The American Journal of Sports
Medicine
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Chronic Ankle Instability Alters Central Organization of Movement
Chris J. Hass, Mark D. Bishop, Douglas Doidge and Erik A. Wikstrom
Am J Sports Med 2010 38: 829 originally published online February 5, 2010
DOI: 10.1177/0363546509351562
The online version of this article can be found at:
http://ajs.sagepub.com/content/38/4/829
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Chronic Ankle Instability Alters Central
Organization of Movement
Chris J. Hass,* PhD, Mark D. Bishop,y PhD, PT, Douglas Doidge,*
and Erik A. Wikstrom,z§ PhD, ATC
From the *Center for Exercise Science, Department of Applied Physiology and Kinesiology,
University of Florida, Gainesville, Florida, yDepartment of Physical Therapy, University of
Florida, Gainesville, Florida, and the §Biodynamics Research Laboratory, Department of
Kinesiology, and Center for Biomedical Engineering Systems, University of North
Carolina at Charlotte, Charlotte, North Carolina
Background: Chronic ankle instability alters spinal level sensorimotor function and is hypothesized to alter supraspinal motor
control mechanisms. Gait initiation is a functional task modulated by supraspinal pathways, but the effect of chronic ankle instability,
a peripheral musculoskeletal impairment, on gait initiation and thus supraspinal motor control mechanisms remains unknown.
Purpose: This study was conducted to determine if supraspinal aspects of motor control are altered in subjects with chronic
ankle instability.
Study Design: Controlled laboratory study.
Methods: Subjects with chronic ankle instability (5 males, 15 females; age, 20.5 6 1.0 years; height, 169.8 6 9.8 cm; weight,
74.2 6 20.2 kg) and uninjured controls (4 males, 16 females; age, 20.85 6 1.6 years; height, 164.3 6 7.9 cm; weight, 64.2 6
10.62 kg) completed 5 gait initiation trials for each leg at a self-selected pace. The resulting trajectory of the center of pressure
trace was investigated and peak center of pressure excursions in the anteroposterior and mediolateral directions, peak resultant
center of pressure excursions, and average direction-specific velocities were calculated.
Results: Significant group 3 limb interactions were noted during the first (resultant center of pressure displacement [F1,37 5 4.60,
P 5 .04]) and second (mediolateral center of pressure displacement [F1,37 5 3.82, P 5 .05]) period of gait initiation. Center of
pressure displacement was reduced (impaired) in the involved limb of the chronic ankle instability group (resultant, 0.29 6
0.02; mediolateral, 0.72 6 0.02) relative to the uninvolved limb of the chronic ankle instability group (resultant, 0.32 6 0.02; mediolateral, 0.76 6 0.02) and both limbs of the control group (resultant, 0.32 6 0.02; mediolateral, 0.74 6 0.02) when the involved limb
of the chronic ankle instability group served as the initial stance limb.
Conclusion: These interactions suggest that supraspinal motor control mechanisms are altered in subjects with chronic ankle
instability to place a greater emphasis on reducing the postural demands on the involved limb.
Clinical Relevance: These changes suggest that supraspinal adaptations to motor control may be an important contributor to the
underlying neurophysiologic mechanism of chronic ankle instability. The presence of supraspinal adaptations in subjects with
chronic ankle instability also indicates that health care providers and rehabilitation specialists treat chronic ankle instability as
a global/central and not just a local/peripheral injury.
Keywords: dynamic postural control; center of pressure; supraspinal motor control; lateral ankle sprains
Lateral ankle sprains, resulting from a combination of sudden inversion and plantar flexion of the foot/ankle
complex, are the most common injury suffered by both
high school and collegiate athletes.6,18 These injuries
most commonly exceed the maximum load to failure of
the anterior talofibular and calcaneofibular ligaments5
and are often believed to have no lasting consequences.
However, the sequela of a lateral ankle sprain, commonly
referred to as chronic ankle instability (CAI), which
includes residual symptoms,1 recurrent injury,36 and
decreased physical activity,32 have been reported for
months and years after the initial trauma.
Impairments in feedback sensorimotor function (ie, proprioception) have long been thought to be a consequence
z
Address correspondence to Erik A. Wikstrom, PhD, ATC, Department of Kinesiology, University of North Carolina at Charlotte, 9201 University City Blvd, Charlotte, NC 28223 (e-mail: ewikstrom@uncc.edu).
One or more authors has declared a potential conflict of interest: This
study was funded in part by the Southeastern Athletic Trainers’
Association.
