INTRODUCTION:

Injury to the lateral ligaments of the lateral lower leg complex is among the most well-known injuries by the athletes ^[1]. Lateral ankle sprains are thought to be endured by men and, women at around the same rates; in any case, one recent report recommends that female interscholastic and intercollegiate ball players have a 25% more grave danger of causing grade I lower ankle sprains than their male partners. More than 23 000 moderate ankle sprains have been assessed to happen per day in the United States, which equates to one sprain for each 10 000 individual’s day by day^[2,3,4]. Much has been composed of the mechanical part of the ligaments that encompass the ankle joint in providing ankle joint stability. The anterior talofibular ligament limits talar tilt throughout the sagittal plane motion, especially with the joint in a position of plantar flexion^[4,5]. The calcaneofibular ligament appears to constrain talar tilting in dorsiflexion as well as in talocalcaneal adduction^[6,7]. Also, embedded within these ligaments are mechanoreceptors believed to be responsible for providing a proprioceptive role in maintaining ankle joint stability ^[8].

Proprioception, which results from the afferent neural info beginning from mechanoreceptors about the joint, adds to an element in joint stability components and facilitated motor patterns^[9]. Michelson and Hutchins^[10] exhibited histologically that Ruffini-type, Pacinian corpuscle type, and Golgi tendon organ receptors are scattered all through the ankle ligaments, with Pacinian and Golgi tendon like bodies making up a majority of the mechanoreceptors present. Johansson and partners ^[11] described how ligamentous mechanoreceptors play a role in providing the joint stability that is similarly as essential as the mechanical part of the ligaments. In the fair, neutral position the bony anatomy of the ankle joint is responsible for stability. Compressive loads enhance the rigid stability in the weight-bearing area. Stormont et al.^[12] demonstrated that under loading the articular surface is given 30% of the rotational stability and 100% of the inversion stability. Under non-weight bearing conditions, more limitations were provided by the ligamentous structures. With increasing plantar flexion, the osseous constraints are lessened, and the soft tissues are more susceptible to injury. The primary lateral soft tissue stabilizers of the ankle are the ligaments of the lateral ligamentous complex: the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL).

The ATFL is nothing more than a thickening of the tibiotalar capsule that originates from the anterior border and tip of the lateral malleolus and runs anterior to insert on the neck of the talus. It is 6 to 10 mm wide, 20 mm long, and 2mm thick^[13].It runs almost parallel to the axis of the neutral foot. When the foot is in plantar flexion, however, the ligament courses parallel to the axis of the leg^[14,15].since most sprains occur when the foot is in plantar flexion, this ligament is most often injured in inversion sprains. The CFL originates from the tip of the lateral malleolus and furthermore, with a slight backward inclination, to the lateral side of the calcaneus^[16]. The ligament is extra-articular and lies just under the peroneal tendons. It is 20 to 25 mm in length with a diameter of 6 to 8 mm. Since this ligament runs more perpendicular to the axis of the neutral foot, isolated tears are less common with typical plantar flexion injuries. It is most commonly torn during moderately severe sprains where the ATFL tears and the damage continue around the outside of the ankle to also tear the CFL. Isolated injuries can occur but are infrequent and occur when the ligament is under maximum strain with the foot in dorsiflexion.

The PTFL arises from the posteromedial aspect of the lateral malleolus and runs posteromedially to the posterior process of the talus. It has an average diameter of 6 mm. The ligament is under most strain when the foot is in dorsiflexion. Isolated injuries of the PTFL are exceedingly rare. Most injuries occur as a result of very severe ankle sprains where the both the ATFL and CFL have been ruptured before tearing of the PTFL as the damage continues around the lateral aspect of the ankle. During an inversion injury, the ATFL is the first ligament to be injured. If the tearing force continues, the CFL will be injured next, followed by the PTFL^[17,18].

