Keyword(s):  
Motor Imagery ◽  
Experimental Pain ◽  
Muscle Inhibition ◽  
Arthrogenic Muscle Inhibition

Arthrogenic Muscle Inhibition in the Leg Muscles of Subjects Exhibiting Functional Ankle Instability

2005 ◽  
Vol 26 (12) ◽  
pp. 1055-1061 ◽  
Author(s):  
Eric D. McVey ◽  
Riann M. Palmieri ◽  
Carrie L. Docherty ◽  
Steven M. Zinder ◽  
Christopher D. Ingersoll
Keyword(s):  
Tibialis Anterior ◽  
Ankle Instability ◽  
H Reflex ◽  
Functional Ankle Instability ◽  
Injured Limb ◽  
Lateral Ankle ◽  
M Wave ◽  
Muscle Inhibition ◽  
Lateral Ankle Ligaments ◽  
Arthrogenic Muscle Inhibition

Background: Functional ankle instability or a subjective report of “giving way” at the ankle may be present in up to 40% of patients after a lateral ankle sprain. Damage to mechanoreceptors within the lateral ankle ligaments after injury is hypothesized to interrupt neurologic feedback mechanisms resulting in functional ankle instability. The altered input can lead to weakness of muscles surrounding a joint, or arthrogenic muscle inhibition. Arthrogenic muscle inhibition may be the underlying cause of functional ankle instability. Establishing the involvement of arthrogenic muscle inhibition in functional ankle instability is critical to understanding the underlying mechanisms or chronic ankle instability. The purpose of this investigation was to determine if arthrogenic muscle inhibition is present in the ankle joint musculature of patients exhibiting unilateral functional ankle instability. Methods: Twenty-nine subjects, 15 with unilateral functional ankle instability and 14 healthy control subjects, consented to participate. Bilateral soleus, peroneal, and tibialis anterior H-reflex and M-wave recruitment curves were obtained. Maximal H-reflex and maximal M-wave values were identified and the H:M ratios were calculated for data analysis. Separate 1 × 2 ANOVA were done for both the functional ankle instability and control groups to evaluate differences between limbs on the H:M ratios. Bonferroni multiple comparison procedures were used for post hoc comparisons ( p ≤ 0.05). Results: The soleus and peroneal H:M ratios for subjects with functional ankle instability were smaller in the injured limb when compared with the uninjured limb (p < 0.05). No limb difference was detected for the tibialis anterior H:M ratio in the functional ankle instability group ( p = 0.904). No side-to-side differences were detected for the H:M ratios in patients reporting no history of ankle injury ( p > 0.05). Conclusions: Depressed H:M ratios in the injured limb suggest that arthrogenic muscle inhibition is present in the ankle musculature of patients exhibiting functional ankle instability. Establishing and using therapeutic techniques to reverse arthrogenic muscle inhibition may reduce the incidence of functional ankle instability.

scholarly journals Management of the Knee Extension Deficit after Acute Trauma

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Thiago Alvim do Amaral ◽  
David Sadigursky
Keyword(s):  
Case Report ◽  
Surgical Treatment ◽  
Knee Extension ◽  
Extension Deficit ◽  
Acute Trauma ◽  
Muscle Inhibition ◽  
Articular Pathology ◽  
Functional Gain ◽  
Arthrogenic Muscle Inhibition

A 25-year-old man initially presented with right knee extension deficit after an acute trauma, caused by a condition known as arthrogenic muscle inhibition. This should not be confused with a mechanical block caused by intra-articular pathology. The loss of knee extension, even if minimal, is disabling and leads to worse results after knee surgical treatment. Therefore, it is necessary to recognize and diagnose arthrogenic muscle inhibition to ensure the best treatment for patients with this condition. In this case report, the patient was managed with a rehabilitation technique resulting in an effective functional gain of the quadriceps and full restoration of knee extension.

