Re:arthrogenic muscle inhibition 논문 모음

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재미있는 개념이다.

Arthrogenic Muscle Response of the Quadriceps and.pdf

Arthrogenic Muscle Inhibition Is Not present in the limb co.pdf

1: Arthritis Rheum. 2009 Jan 15;61(1):78-83. Links

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

Rice D, McNair PJ, Dalbeth N.

AUT University, Auckland, New Zealand.

OBJECTIVE: Arthrogenic muscle inhibition (AMI) contributes to quadriceps weakness and atrophy in knee arthritis and following joint injury. This laboratory-based study examined the efficacy of cryotherapy in reducing quadriceps AMI caused by intraarticular swelling. METHODS: Sixteen subjects without knee pathology participated, and were randomly assigned to a cryotherapy (n = 8) or control (n = 8) group. Surface electromyography (EMG) from vastus medialis and quadriceps torque measurements were recorded during maximum effort isometric contractions. All subjects then received an experimental joint infusion, whereby dextrose saline was injected into the knee to an intraarticular pressure of 50 mm Hg. EMG and torque measurements were repeated. Thereafter, the cryotherapy group had ice applied to the knee for 20 minutes while the control group did not receive an intervention. EMG and torque measurements were again collected. Quadriceps peak torque, muscle fiber conduction velocity (MFCV), and the root mean square (RMS) of EMG signals from vastus medialis were analyzed. RESULTS: Quadriceps peak torque, MFCV, and RMS decreased significantly following joint infusion (P </= 0.001). Cryotherapy led to a significant increase in quadriceps torque and MFCV compared with controls (P < 0.05). The difference in RMS did not reach statistical significance (P = 0.13). CONCLUSION: The study demonstrated that cryotherapy is effective in reducing AMI induced by swelling. Cryotherapy may allow earlier and more effective quadriceps strengthening to occur in patients with knee joint pathology.

1: J Athl Train. 2007 Jul-Sep;42(3):355-60. Links

Arthrogenic muscle response of the quadriceps and hamstrings with chronic ankle instability.

Sedory EJ, McVey ED, Cross KM, Ingersoll CD, Hertel J.

University of Virginia, Charlottesville, VA, USA.

CONTEXT: An arthrogenic muscle response (AMR) of the soleus and peroneal muscles has been previously demonstrated in individuals with chronic ankle instability (CAI), but the presence of AMR in muscles acting on joints proximal to unstable ankles has not been previously explored. OBJECTIVE: To determine if AMR is present in the quadriceps and hamstrings muscles of those with and without unilateral CAI. DESIGN: Case control. SETTING: University research laboratory. PATIENTS OR OTHER PARTICIPANTS: Twenty subjects with unilateral CAI (12 males, 8 females: age = 19.9 +/- 3.7 years; height = 170.3 +/- 15.6 cm; mass = 78.0 +/- 23.1 kg) and 21 controls (16 males, 5 females: age = 23.2 +/- 5.4 years; height = 173.9 +/- 12.7 cm; mass = 87.2 +/- 24.6 kg) with no previous ankle injuries. MAIN OUTCOME MEASURE(S): The central activation ratio (CAR), a measure of motoneuron pool excitability during maximal voluntary isometric contraction, for the hamstrings and quadriceps muscles was measured in both limbs using the superimposed burst technique. RESULTS: The CAI group demonstrated quadriceps CARs that were significantly larger in their involved limbs (.87 +/- .09), as compared with their uninvolved limbs (.84 +/- .08), whereas no significant side-to-side difference was seen in the control group (sham involved = .80 +/- .11, sham uninvolved = .81 +/- .11). When values from both the involved and uninvolved limbs were averaged, the hamstrings CAR was significantly lower for the CAI group (.94 +/- .03) than for the control group (.96 +/- .03). CONCLUSIONS: Arthrogenic inhibition of the hamstrings muscles bilaterally and facilitation of the quadriceps muscle ipsilateral to the involved limb were noted in subjects with unilateral CAI. Motoneuron pool excitability appears to be altered in muscles that act on joints proximal to the ankle in those with unilateral CAI.

1: Foot Ankle Int. 2005 Dec;26(12):1055-61. Links

Arthrogenic muscle inhibition in the leg muscles of subjects exhibiting functional ankle instability.

McVey ED, Palmieri RM, Docherty CL, Zinder SM, Ingersoll CD.

University of Virginia, Department of Human Services, P.O. Box 400407, 210 Emmet Street South, Charlottesville, VA 22904, USA. edm9u@virginia.edu

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 x 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 < or = 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.

1: Knee Surg Sports Traumatol Arthrosc. 2005 Jul;13(5):370-6. Epub 2005 Feb 1. Links

Pre-synaptic modulation of quadriceps arthrogenic muscle inhibition.

Palmieri RM, Weltman A, Edwards JE, Tom JA, Saliba EN, Mistry DJ, Ingersoll CD.

Neuromuscular Research Laboratory, Division of Kinesiology, University of Michigan, 401 Washtenaw Avenue, Ann Arbor, MI 48109, USA. riannp@umich.edu

Arthrogenic muscle inhibition (AMI) impedes rehabilitation following knee joint injury by preventing activation of the quadriceps. AMI has been attributed to neuronal reflex activity in which altered afferent input originating from the injured joint results in a diminished efferent motor drive to the quadriceps muscles. Beginning to understand the mechanisms responsible for muscle inhibition following joint injury is vital to control or eliminate this phenomenon. Therefore, the purpose of this investigation is to determine if quadriceps AMI is mediated by a presynaptic regulatory mechanism. Eight adults participated in two sessions: in one session their knee was injected with saline and in the other session it was not. The maximum Hoffmann reflex (H-reflex), M-wave, reflex activation history, plasma epinephrine, and norepinephrine were recorded at: baseline, post needle stick, post lidocaine, and 25 and 45 min post effusion. Measures for the control condition were matched to the effusion condition. The percent of the unconditioned reflex amplitude for reflex activation history and the maximum H-reflex were decreased at 25 and 45 min post effusion as compared to measures taken at baseline, post needle stick, and post lidocaine (P<0.05). No differences were noted for the maximum M-wave or plasma epinephrine and norepinephrine levels in either the effusion or noneffusion admission (P>0.05). No differences were detected at any time interval for any measure during the control admission (P>0.05). Quadriceps AMI elicited via an experimental knee joint effusion is, at least in part, mediated by a presynaptic mechanism.