Injury to the lateral ligaments of the ankle results in adverse changes to the neuromuscular system that provides dynamic support to the ankle. The path-etiologic model is not finished without including impeded neuromuscular control, subsequently bringing about insufficiencies of the active defense mechanism protecting against hyper supination of the rearfoot^[19]. In the course of recent decades, functional deficiencies among people with either severe ankle sprains or Chronic Ankle Instability (CAI) have been exhibited by measuring deficits in ankle proprioception, cutaneous sensation, nerve conduction speed, neuromuscular reaction times, postural control, and strength. Proprioception at the ankle is impaired in individuals prone to repetitive ankle sprains on measures of kinesthesia^[20-22]. Recent evidence proposes that change in muscle spindle activity in the peroneal muscles may be more important than altered particular mechanoreceptor activity in the indications of proprioceptive deficits at the ankle^[23]. The clinical importance of proprioceptive deficits is not completely understood at this time, and whether proprioception was enhancing through rehabilitation exercises has not yet been decisively illustrated ^[24].Impeded cutaneous sensation^[25-28] and slowed nerve conduction velocity^[29] have been reported as indicators of common peroneal nerve palsy after an acute lateral ankle sprain, but no evidence exists that such impairments are present in patients with CAI. Impaired neuromuscular recruitment patterns have been demonstrated in individuals with a history of repetitive lateral ankle sprain^[30-35]. If the peroneal response is impaired in those with CAI, it may be due to impaired proprioception, slowed nerve conduction velocity, or central impairments in neuromuscular recruitment strategies. Impaired postural control during single-leg stance has frequently been demonstrated in individuals after acute ankle sprain^[30-39] and in those with a history of repetitive ankle sprains^[40-45].

Freeman et al.^[46] have proposed that the fundamental mechanism of ankle instability after ankle injury develops due to the lesion of mechanoreceptors in the joint capsule and ligaments surrounding the ankle. This theory is known as articular deafferentation. According to this theory, the dynamic stability of the ankle joint depends on the ability of the evertors (peroneal) to react quickly to sudden inversion perturbations, to develop sufficient tension to prevent injurious ranges of ankle motion, and thus to prevent sprains of the lateral ligament complex of the ankle. This theory suggests that individuals with functional instability could have delayed and diminished reflex responses in the evertor muscles of their affected ankles in reaction to an inversion stress because of altered capsular and ligamentous afferent input. However, more current evidence suggests that the dynamic control of ankle stability depends on feed-forward motor control of the central nervous system^[47]. It has been suggesting that inappropriate positioning of the ankle joint before ground contact during walking may have important implications for ankle joint stability^[48]. Furthermore, we are unaware of any research that has examined the influence of the lateral ankle ligaments on muscle firing characteristics during dynamic stability. Alterations in muscles proximal to the ankle joint have also been identified by Bullock-Saxton et al.^[28] who found changes in hip extensor activity in both injured and uninjured limbs after a severe unilateral ankle sprain. These central impairments and the resulting impaired postural control may put the individual at greater risk for chronic injury or other lower extremity injury and may be the cause of chronic ankle instability^[49].Most studies to assess postural control deficits use static tasks. However, gait initiation has detected impairments in other populations.

The purpose of this study was to evaluate the role of peripheral afferent information from the lateral ankle ligaments in spatial and temporal muscle activation characteristics during an inversion perturbation dynamic stability.

MATERIALS AND METHODS:

Twenty athletes volunteered to participate in this study, who sustained a lateral ankle sprain who were recruited for participation in this study. The subjects participated in a variety of collegiate sports including, baseball, cheer, diving, football, men’s soccer, softball, women’s basketball, women’s tennis, and volleyball and were included in the study if the individual sustained a lateral ankle sprain during the sports activity. Exclusion criteria for the control group included; history of chronic ankle instability as identified by using the foot and ankle ability measure (FAAM) to evaluate self-perceived function and stability with a score no lower than 95% on either ankle and lower extremity injury within the previous six months. Exclusion for both groups included neurological conditions, including concussion, in the last 12 months. All subjects provided written informed consent before participating in the study as approved by the University Human Ethics Committee.

Participants’ information:

Table 1. Demographic information: There were no significant differences between groups for age, height or weight.

