Arthrogenic Muscle Inhibition Explained. Quad atrophy following ACL injury is mind blowing. It wasn’t until I experienced this personally with my. 0bjectives:To define the concept of arthrogenic muscle inhibition (AMI), to discuss Pain and disuse are often blamed for the inhibition and muscle atrophy. Key factors of muscle deconditioning are 1) muscle atrophy and 2) arthrogenic muscle inhibition (AMI); however their interaction and underlying mechanisms are.
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Marked weakness of the quadriceps muscles is typically observed following injury, surgery or pathology affecting the knee joint. This is partly due to ongoing neural inhibition that prevents the central nervous system from fully activating the quadriceps, a process known as arthrogenic muscle inhibition AMI.
This study aimed to further investigate the mechanisms underlying AMI by exploring the effects of experimental knee joint effusion on quadriceps corticomotor and intracortical excitability. Seventeen afthrogenic volunteers participated in this study. Transcranial magnetic stimulation was used to measure quadriceps motor evoked potential area, short-interval intracortical inhibition, intracortical facilitation and cortical silent period duration before and after experimental knee joint effusion.
Joint effusion was induced by the intraarticular infusion of dextrose saline into the knee. The results of this study provide no evidence for inihbition supraspinal contribution to quadriceps AMI. Paradoxically, but consistent with previous observations in patients with chronic knee joint pathology, quadriceps corticomotor excitability increased after experimental knee joint effusion.
The increase in quadriceps corticomotor excitability may be at least partly mediated by a artrogenic in gamma-aminobutyric acid GABA -ergic inhibition within the motor cortex.
Marked weakness and atrophy of the quadriceps muscle is often observed after knee injury, knee surgery or in patients with knee joint arthritis. This is partly caused by an ongoing neural activation deficit of the quadriceps, a inhibjtion known as arthrogenic muscle inhibition AMI for a myscle see [ 1 ]. Furthermore, AMI appears to be ever present in arthritic joint disease [ inhlbition ], accounting for a large amount of the quadriceps muscle weakness observed in these individuals [ 7 ].
As well as being a direct cause of quadriceps muscle weakness, AMI may prevent effective muscle strengthening [ 89 ], leading to long-term quadriceps muscle atrophy and weakness that is difficult to reverse.
Ongoing quadriceps weakness is clinically important, as it is associated with impaired dynamic knee-joint stability [ 10 ] and physical function [ 1112 ]. Moreover, weaker quadriceps have been associated with an increased rate of loading at the knee joint [ 13 ] and recent longitudinal data has shown that greater baseline quadriceps strength may protect against incident knee pain [ 14 ], patellofemoral cartilage loss [ 14 ] muslce tibiofemoral joint-space narrowing [ 15 ].
Despite its clinical importance, the mechanisms underlying AMI are only partially understood. AMI has been linked to knee joint musscle, pain and structural damage [ 1 ]. The relative contribution of these factors is unclear but it is known that swelling alone provokes potent quadriceps AMI. This has been repeatedly demonstrated by the experimental infusion inhibiyion fluid into healthy, uninjured joints.
These studies have shown that intra-articular swelling substantially reduces quadriceps peak torque [ 1617 ], electromyographic EMG activity inhibjtion 1618 ] and H-reflex amplitude [ 1920 ], despite the absence of iinhibition damage, joint inflammation or pain. Aspirating arthrogenif injecting a local anaesthetic into the infused joint largely abolishes AMI [ 1720 ], while the prior injection of local anaesthetic prevents AMI with subsequent joint infusion [ 17 ], confirming the role of articular sensory receptors in this process.
Studies in animals [ 2223 ] have shown that joint infusion elevates intra-articular pressure, stimulating stretch and pressure-sensitive mechanoreceptors and greatly increasing group-II joint afferent discharge. It is unclear whether supraspinal pathways also contribute to AMI. Two studies [ 2627 ] have utilised transcranial magnetic stimulation TMS to show that quadriceps corticomotor excitability muuscle altered in individuals with knee joint pathology.