Clinical Perceptions of Arthrogenic Muscle Inhibition

2010 ◽  
Vol 2 (4) ◽  
pp. 160-162 ◽  
Author(s):  
Joseph M. Hart ◽  
David R. Diduch ◽  
Andy G. Baker
Keyword(s):  
Muscle Inhibition ◽  
Arthrogenic Muscle Inhibition

Arthrogenic Muscle inhibition: A Limiting Factor in Joint Rehabilitation

2000 ◽  
Vol 9 (2) ◽  
pp. 135-159 ◽  
Author(s):  
J. Ty Hopkins ◽  
Christopher D. Ingersoll
Keyword(s):  
Complete Recovery ◽  
Data Sources ◽  
Therapeutic Interventions ◽  
Limiting Factor ◽  
Reflex Inhibition ◽  
Hoffmann Reflex ◽  
Joint Injury ◽  
Muscle Inhibition ◽  
Type Data ◽  
Arthrogenic Muscle Inhibition

Objectives:To define the concept of arthrogenic muscle inhibition (AMI), to discuss its implications in the rehabilitation of joint injury, to discuss the neurophysiologic events that lead to AMI, to evaluate the methods available to measure AM1 and the models that might be implemented to examine AMI, and to review therapeutic interventions that might reduce AMI.Data Sources:The databases MEDLINE, SPORTDiscus, and CIHNAL were searched with the termsreflex inhibition, joint mechanoreceptor, Ib interneuron, Hoffmann reflex, effusion, andjoint injury. The remaining citations were collected from references of similar papers.Conclusions:AMI is a limiting factor in the rehabilitation of joint injury. It results in atrophy and deficiencies in strength and increases the susceptibility to further injury. A therapeutic intervention that results in decreased inhibition, allowing for active exercise, would lead to faster and more complete recovery.

Effects of cryotherapy on arthrogenic muscle inhibition using an experimental model of knee swelling

2008 ◽  
Vol 61 (1) ◽  
pp. 78-83 ◽  
Author(s):  
David Rice ◽  
Peter J. McNair ◽  
Nicola Dalbeth
Keyword(s):  
Experimental Model ◽  
Muscle Inhibition ◽  
Arthrogenic Muscle Inhibition

Peroneal Activation Deficits in Persons with Functional Ankle Instability

2009 ◽  
Vol 37 (5) ◽  
pp. 982-988 ◽  
Author(s):  
Riann M. Palmieri-Smith ◽  
J. Ty Hopkins ◽  
Tyler N. Brown
Keyword(s):  
Ankle Sprain ◽  
Muscle Activation ◽  
Ankle Instability ◽  
Cross Sectional Study ◽  
Functional Ankle Instability ◽  
Level Of Evidence ◽  
Cross Sectional ◽  
Emg Amplitude ◽  
Muscle Inhibition ◽  
Arthrogenic Muscle Inhibition

Background Functional ankle instability (FAI) may be prevalent in as many as 40% of patients after acute lateral ankle sprain. Altered afference resulting from damaged mechanoreceptors after an ankle sprain may lead to reflex inhibition of surrounding joint musculature. This activation deficit, referred to as arthrogenic muscle inhibition (AMI), may be the underlying cause of FAI. Incomplete activation could prevent adequate control of the ankle joint, leading to repeated episodes of instability. Hypothesis Arthrogenic muscle inhibition is present in the peroneal musculature of functionally unstable ankles and is related to dynamic peroneal muscle activity. Study Design Cross-sectional study; Level of evidence, 3. Methods Twenty-one (18 female, 3 male) patients with unilateral FAI and 21 (18 female, 3 male) uninjured, matched controls participated in this study. Peroneal maximum H-reflexes and M-waves were recorded bilaterally to establish the presence or absence of AMI, while electromyography (EMG) recorded as patients underwent a sudden ankle inversion perturbation during walking was used to quantify dynamic activation. The H:M ratio and average EMG amplitudes were calculated and used in data analyses. Two-way analyses of variance were used to compare limbs and groups. A regression analysis was conducted to examine the association between the H:M ratio and the EMG amplitudes. Results The FAI patients had larger peroneal H:M ratios in their nonpathological ankle (0.399 ± 0.185) than in their pathological ankle (0.323 ± 0.161) (P = .036), while no differences were noted between the ankles of the controls (0.442 ± 0.176 and 0.425 ± 0.180). The FAI patients also exhibited lower EMG after inversion perturbation in their pathological ankle (1.7 ± 1.3) than in their uninjured ankle (EMG, 3.3 ± 3.1) (P < .001), while no differences between legs were noted for controls (P > .05). No significant relationship was found between the peroneal H:M ratio and peroneal EMG (P > .05). Conclusion Arthrogenic muscle inhibition is present in the peroneal musculature of persons with FAI but is not related to dynamic muscle activation as measured by peroneal EMG amplitude. Reversing AMI may not assist in protecting the ankle from further episodes of instability; however dynamic muscle activation (as measured by peroneal EMG amplitude) should be restored to maximize ankle stabilization. Dynamic peroneal activity is impaired in functionally unstable ankles, which may contribute to recurrent joint instability and may leave the ankle vulnerable to injurious loads.