Group	Mean Age (yrs.)	Mean Height(cm)	Mean Weight (kg)
Experimental Group	20 ± 1.5	175.40 ± 11.14	81.84 ± 21.57
Control Group	19 ± 1.1	175.16 ± 10.17	76.20 ± 20.41

Electromyographic Assessment:

We recorded surface EMG from the tibialis anterior, peroneus longus, and Peroneus Brevis muscles in each group. The EMG activity was inspected by an independent evaluator, who examined the EMG profiles for any evidence of baseline shift, motion artifact, or 50-Hz interference. If any of those above were present, the trial was rejected; thus, this accounted for the difference in the number of muscles recorded from each subject. The activity has been registered using preamplified electrodes applied to lightly abraded skin over the respective muscle belly. Electrode placement was carried out by the Surface EMG for Noninvasive Assessment of Muscles Research Group recommendations. Data acquisition was performed with an amplifier/processor module that consisted of onsite preamplifiers and an amplifier/processor. Raw EMG signals were converted to a root mean square value using a time constant of 55 msec. The root mean square EMG signals were then converted from analog to digital at a sampling rate of 50 Hz using a converter Visual inspection was used to determine the onset of EMG activity above the resting baseline level. The latency time between platform release and the onset of EMG activity was calculated in milliseconds.

Testing Procedure:

The participant was asked to lay back supine position on a table bed with barefoot. Before sensor placement was done, the skin was cleaned with an alcohol pad or sanitizer to allow for better adhesion of the electrode. Then, the electrodes were placed on a target muscle. The actual placement of the electrodes can be complicated and depend on some factors including specific muscle selection and the size of that muscle. Proper EMG placement is imperative for accurate representation of the tissue of interest which is in this study is the Tibialis anterior, Peroneus Longus and Peroneus Brevis. Two types of contraction trial were done in this study, which is eversion and inversion contraction. The participant was instructed to contract the muscles for about 10 seconds for three sets. The rest period for 20 seconds was given after each contraction. Finally, after the test was done, the electrodes had to be disposed of as it cannot already use by another participant.

Table 2. The Conventional Training Program^[50]:

No Material

Ball

Balance Board

Ball & Balance Board

Exercise1

One-legged stance with the knee

flexed. Step-out on the other leg

with the knee flexed and keep balance for 5 seconds. Repeat 10 times for both legs.

Variations1234

Exercise3

Make pairs. Both stand in one-

legged stance with the knee

flexed. Keep a distance of 5 meters. Throw and/or catchaball

5 times while maintaining balance.Repeat10 times for both legs.

Variations12

Exercise5

One legged stance on the balance

Board with the knee flexed.

Maintain balance for 30 seconds and change stance leg. Repeat twice for both legs.

Variations1234

Exercise7

Make pairs. One stands with both Feet on the balance board. Throw and/or catch a ball 10 times with one hand while maintaining balance. Repeat twice for both players on the balance board.

Exercise2

One-legged stance with the hip and the knee flexed. Step-out on the other leg with the hip and knee flexed, and keep balance for 5 seconds. Repeat 10 times for both legs.

Variations1234

Exercise4

Make pairs. Stand both in one- legged stance with the hip and knee flexed. Keep a distance of 5meters. Throw and/or catchaball 5 times while maintaining balance.Repeat10 times for both legs.

Variations12

Exercise6

One-legged stance on the balance board with the hip and knee flexed. Maintain balance for 30

Seconds and change stance leg. Repeat twice for both legs.

Variations1234

Exercise8

Make pairs. One stands in one- legged stance with the knee flexed on the balance board, the other has The same position on the floor. Throw and/orcatchaball10times with one hand while maintaining balance. Repeat twice for both legs and for both players on the balance board.

Variations12

Exercise10

Step slowly over the balance board with one foot on the balance board. Maintain the balance board in a horizontal position while steppingover.Repeat10timesfor both legs.

Exercise9

Make pairs. One stands in one-legged stance with the hip and knee flexed on the balance board, The other has the same position on the floor. Throw and/or catch a ball 10 times with one hand while maintaining balance. Repeat twice for both legs and for both players on the balance board.

Variations12

Exercise11

Stand with both feet on the Balance board. Make 10 knee flexions while maintaining balance.

Exercise13

Make pairs. One stands with both

Feet on the balance board. Play the ball with anupperh and technique 10 times while maintaining balance. Repeat twice for both legs and for both players on the balance board.

Variations5678

Variations on basic exercises:

1 The standing leg is stretched

2The standing legisflexed

3The standing is stretched &the eyes are closed

4 The standing leg is flexed & the eyes are closed

5 The standing leg is stretched & upper hand technique

6 The standing leg is flexed & upper hand technique

7Thestandinglegisstretched &lower hand technique

8 The standing leg is flexed & lower hand technique

Exercise12

One-legged stance on the balance board with the knee flexed. Make

10 knee flexions while maintaining balance. Repeat twice

For both legs.