The American Journal of Sports Medicine, Vol. 38, No. 4
DOI: 10.1177/0363546509351562
Ó 2010 The Author(s)
829
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830
Hass et al
The American Journal of Sports Medicine
of an initial lateral ankle sprain and a mechanism of
CAI.7,8 However, there is little empirical evidence to support this theory. Recent research has indicated that central
changes in sensorimotor function are present in subjects
with CAI, most notably alterations in gait3,27,29 and altered
alpha motoneuron pool excitability,28 which suggests that
spinal-level motor control mechanisms have changed. Furthermore, because in vivo measures of sensorimotor function require conscious perception of peripheral joint and
muscle information, it has been hypothesized that supraspinal aspects of motor control are also altered.15
Gait initiation (GI) requires effective balance control as
one transitions from quiet stance to continuous gait.12-14
Specifically, anticipatory postural adjustments, via a series
of muscle contractions prior to initiation of the locomotor
pattern (preparatory phase), move the net center of pressure (COP) backward and toward the initial swing limb
to move the body’s center of mass forward over the stance
limb.21 Execution of the first step (stepping phase) begins
when the body’s center of mass has been transferred to
the stance limb.19 Most importantly, GI is proposed to be
modulated via supraspinal pathways because secondary
motor areas control the preparatory phase of GI, while
the primary motor cortex controls the stepping phase.21
Previous research has demonstrated inefficient anticipatory postural adjustments as evidenced by decreased
velocity and magnitude of COP displacement during GI
in patients with impairment of the central nervous
system.12-14 Indeed, these GI deficits may be caused by
compromised motor programming in the premotor and
secondary motor areas of the cortex.24 In contrast, little
is known about the effect of peripheral musculoskeletal
impairments of the nervous system. Therefore, the purpose
of this investigation was to determine if supraspinal
aspects of motor control are altered in subjects with CAI.
Specifically we used a GI task to test the hypothesis that
CAI causes alterations in the organization of movement
(ie, alters supraspinal motor control mechanisms).
METHODS
Experimental Design and Participants
This single-session, mixed-model design was part of a larger
project that investigated the influence of CAI on locomotion.
Twenty participants with CAI (5 males, 15 females; age,
20.5 6 1.0 years; height, 169.8 6 9.8 cm; weight, 74.2 6
20.2 kg) and 20 uninjured controls (4 males, 16 females;
age, 20.85 6 1.6 years; height, 164.3 6 7.9 cm; weight,
64.2 6 10.62 kg) volunteered in response to flyers posted
on campus and/or classroom presentations made by the
investigative team. Additionally, all participants read and
signed the University Institutional Review Board–approved
informed consent form before data collection. All participants were recreationally active, which was operationally
defined as performing 3 aerobic exercise sessions per week
for a total of 90 minutes.
Those with CAI met specific criteria, including (1) a history
of at least 1 unilateral lateral ankle sprain that required
immobilization for at least 3 days (11.5 6 9.2 days); (2) at
least 1 episode of giving way within the past year (8.5 6
6.7 episodes); (3) at least 1 recurrent ankle sprain between
3 and 6 months before study participation (2.9 6 1.8 recurrent sprains); (4) report of pain, instability, and/or weakness
in the involved ankle; (5) attribution of these signs to the initial ankle injury; (6) failure to resume all preinjury level of
activities; (7) no previous ankle fractures; (8) no previous
head and acute lower extremity injury within the past 3
months; and (9) no formal rehabilitation of the involved
ankle. These requirements have been used previously as
inclusion criteria for individuals with CAI.34,35 An episode
of reinjury between 3 and 6 months before enrollment in
this investigation was required to ensure that subjects still
had physical manifestations of CAI but that acute symptoms
were resolved. Uninjured controls were excluded if they
were not free from acute lower extremity or head injuries
for the previous 3 months or if they suffered from any equilibrium disorders or chronic lower extremity disorders.
Protocol
Testing was completed in the Applied Neuromechanics Laboratory at the University of Florida. Before data collection,
demographic and anthropometric measurements were taken
and participants were tested barefoot in form-fitting
clothing. All trials of GI were performed along a 12-m walkway surrounded by an 8-camera optical motion capture system (Vicon Peak, Lake Forest, California). Ground-reaction
forces were collected at 1200 Hz using 2 force platforms
(Bertec Corporation, Columbus, Ohio) mounted flush with
the surrounding floor. Once orientated, participants were
instructed on and familiarized with the GI protocol and
allowed to practice.