Arthrogenic Muscle Inhibition: Best Evidence, Mechanisms, and Theory for Treating the Unseen in Clinical Rehabilitation

2021 ◽  
pp. 1-19
Author(s):  
Grant Norte ◽  
Justin Rush ◽  
David Sherman
Keyword(s):  
Evidence Synthesis ◽  
Well Being ◽  
Limiting Factor ◽  
Joint Injury ◽  
Patient Decision Making ◽  
Patient Decision ◽  
Joint Health ◽  
Muscle Inhibition ◽  
Post Traumatic ◽  
Arthrogenic Muscle Inhibition

Context: Arthrogenic muscle inhibition (AMI) impedes the recovery of muscle function following joint injury, and in a broader sense, acts as a limiting factor in rehabilitation if left untreated. Despite a call to treat the underlying pathophysiology of muscle dysfunction more than three decades ago, the continued widespread observations of post-traumatic muscular impairments are concerning, and suggest that interventions for AMI are not being successfully integrated into clinical practice. Objectives: To highlight the clinical relevance of AMI, provide updated evidence for the use of clinically accessible therapeutic adjuncts to treat AMI, and discuss the known or theoretical mechanisms for these interventions. Evidence Acquisition: PubMed and Web of Science electronic databases were searched for articles that investigated the effectiveness or efficacy of interventions to treat outcomes relevant to AMI. Evidence Synthesis: 122 articles that investigated an intervention used to treat AMI among individuals with pathology or simulated pathology were retrieved from 1986 to 2021. Additional articles among uninjured individuals were considered when discussing mechanisms of effect. Conclusion: AMI contributes to the characteristic muscular impairments observed in patients recovering from joint injuries. If left unresolved, AMI impedes short-term recovery and threatens patients’ long-term joint health and well-being. Growing evidence supports the use of neuromodulatory strategies to facilitate muscle recovery over the course of rehabilitation. Interventions should be individualized to meet the needs of the patient through shared clinician–patient decision-making. At a minimum, we propose to keep the treatment approach simple by attempting to resolve inflammation, pain, and effusion early following injury.

Arthrogenic Quadriceps Inhibition and Rehabilitation of Patients with Extensive Traumatic Knee Injuries

1994 ◽  
Vol 86 (3) ◽  
pp. 305-310 ◽  
Author(s):  
M. V. Hurley ◽  
D. W. Jones ◽  
D. J. Newham
Keyword(s):  
Joint Instability ◽  
Knee Injuries ◽  
Joint Damage ◽  
Voluntary Contraction ◽  
Strength Increase ◽  
Quadriceps Weakness ◽  
Before And After ◽  
Muscle Inhibition ◽  
Intensive Rehabilitation ◽  
Arthrogenic Muscle Inhibition

1. The relationship between joint damage, quadriceps weakness and arthrogenic muscle inhibition was investigated in eight patients who had sustained extensive traumatic knee injury. Isometric and isokinetic quadriceps and hamstring voluntary strength, and quadriceps arthrogenic muscle inhibition during isometric contractions, were measured before and after 4 weeks (approximately 100 h) of intensive rehabilitation. 2. Compared with the uninjured leg, before rehabilitation the injured leg had larger amounts of quadriceps arthrogenic muscle inhibition (P < 0.025), quadriceps (P < 0.0001) and hamstring (P < 0.0001) weakness and severe functional joint instability. There was a negative correlation between the amount of arthrogenic muscle inhibition and quadriceps voluntary contraction force (P < 0.025). 3. After rehabilitation in the injured leg there were small hamstring strength increases (P < 0.05–0.025), but no overall significant quadricep strength increase. Arthrogenic muscle inhibition was statistically unchanged. Severe functional joint instability was still reported by all patients. 4. Previous studies have shown that minimal joint damage evokes relatively less arthrogenic muscle inhibition that does not impede rehabilitation. These data indicate that greater joint damage is associated with greater arthrogenic muscle inhibition, quadriceps weakness and joint instability. Furthermore, intensive rehabilitation had little affect on either quadriceps arthrogenic muscle inhibition or atrophy.

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