Arthrogenic muscle response to a simulated ankle joint effusion

[문형철]

반사성 근수축(reflexive muscle contraction)의 병리적 이름 arthrogenic muscle inhibition에 관한 논문

발목 염좌후에 foot/ankle complex가 만성적으로 불안정성이 초래되는 중요한 한가지 이유를 설명

Simulated ankle joint effusion results in facilitation of the soleus, peroneus longus, and tibialis

anterior motoneurone pools. This may occur to stabilise the foot/ankle complex in order to maintain

posture and/or locomotion.

- 발목관절 부종은 가자미근,  장비골근, 전경골근 운동신경 pool의 촉진을 야기함. 

- 이는 이동이자 자세유지를 이루기 위한 안정화를 야기할 수 있음. 

Ankle sprains are common during athletic competition and recreational activity.1–3 Acute ankle sprains comprise 12% of all injuries seen in emergency rooms and15% of all athletic injuries.1 2 Functional ankle instability (FAI) or a subjective report of ‘‘giving way’’ at the ankle may be preval‎ent in as many as 40% of patients after an acute sprain of the lateral ligament complex.4 5 A definitive cause of FAI continues to elude clinicians. 

The absence of a pathophysiological mechanism for this chronic instability precludes the development of an effective treatment protocol. Peroneal muscle weakness may exist after an ankle sprain precipitating FAI. Weakness of the evertor musculature has been extensively examined, but its existence is still questioned because of conflicting results.6–9 The possible weakness of the evertor musculature has been suggested to occur as a result of peroneal nerve injury,7 inadequate rehabilitation,9 and/or inhibition because of pain or oedema.10 

After ankle injury it is difficult to determine which of the above mechanisms lead to the evertor weakness as all of those proposed may result. The use of an ankle effusion model is an effective method to determine whether inhibition is associated

with swelling within the ankle joint. Neuromuscular inhibition of the evertor musculature may exist in concurrence with inhibition or facilitation of the other muscles that stabilise the ankle complex. 

This inhibition may occur after ankle joint injury and is a possible cause of FAI, therefore further examination is warranted.

Neuromuscular inhibition has been widely reported in the quadriceps as a result of knee joint injury11–13 or simulated

joint effusion.14–16 This phenomenon has been termed arthrogenic muscle inhibition (AMI) and is a continuing reflex inhibition of the musculature surrounding a joint after distension or damage to structures of that joint.17 

The quadriceps musculature sustains no direct damage, but severe weakness and wasting occurs, creating disability and

prolonging the rehabilitation process. AMI has been generalised to occur at all joints in the musculoskeletal system,18 19

yet minimal research20–22 has been conducted to confirm‎ this hypothesis. A simulated effusion at the ankle joint has been

shown to result in facilitation of the soleus H-reflex,22 but it is not known how the other muscles that stabilise the ankle/foot complex react to joint trauma. Petrik et al22 hypothesised that facilitation of the soleus occurs in addition to inhibition of the tibialis anterior and peroneus longus musculature, preventing dorsiflexion of the ankle, thereby decreasing joint volume. 

Establishing the relation between the plantarflexors/dorsiflexors and invertors/evertors would be useful in understanding

the interaction of the muscles after trauma. The purpose of this investigation was to compare changes in the soleus, tibialis anterior, and peroneus longus H-reflex measurements resulting from ankle joint effusion over a one hour time period.