Exercise14

Make pairs. One stands in one- legged stance with the knee flexed on the balance board, the other has the same position on the floor. Play the ball with an upper hand technique 10 times while maintaining balance. Repeat twice for both legs and for both players on the balance board.

Variations5678

Table 3. The Neuromuscular Training Program^[51].

Level	A	B	C	D
1	DLS with lumbar control 2x10 Toe raises 2 x20 DL heel raises 2 x20	DLS on BOSU 2 x10	DL compressions on BOSU 2 x20	Forward/backward hop on BOSU 2 x20
2	DL skiing exercises on BOSU 2x10 (side to Side Squats)	DL box jumps onto Reebok step 2 x15 (stabilize on landings)	SL step down on Reebok step 2 x10	SL lunges forward 2 x 10
3	SLS 2 x 10	As in B2 above but increase reebok step height	As in C2 above but increase Reebok step height	SL hopping forwards 2 x10 SL hopping sideways 2 x10
4	SLS 2 x10 and hold squat position for 10secons after 10 squats	DL bunny hop onto BOSU 2 X10 DL lateral bunny hop onto Bosu 2 x10	SL step up on BOSU 2 x10 SL step down on BOSU 2 x10	Lateral SL hops onto BOSU 2 x10
5	SLS on BOSU 2 x10	High knee lifts on BOSU 2x 20	Lunge from Reebok step onto BOSU 2 x10	As in D4 above but increase distance of jump onto BOSU

SL indicates single leg; DL double leg; SLS single-leg squat: DLS, double-leg squat: BOSU both Sides Up Balance Trainer.

NEUROMUSCULAR TRAINING:

This training program was referred to a set off for four weeks of intervention training program. In this present study, we had extended this program to 12 weeks training program. This program involved four sets of exercises. Each set was conducted for three sessions from the overall 12 sessions of training. Level 1 program included bilateral stance exercises with no change in the base of support, including squats, heel raises and toe raises, as well as an introduction to dynamic exercise on the unstable surface of the BOSU ball. Levels 2 and three were introduced single-leg exercises on stable surfaces aimed at developing neuromuscular control of the limb in a controlled situation. Lastly, level 4 and 5 involved more complex single-leg exercises on both stable and unstable surfaces. Participants were instructed to stabilize, with their knees flexed upon landing, at each phase of the particular activity for one second before completing the next movement in the exercise. Over the course of 12 weeks, participants progressed through 7 difficulty levels for each activity ^[51].

STATISTICAL ANALYSIS:

Paired t-tests were used to determine statistically significant differences between the ankle condition (control vs. experimental training) and the muscle onset time (peroneus longus vs. tibialis anterior). This method of analysis was utilized to simplify the comparisons in a clinically applicable manner. The Bonferroni- Dunn correction factor was used to adjust the nominal alpha level of p <0.05 to p < 0.0125 to control the overall Type I error rate. A paired t-test was also used to assess the range of motion differences between the control group and experimental ankles.

Table 4: Electromyographic (EMG) response time (milliseconds) of the peroneal and tibialis anterior muscle in the control group and experimental group following inversion and eversion.

Comparison	X	SD	t value	P
Control Peroneal Control tibialis anterior	57.9 66.6	10.0 13.0	-2.11	0.054
Experimental peroneal Experimental tibialis anterior	64.9 70.6	16.0 14.0	-2.31	0.039
Control Peroneal Experimental peroneal	58.6 64.9	11.0 16.0	-1.24	0.238
Control tibialis anterior Experimental tibialis anterior	67.6 70.9	13.0 14.0	-0.75	0.467

RESULTS:

The results for the mean firing time for the peroneus longus and the tibialis anterior muscles in both the control group and experimental group ankles are presented in the Table. The results indicated no statistically significant differences in the mean firing time between the control and experimental group for both the peroneus longus (t12 = 1.24, p = 0.238) or the tibialis anterior (t12= 0.75, p = 0.467) muscles. The results also showed no significant differences to exist between the tibialis anterior and peroneal muscles in both the control group (t= 2.31, p = 0.039) and experimental group (t12 = 2.13, p = 0.054) ankles. The average time from completion of the most recent rehabilitation period to the time of testing was 3.5 weeks (range = 4-8 weeks). All subjects reported that rehabilitation consisted of activities to improve range of motion and flexibility as well as strength and dynamic stability.