Participants began each trial by standing quietly with
a foot on each of the 2 adjacent force platforms in a relaxed
position. Stance width was self-selected for each trial and
was not constrained in any way. In response to an auditory
cue, participants began walking and continued along the
length of the walkway. The auditory cue triggered an
electronic event marker that identified the beginning of
the trial. For each participant, 10 trials (5 for the involved
limb and 5 for the uninvolved limb) performed at a selfselected pace were collected. For this investigation, the dominant limb of uninjured controls, defined as the limb the
individual would use to kick a ball, served as their involved
limb while the nondominant limb of uninjured controls
served as their uninvolved limb for statistical analyses.
Data Reduction
The COP trace was divided into 3 periods by identifying 2
landmark events as previously reported.12-14 Briefly, the
first section (S1) begins with the auditory cue and ends
with the COP located in its most posterior and lateral position toward the initial stepping foot (landmark 1). This
posterolateral shift requires bilateral soleus inhibition, followed closely by bilateral tibialis anterior activation.2 The
second section (S2) represents the movement of the COP
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Chronic Ankle Instability
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TABLE 1
Normalized COP Excursions During the S1, S2, and S3 Phases of Gait Initiationa
S1
ML
AP
Resultant
S2
ML
AP
Resultant
S3
MLd,e
AP
Resultant
CAI Involved
CAI Uninvolved
Control Involvedb
Control Uninvolvedb
0.20 6 0.02
0.21 6 0.02
0.29 6 0.02c
0.22 6 0.01
0.22 6 0.02
0.32 6 0.02
0.22 6 0.02
0.23 6 0.02
0.33 6 0.02
0.21 6 0.01
0.21 6 0.02
0.31 6 0.02
0.72 6 0.02c
0.07 6 0.01
0.73 6 0.02
0.76 6 0.02
0.04 6 0.01
0.75 6 0.02
0.75 6 0.02
0.05 6 0.01
0.76 6 0.02
0.73 6 0.02
0.06 6 0.01
0.73 6 0.02
0.13 6 0.03
0.96 6 0.06
0.97 6 0.06
0.11 6 0.02
0.99 6 0.07
1.00 6 0.07
0.12 6 0.03
0.97 6 0.06
1.01 6 0.06
0.12 6 0.02
1.06 6 0.07
1.08 6 0.07
a
Data are reported as mean 6 standard deviation. COP, center of pressure; S1, S2, and S3 are the 3 sections/phases of the COP trace; ML,
mediolateral; AP, anteroposterior.
b
For the control group, involved is the dominant lower extremity and uninvolved is the nondominant lower extremity.
c
Indicates a statistical difference (P \ .05) from the CAI uninvolved limb and both the involved and uninvolved limbs of the uninjured
controls.
d
Indicates that the CAI was significantly larger than the control group (P \ .05).
e
Indicates that the involved limb was significantly larger than the uninvolved limb (P \ .05).
toward the initial stance foot and ends at landmark 2,
which is the position under the initial stance foot on which
the COP begins to move forward. The abductors and
adductors of the hip contribute to this movement.20 The
third section (S3) extends from landmark 2 until toe-off
of the initial stance foot as the COP translates forward.
During S3, the stance limb gluteus medius maintains control of the center of mass in the frontal plane while the ipsilateral tibialis anterior and soleus activate to pull the
center of mass forward while also controlling forward
motion, respectively.2,23 During each of these 3 sections,
the following outcome measures were calculated: (1) peak
COP excursions in the anteroposterior and mediolateral
directions, (2) peak resultant COP excursions, and (3) average anteroposterior and mediolateral velocities.12,14
Because stance width was not constrained, a statistical
trend (t385 –1.92, P 5 .06) was noted between groups (control, 17.0 6 3.97 cm; CAI, 19.7 6 5.18cm). Therefore, the
decision was made to normalize the COP excursions and
average velocities to the self-selected stance width of the
corresponding trial for each participant. The normalized
averages were then used for further analysis.