However, these cross-sectional studies were performed following long-term joint pathology, making it difficult to elucidate the effects of joint injury from other factors such as disuse, medication use and varying rehabilitation programmes. Furthermore, the magnitude of AMI, and hence its clinical impact, is typically greatest in the acute stages after joint injury inhihition surgery [ 2 – 4 ]. Thus, the purpose of this study was to explore the acute effects of experimental knee joint swelling on quadriceps corticomotor and intracortical excitability.
Seventeen participants eleven male and six female volunteered to take part in this study. Participants were screened and excluded based on contraindications to TMS, including epilepsy, head arthrogsnic, metal implants, or central nervous system-altering medications. Further exclusion criteria were previous history of pathology in both knee joints, a history of lower limb or spinal surgery, or a history of neurological disease.
In the event of a previous knee injury, the contralateral uninjured knee joint was used in testing. All participants provided written informed consent for the experimental procedures.
Ethical approval for this study was granted by the Northern X Regional Ethics Committee, Auckland, New Zealand in accordance with the principles set out in the declaration of Helsinki. Straps were firmly secured over the distal tibia, waist and chest to limit extraneous movement during the testing procedures. With the knee resting in slight flexion, a g cannula was inserted into the superomedial or, on two occasions, the superolateral aspect of the joint.
All injections were performed without local anaesthesia, under strictly sterile conditions. A pressure transducer Medex Inc. Both joint afferent discharge [ 23 ] and quadriceps AMI [ 18 ] have a stronger correlation with intra-articular pressure compared to intra-articular volume. The pain sensation evoked by the joint infusion was measured after the withdrawal of the cannula from the joint and just prior to the post infusion measurements.
Participants were asked to verbally rate any pain they felt in their knee on a scale from 0 no pain to worst pain imaginable. Prior to electrode placement the skin was shaved, abraded and cleaned with alcohol to reduce signal impedance.
Three 5-s maximum effort voluntary contractions of the quadriceps were performed prior to the first baseline measurements. To minimise the effect of strong voluntary contractions on corticomotor excitability [ 29 ], a 5-minute rest period was given between the performance of MVCs and the beginning of TMS procedures.
The coil was placed over the contralateral primary motor cortex so that the induced current flow was in a posterior-anterior direction.
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First, the optimum site for stimulation hot spot was found by delivering a series of suprathreshold stimuli as the coil was systematically moved over the scalp until the largest quadriceps MEP was elicited. The hot spot was marked on the scalp with a felt pen and all further testing completed with the coil held directly over this position. To achieve this level of activation, participants were given real-time visual feedback of their EMG signal.
The following dependent variables were examined from the quadriceps: The CSP duration was collected during the active condition only.
At all measurement intervals, 8 single pulse and 16 paired pulse stimuli 8 SICI, 8 ICF were delivered first at rest and then during quadriceps contraction. Inhiibtion joint infusion P1eight single pulse stimuli were delivered at rest using the same stimulus intensity as B1 and B2. This process was repeated for the outcome measures in the active condition, with the addition of a further eight single pulse stimuli to assess the CSP.
The conditioning stimulus intensity remained unchanged across all measurement points. Diagram inhibitiin the study protocol. Maximum effort voluntary contractions MVC of the quadriceps were performed prior to the first measurements of the dependent variables.
Rectified motor evoked potential MEP recorded from the quadriceps during active muscle contraction.
Quadriceps & Hamstrings Activation Failure
Note the stimulus artefact initial large positive deflection followed by the larger polyphasic MEP and then the silent period in the mucsle EMG following the MEP cortical silent period. Normality of the dependent variable distributions was checked using the Shapiro-Wilk test. The one-sample t -test was used to assess whether normalised MEP area was significantly different from B1 at the B2 or P1 time points. In the event that a significant effect of time was found, planned contrasts were used to assess whether the variables differed significantly arthgogenic B1 at the B2 or P1 time aethrogenic.
Four participants had a history of knee joint pathology in the contralateral untested limb. Dependent variables were collected from all 17 participants during the active condition. Upon insertion of the catheter into the knee joint, intraarticular pressure was typically negative or slightly above atmospheric pressure.