DISCUSSION:

The role of the peroneal and tibialis anterior muscles in providing anactive restraint to eversion and inversion has yet to be defined. The purpose of this study evaluates the knock in a response time of the peroneal and the tibialis anterior reflex response time of these muscles with a neuromuscular training. The results of this investigation revealed no statistically significant differences between the control and experimental group.

The loss of ligamentous integrity resulting in varus instability of the talus in the ankle mortise, thereby attributing to malalignment of the ankle joint, has been defined as mechanical instability. It could, therefore, be hypothesized that peripheral neural pathology may not have been present in this sample of subjects. Also, the assessment of automatic muscle response during an inversion simulation could have been accomplished under more functional tasks such as walking or running in the present investigation. The instrumentation utilized in this study limited this assessment to a standing position with no movement by the subject.

An early study conducted by Freeman^[8] demonstrated no relationship between functional instability and mechanical problems in adult male soldiers. The results from the present study appear to follow a similar pattern as there was no difference in peroneal and tibialis anterior reaction time between the control group and experimental group. To reiterate this notion, Lephart^[9] found that reflexive contraction of the peroneal muscles played no role in protecting the ankle joint during a sprain. Garn SN ^[21] also examined the peroneal response to inversion and found no statistical differences between injured and non-injured ankles.

Freeman et al.^[8] theorized that mechanical instability resulting in functional instability of the ankle could be due to motor in coordination due to particular deafferentation of the mechanoreceptors as a result of injury to the ligaments and joint capsule. Typically, proprioceptors are stimulated when the structures of the ankle are stretched during displacement. The central effect of this stimulation elicits reflex responses which cause the muscles to fire and stabilize the joints^[10]. If an extreme amount of inversion occurs, damage to nerve fibers, ligaments, and the joint capsule can cause a disturbance of these reflexes^[8]. Damage to the nerve fibers in these structures can have central effects, including changes in the activity of neighboring muscles. The results from the present study, however, do not support this theory as there did not appear to be any differences between the control group and experimental or between the peroneal and tibialis anterior muscles reaction time. It should be noted that all of the subjects in this study had undergone some type of proprioceptive rehabilitation following their injuries as outlined by their completed questionnaires in addition to being athletically active at the time of testing. These two findings may partially explain the lack of differences between the unstable and stable ankles since proprioceptive training may have helped to reestablish the deficits that have occurred with the injury.

The findings of the present study appear to indicate that the mechanical response time of the peroneal and tibialis anterior muscles do not differ between the control group and experimental group. The literature also seems to support the finding that sheer strength of the ankle is not affected by ankle instability. Future research should be directed toward identifying the role of muscle force generation or reaction time as compensatory mechanisms in ankles demonstrating mechanical instability. Such documentation may aid the clinician in critical decision making on exercise prescription for rehabilitation in athletes with the chronically unstable ankle. Also, the relationship between quantifiable mechanical ankle instability, possibly through graded stress radiography, and functional outcome is necessary to generate definitive conclusions regarding this association.

CONCLUSION:

Injury to the lateral ligamentous complex of the ankle continues to be a chronic problem for many athletes. The ability to control excessive articular movement under conditions of inversion has been suggested to be impaired as a result of a reduction in reflex muscular contraction. The results of the present investigation demonstrate that spontaneous reflex response time of the anterior tibialis and peroneal muscles do not differ between the control group ankle vs. the experimental group ankle.

The inclusion of a comprehensive rehabilitation program following injury may have played a critical role in the results of this study. Further investigation into the effects of functional activities on the motor response of the ankle musculature may provide researchers and clinicians with evidence regarding the efficacy of such rehabilitative modalities.

ACKNOWLEDGEMENT:

This study was funded by Ministry of Higher Education Research Grant (FRGS - Fundamental Research Grant Scheme - (1001/PPSK/816240). Corresponding author of the present study is indebted to the Grant Authorities for having awarded to carry out the study.

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Received on 17.07.2017 Modified on 19.08.2017

Research J. Pharm. and Tech 2017; 10(11): 4011-4018.

DOI: 10.5958/0974-360X.2017.00727.2