Statistical Analysis
Several preliminary analyses were conducted to ensure
appropriate analysis of the dependent variables. Group
demographics were compared with independent-sample
t tests and no significant differences were noted between
participants with CAI and uninjured controls with regard
to their age, height, or weight. Additionally, weight
distribution during quiet stance and over-ground gait velocity was compared between groups using an independentsample t test to ensure that the groups had comparable standing and temporal-spatial gait characteristics. Over-ground
gait velocity did not differ [t38 5 –0.52, P 5 .60] between
the control (1.22 6 0.09 m/s) and CAI (1.24 6 0.12 m/s)
groups. Similarly, the distribution of weight under both
limbs was statistically similar for both groups (control
[involved, 320 6 62 N; uninvolved, 322 6 58 N) and CAI
[involved, 365 6 86 N; uninvolved, 374 6 79 N]), regardless
of whether the injured limb was to be the stance or swing
limb. This finding indicates that between-group and
between-limb differences observed in COP displacements
during GI are not attributed to differences in a priori
weight distributions. Separate 2 3 2 (group 3 limb) analyses of variances were used to test for overall group differences during each period of the COP trace during GI. A
traditional level of significance (a 5 .05) was used on all
statistical tests and Bonferonni post hoc analyses were performed when necessary.
RESULTS
A significant group 3 limb interaction (F1,37 5 4.60, P 5
.04] was noted for the resultant displacement of the COP
trace during the S1 phase of GI (Table 1). This interaction
was strongly influenced by the mediolateral component of
the shift (F1,37 5 3.23, P 5 .08). Post hoc analysis indicated
that in participants with CAI, the resultant posterolateral
shift was decreased when the involved limb served as the
initial stance limb, suggesting impaired motor performance. During the S2 period of GI (Table 1), a significant
group 3 limb interaction (F1,37 5 3.82, P 5 .05) was also
observed in the mediolateral component of the COP displacement shift. Similarly, post hoc testing indicated that
when the involved limb of participants with CAI served
as the initial stance limb, the mediolateral COP displacement was reduced, suggesting a more constrained
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Hass et al
The American Journal of Sports Medicine
sensorimotor system. During the final phase of gait initiation (S3), limb main effects revealed that mediolateral displacement (F1,37 5 4.47, P 5 .04) and mediolateral COP
velocity (F1,37 5 4.80, P 5 .03) were greater on the involved
limb (Table 1). Additionally, a group main effect was
revealed for mediolateral displacement (F1,37 5 3.86, P 5
.05) and a statistical trend toward a group main effect
was illustrated for the mediolateral COP velocity (F1,37 5
3.67, P 5 .06), both indicating that the healthy control
group had greater mediolateral displacement during S3,
suggesting a less constrained sensorimotor system or
greater tolerance to mediolateral COP movement.
AP Position
832
Uninjured Control
CAI
DISCUSSION
ML Position
Deficits in feedback sensorimotor function (ie, proprioception) have long been hypothesized as the causal mechanism of CAI,7,8 but this theory is largely unsupported.
Recent research has identified altered spinal-level motor
control mechanisms in persons with CAI.3,27-29,33 However,
some aspects of supraspinal motor control have also been
hypothesized to be altered in individuals with CAI because
in vivo measures of sensorimotor function require conscious perception of joint and muscle information.15 The
principal finding of the current investigation (ie, decreased
normalized COP excursion magnitudes during the S1 and
S2 phases of GI) clearly demonstrates that chronic peripheral joint injury, CAI, negatively alters supraspinal aspects
of motor control.
The initiation of gait is preceded by several anticipatory
postural adjustments that shift the COP in a posterolateral
direction (S1) to achieve 2 distinct goals: (1) the generation
of forward momentum (posterior shift) and (2) the propulsion of the center of mass toward the initial stance limb
(lateral shift).26 The magnitude of the S1 posterior shift
naturally declines with age and disability,13,14,26 which is
hypothesized to be caused by a deterioration of centrally
mediated anticipatory postural adjustments such as the
failure to inhibit the soleus muscles prior to the activation
of the tibialis anterior muscles. This nonstereotypical pattern of muscle activation limits posterior COP excursions
during S1 and subsequent forward momentum.26 Because
older adults and patient populations are highly susceptible
to falls, these individuals may purposefully limit the posterior COP excursion to minimize mechanical and postural
challenges during GI and their risk of falls.10
However, falls do not appear to be a concern of individuals with CAI and it is highly unlikely that age-related
declines in the effectiveness of the posterior-directed anticipatory postural adjustments were present in the current
CAI study participants. For example, uninjured controls
(3.7 cm) and CAI participants (3.8 cm) produced smaller
but similar raw posterior COP excursions as those reported
in the literature for young adults (4.7 cm).11 Despite the
similar raw displacements, deviations from a ‘‘normal’’
COP trace similar to those seen in older adults and Parkinson disease patients were seen in subjects with CAI when
the data were normalized to an individual’s stance width.
