Introduction: Ankle sprains are among the most common injuries in sports and recreational activities. 10 to 40% of the acute ankle sprains lead to chronic ankle instability (CAI), which can be divided into its mechanical and its functional division. The clinical-orthopaedic diagnosis of mechanical ankle instability (MAI) has been well established, whereas the etiology of the functional ankle instability (FAI) is still not objectively allocatable. The aim of this study was to identify neuromuscular patterns in lower leg muscles to objectively describe the FAI.

Methods: 15 patients suffering from unilateral CAI (mean age, 35.5 years) since 2.4 years (1–9 years) were examined. The patients were evaluated etiologically and clinically (VAS pain score, AOFAS Ankle Score, calf circumference, and SF-36). Electromyographic (EMG) measurements of surface EMG with determination of mean EMG frequency and intensity by wavelet transformation were taken synchronously with dynamic stabilometry measurements. Four lower leg muscles were detected: tibialis anterior (TA), gastrocnemius medialis (GM), soleus (SO), and peroneus longus (PL) muscle. 15 healthy subjects were tested identically.

Results: Patients showed higher stability indices, higher VAS score, and lower AOFAS Ankle Score.

The mean EMG frequency was significantly lower for the PL (pathologic leg, 138.3 Hz; normal leg, 158.3 Hz, p< 0.001). Lower mean EMG intensity was found in the pathologic PL and GM. The mean EMG frequency of the TA was lower in the patient group, its intensity higher.

Discusssion and conclusion: Patients suffering CAI demonstrate weakened stability and impaired life quality. Neuromuscular patterns of the GM, PL and TA lead evidently to an objective etiology of the functional ankle instability. EMG patterns of four lower leg muscles indicate chronic changes in muscle morphology, such as degradation of type-II muscle fibres or modified velocity of motor unit action potentials. Accurate prevention and rehabilitation may compensate a MAI with a sufficient functional potential of lower leg muscles. This may also avoid operative treatment of MAI. The present study evidences the etiology of the FAI with objective parameters and indicates chronic changes in muscle morphology within CAI-Patients.

Purpose: Ankle sprains are among the most common injuries in sports and recreational activities. 10 to 40% of the acute ankle sprains lead to chronic ankle instability (CAI), which can be divided into its mechanical and its functional division. The clinical-orthopaedic diagnosis of mechanical ankle instability (MAI) has been well established, whereas the etiology of the functional ankle instability (FAI) is still not objectively allocatable. The aim of this study was to identify neuromuscular patterns in lower leg muscles to objectively describe the FAI.

Method: 15 patients suffering from unilateral CAI (mean age, 35.5 years) since 2.4 years (1–9 years) were examined. The patients were evaluated etiologically and clinically (VAS pain score, AOFAS Ankle Score, calf circumference, and SF-36). Electromyographic (EMG) measurements of surface EMG with determination of mean EMG frequency and intensity by wavelet transformation were taken synchronously with dynamic stabilometry measurements. Four lower leg muscles were detected: tibialis anterior (TA), gastrocnemius medialis (GM), soleus (SO), and peroneus longus (PL) muscle. 15 healthy subjects were tested identically.

Results: Patients showed higher stability indices, higher VAS score, and lower AOFAS Ankle Score. The mean EMG frequency was significantly lower for the PL (pathologic leg, 138.3 Hz; normal leg, 158.3 Hz, p< 0.001). Lower mean EMG intensity was found in the pathologic PL and GM. The mean EMG frequency of the TA was lower in the patient group, its intensity higher.

Conclusion: Patients suffering CAI demonstrate weakened stability and impaired life quality. Neuromuscular patterns of the GM, PL and TA lead evidently to an objective etiology of the functional ankle instability. EMG patterns of four lower leg muscles indicate chronic changes in muscle morphology, such as degradation of type-II muscle fibres or modified velocity of motor unit action potentials. Accurate prevention and rehabilitation may compensate a MAI with a sufficient functional potential of lower leg muscles. This may also avoid operative treatment of MAI. The present study evidences the etiology of the FAI with objective parameters and indicates chronic changes in muscle morphology within CAI-Patients.