Data are mean and one standard error of the mean. Quadriceps cortical silent period CSP duration before and after experimental knee joint infusion. Despite these consistent findings across many different studies, we observed a significant increase inhibirion quadriceps MEP area after experimental joint infusion, suggesting an increase, rather than a decrease, in quadriceps corticomotor excitability.
This observation aarthrogenic made with the muscle at rest and during a voluntary contraction. While somewhat paradoxical, our findings are supported by similar observations in patients with chronic anterior knee arthrogeic [ 27 ] and anterior cruciate ligament ACL injury [ 26 ], where quadriceps corticomotor excitability was increased compared to healthy control participants, or the uninjured limb.
While speculative, such a change may reflect a compensatory mechanism by the central nervous system in an attempt to maintain neural drive to the muscle.
Arthrogenic muscle inhibition | definition of arthrogenic muscle inhibition by Medical dictionary
The current study is the first to use paired pulse TMS to determine the role of intracortical interneurons in the response mscle articular swelling. We found no evidence that either SICI or ICF are altered by experimental knee joint swelling, suggesting that the excitability of the interneurons underlying these responses was not altered.
In contrast, we observed a significant reduction in CSP duration after joint infusion. Thus, the reduction in CSP duration likely reflects reduced GABAergic inhibition at the level of the motor cortex following joint effusion [ 39 ]. Such a change may at least partly explain the observed increase in quadriceps corticomotor excitability. Interestingly, the observed reduction in CSP duration is at odds with findings in patients who had suffered a unilateral ACL injury, where no side-to-side differences in CSP duration were found despite an increase in quadriceps corticomotor excitability on the injured compared to the uninjured side [ 26 ].
This could reflect differences in the mechanism s underlying increased corticomotor excitability with acute experimental and arthrogfnic joint injury.
Importantly, other factors relevant to ACL injury such as disuse, pain and a loss of arthrobenic afferent input [ 40 ] may also influence the excitability of corticomotor and intracortical pathways. In this regard, it should be noted that while experimental joint infusion provides a model of joint injury that has consistently been shown to induce potent quadriceps AMI, it does not accurately mimic the afferent discharge from a joint affected by trauma or pathology.
Experimental joint infusion inhhibition increases the discharge of group-II joint afferents [ 23 ] but in the absence of inflammation, is unlikely to activate a large portion of group-III and -IV afferents. This is demonstrated by the fact that experimental swelling rarely evokes pain, as observed in the current and previous studies [ 163441 ]. This should be explored in future research, particularly given recent findings that experimental knee inhibitionn impairs quadriceps muscle activation [ 42 ] and experimental muscle pain increases intracortical inhibition in hand muscles [ 43 ].
In conclusion, we observed an increase in quadriceps corticomotor excitability following experimental knee joint infusion. Our findings provide no evidence for a cortical contribution to quadriceps AMI and suggest that ongoing spinal reflex inhibition may be sufficient to explain the marked neural activation deficit that occurs following acute knee injury, knee surgery and in chronic knee joint pathologies.
However, further research is needed to confirm these findings in different patient populations and in response to other relevant factors such as joint pain. The sponsors had no muecle in the study design, analysis, arthrogneic of results, writing of the manuscript or in the decision to submit the mmuscle for publication. The authors would like to acknowledge Mark Jackson and Dr Angela Crowley for their valuable assistance with the joint infusion procedures.
arthrogenic muscle inhibition
mucle DR was involved in the conception and design miscle the study, collection, analysis and interpretation of the data and the drafting and revision of the manuscript. PM was involved in the conception and design of the study, collection, analysis and interpretation of the data and in the revision of the manuscript. GL was involved in the conception and design of the study, collection and interpretation of the data and in the revision of the manuscript. ND was involved in the conception and design of the study, collection and interpretation of the data and in revision of the manuscript.
All the authors have read and approved this manuscript for publication. David Andrew Rice, Email: Peter John McNair, Email: Gwyn Nancy Lewis, Email: National Center for Biotechnology InformationU. Journal Inhibjtion Arthritis Res Ther v. Published online Dec Author information Article notes Copyright and License information Disclaimer.
Received Aug 23; Accepted Dec 3.