Specifically, participants with CAI reduced the magnitude
Figure 1. Representative normalized center of pressure
(COP) trace for the uninjured control and chronic ankle instability (CAI) groups when the involved limb served as the initial
stance limb. AP, anteroposterior; ML, mediolateral.
of their normalized posterolateral COP excursion when
their involved limb (ie, unstable ankle) served as the initial
stance limb, which is suggestive of decreased postural control (Figure 1).
Participants with CAI also reduced stance-side momentum when the involved limb (ie, unstable ankle) served as
the initial stance limb, possibly to minimize postural
demands while transitioning from double- to single-limb
stance. Lateral COP displacement during S1 has significant effects on center of mass displacement, the preservation of lateral stability,37 and stance-side momentum (S2
mediolateral displacement). Both controls (3.7 cm) and
CAI participants (3.8 cm) produced similar raw excursions
to previously reported means for young adults (3.6 cm).11
Additionally, postural instability during static stance16,22
and when exposed to internal33 and external perturbations25
has been shown in individuals with CAI. Thus, it appears
that the altered supraspinal motor control mechanisms
used by individuals with CAI serve to (1) reduce anticipatory
postural forces and (2) place a greater emphasis on reducing
the postural demands on the involved limb. Previously,
altered lower extremity muscle activation patterns have
also been reported in individuals with CAI during gait,3,27
jump landings,4,9,29 and when transitioning from double- to
single-limb stance,31 so it is possible that deviations from
the stereotypical pattern of lower limb muscle activation
also occurred during GI. However, this is speculative as
muscle activity was not recorded in the current investigation. Regardless of the lower extremity muscle activation
pattern, these data suggest that supraspinal aspects of
motor control are susceptible to chronic peripheral joint
injury, specifically CAI.
Despite the apparent advantage the identified alterations in GI demonstrated by participants with CAI have
for preserving lateral stability, these individuals were still
experiencing recurrent episodes of giving way and recurrent injury, which are both important clinical symptoms
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Chronic Ankle Instability
of CAI. Thus, the supraspinal alterations observed in the
current investigation should be considered either maladaptive or ineffective changes to the organization of movement. We speculate that centrally mediated decreases in
COP excursion during GI represents a more constrained
sensorimotor system that will decrease the individual’s
ability to cope with changing task demands,16,22,33 thus
contributing to the major clinical symptoms of CAI (ie, episodes of giving way and recurrent injury). Currently, the
long-term mechanical and neurologic consequences of
a constrained sensorimotor system remain unknown, but
recent evidence illustrates that CAI leads to diminished
activity levels32 and is a leading cause of posttraumatic
osteoarthritis in the ankle.17,30
While our results are important, this study was not
without its limitations. We are inferring that alterations
in the behavioral performance during GI are reflective of
differences in supraspinal control. Future studies should
evaluate lower extremity muscle activity and central mediated processes more directly (eg, transcranial magnetic
stimulation studies or electroencephalography). For the
current investigation, no level of self-reported ankle function was assessed and no validated questionnaire was
used to categorize participants. Previously, our laboratory
group correlated the current inclusionary criteria to validated instruments for a group of controls, ankle copers,
and CAI patients, and noted significant negative correlations. Thus, we are confident that the current inclusionary
criteria properly identify functionally impaired CAI individuals and also appropriately categorized CAI participants. Finally, the control group in the current
investigation was about 10 kg lighter than those with
CAI, but this difference was not statistically significant.
Our primary outcome variables were peak excursion (cm)
and average velocity (cm/s), which are not influenced by
participant weight; thus, we are confident that the average
weight of the groups did not affect our results. However,
future investigations should consider matching CAI participants and controls by weight if they will be using variables such as peak forces that can be influenced by patient
weight.
CONCLUSION
The results of the current investigation provide evidence
that chronic peripheral joint injury, specifically CAI, negatively alters supraspinal aspects of motor control during
an internally mediated postural destabilization (GI). The
COP excursions during the preparatory phase of GI (S1
and S2), modulated by secondary motor areas,21 were
reduced (impaired) in participants with CAI. Similarly,
the stepping phase (S3) of GI, modulated by the primary
motor cortex,21 was also reduced (limited) in CAI participants. These changes strongly suggest that centrally
mediated changes to motor control may be an important
contributor to the underlying neurophysiologic mechanism of CAI. Further, and more importantly, these data
indicate the need for rehabilitation specialists to conduct
global coordination/training programs for both the
833
involved and uninvolved limbs of patients with acute lateral ankle sprains and CAI to prevent motor control alterations and restore proper motor control following
a peripheral joint injury.
ACKNOWLEDGMENT
This study was funded in part by the Southeastern Athletic
Trainers’ Association.
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