Alan R. Needle, Thomas W. Kaminski, Jochen Baumeister, Jill S. Higginson, William B. Farquhar and C. Buz Swanik
Rolling sensations at the ankle are common after injury and represent failure in neural regulation of joint stiffness. However, deficits after ankle injury are variable and strategies for optimizing stiffness may differ across patients.
To determine if ankle stiffness and muscle activation differ between patients with varying history of ankle injury.
Fifty-nine individuals were stratified into healthy (CON, n = 20), functionally unstable (UNS, n = 19), and coper (COP, n = 20) groups.
Main Outcome Measures:
A 20° supination perturbation was applied to the ankle as position and torque were synchronized with activity of tibialis anterior, peroneus longus, and soleus. Subjects were tested with muscles relaxed, while maintaining 30% muscle activation, and while directed to react and resist the perturbation.
No group differences existed for joint stiffness (F = 0.07, P = .993); however, the UNS group had higher soleus and less tibialis anterior activation than the CON group during passive trials (P < .05). In addition, greater early tibialis anterior activation generally predicted higher stiffness in the CON group (P ≤ .03), but greater soleus activity improved stiffness in the UNS group (P = .03).
Although previous injury does not affect the ability to stiffen the joint under laboratory conditions, strategies appear to differ. Generally, the COP has decreased muscle activation, whereas the UNS uses greater plantar-flexor activity. The results of this study suggest that clinicians should emphasize correct preparatory muscle activation to improve joint stiffness in injury-rehabilitation efforts.
Alan R. Needle, Jacqueline A. Palmer, Trisha M. Kesar, Stuart A. Binder-Macleod and C. Buz Swanik
Current research into the etiology of joint instability has yielded inconsistent results, limiting our understanding of how to prevent and treat ligamentous injury effectively. Recently, cortical reorganization was demonstrated in patients with ligamentous injury; however, these neural changes have not been assessed relative to joint laxity.
The purpose of the current study was to determine if changes in cortical excitability and inhibition occur in subjects with functional ankle instability, as well as to investigate the relationship between these measures and joint laxity.
Posttest only with control group.
12 subjects with no history of ankle sprain (CON) and 12 subjects with a history of unilateral functional ankle instability (UNS).
Subjects were tested for joint laxity using an instrumented ankle arthrometer. Cortical excitability and inhibition were assessed using transcranial magnetic stimulation (TMS) to obtain motor-evoked potentials and the cortical silent period from the lower leg muscles.
Main Outcome Measures:
Joint laxity was quantified as peak anterior displacement and inversion rotation. Active motor threshold, slope, and intensity at 50% of peak slope of TMS-derived recruitment curves were used to quantify cortical excitability from lower leg muscles, while the cortical silent period from the peroneus longus was used to represent intracortical inhibition.
No significant differences were observed between groups for laxity or cortical measures. CON demonstrated a significant relationship between laxity and tibialis anterior excitability, as well as laxity and silent period, while UNS ankles demonstrated significant relationships between peroneal and soleus excitability and laxity measures.
Our results support relationships between laxity and measures of excitability and inhibition that differ between healthy and unstable subjects. Future research should further investigate the mechanisms behind these findings and consider cortical influences when investigating altered joint laxity.