The Physician and Sportsmedicine

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Acute lateral ankle sprain to chronic ankle

instability: a pathway of dysfunction

Tyler M. Miklovic, Luke Donovan, Omar A. Protzuk, Matthew S. Kang & Mark
A. Feger

To cite this article: Tyler M. Miklovic, Luke Donovan, Omar A. Protzuk, Matthew S. Kang & Mark
A. Feger (2018) Acute lateral ankle sprain to chronic ankle instability: a pathway of dysfunction, The
Physician and Sportsmedicine, 46:1, 116-122, DOI: 10.1080/00913847.2018.1409604

To link to this article: https://doi.org/10.1080/00913847.2018.1409604

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THE PHYSICIAN AND SPORTSMEDICINE, 2018
VOL. 46, NO. 1, 116–122
https://doi.org/10.1080/00913847.2018.1409604

CLINICAL FEATURE
REVIEW

Acute lateral ankle sprain to chronic ankle instability: a pathway of dysfunction

Tyler M. Miklovica, Luke Donovanb, Omar A. Protzuka, Matthew S. Kanga and Mark A. Fegera
a
School of Medicine, Virginia Commonwealth University, Richmond, VA, USA; bDepartment of Kinesiology, University of North Carolina, Charlotte,
NC, USA

ABSTRACT ARTICLE HISTORY

Lateral ankle sprains (LAS) have been reported as one of the most common musculoskeletal injuries Received 17 October 2017
observed in sports and in individuals who are recreationally active. Approximately 40% of individuals who Accepted 22 November 2017
sustain a LAS develop a condition known as chronic ankle instability (CAI). Years of research has identified KEYWORDS
numerous impairments associated with CAI such as decreases in range of motion (ROM), strength, Balance; gait;
postural control, and altered movement patterns during functional activities when compared to indivi- impairment-based
duals with no LAS history. As a result, an impairment-based rehabilitation model was developed to treat rehabilitation; postural
the common impairments associated with CAI. The impairment-based rehabilitation model has been control; strength
shown to be an effective rehabilitation strategy at improving both clinical and patient-oriented outcomes
in patients with CAI. To date, the efficacy of an impairment-based rehabilitation model has not been
evaluated in patients with an acute LAS. Prior to implementing an impairment-based model for the
treatment of an acute LAS, similarities between impairments associated with acute LAS and CAI across the
spectrum of the healing process is warranted. Therefore, the purpose of this review paper is to compare
and contrast impairments and treatment techniques in individuals with an acute LAS, sub-acute LAS, and
CAI. A secondary purpose of this review is to provide clinical commentary on the management of acute
LAS and speculate how the implementation of an impairment-based rehabilitation strategy for the
treatment of acute LAS could minimize the development of CAI. The main findings of this review were
that similar impairments (decreased ROM, strength, postural control, and functional activities) are
observed in patients with acute LAS, sub-acute LAS, and CAI, suggesting that the impairments associated
with CAI are a continuation from the original impairments developed during the initial LAS. Therefore, the
use of an impairment-based model may be advantageous when treating patients with an acute LAS.

Introduction treatment algorithm underscores the fact that the vast major-
ity of these deficits are treatable with targeted rehabilitation. If
Lateral ankle sprains (LAS) are the most common musculoske-
we acknowledge that these deficits are treatable in patients
letal injury [1] and contribute to a tremendous healthcare
with CAI, one must wonder whether these deficits were pre-
burden stemming from the high treatment costs [2,3] and
sent following the initial LAS and not adequately treated in
long-term consequences following the initial sprain [4–6]. Up
the acute or subacute settings or perhaps the deficits devel-
to 40% of LAS patients develop a condition known as chronic
oped as a long-term sequela of the initial injury.
ankle instability (CAI) [7,8]. CAI is characterized by a history of
Recent evidence indicates that the vast majority of patients
one significant LAS, subsequent recurrent sprains, episodes of
who sustain a LAS do not receive the recommended super-
the ankle giving way, or self-reported deficits in ankle function
vised rehabilitation following the LAS [13], but it remains
for greater than 1 year following the initial sprain [9,10].
unclear as to whether insufficient treatment contributes to
Countless studies have delved into the complex pathophysiol-
the development of CAI. While it would take extensive pro-
ogy that depict patients with CAI and the equally complex
spective studies to answer what circumstances are required to
rehabilitation and treatment strategies required to address the
prevent the development of CAI, in this narrative review, we
myriad of mechanical and functional insufficiencies that per-
aim to describe acute LAS in terms of the four impairment
sist years after the initial LAS [9,11,12]. A review paper by
domains so that clinically relevant parallels can be drawn
Donovan and Hertel [12] synthesized the vast majority of the
between deficits following LAS and chronic impairments in
rehabilitation literature for treating CAI into an assess–treat–
patients with CAI. Stated more clearly, the purpose of this
reassess treatment algorithm to address the most common
review is to use the same four impairment domains (ROM,
functional impairments observed in patients with CAI. These
strength, postural control, and functional tasks) from the
deficits were categorized into four impairment domains that
Donovan and Hertel CAI rehabilitation paradigm and describe
include limited range of motion (ROM), decreased strength,
which deficits can be observed following acute LAS and at
impaired postural control, and altered movement strategies
which time points during recovery the deficits resemble
when completing functional tasks [12]. This evidence-based

CONTACT Luke Donovan ldonova2@uncc.edu Department of Kinesiology, University of North Carolina at Charlotte, Belk Gym 229, Charlotte, NC, USA
© 2017 Informa UK Limited, trading as Taylor & Francis Group

patients with CAI. We believe this is beneficial to our under-
standing of LAS and CAI rehabilitation because interventions
that have been shown to be effective in patients with CAI are
likely equally effective in the weeks to months following acute
LAS. Therefore, early recognition of residual impairments fol-
lowing LAS and implementation of associated interventions
may decrease the long-term consequences for patients with
LAS and CAI.
Impairment domains
Range of motion
It is well established that the most common risk factor for
sustaining a LAS is a history of a previous LAS [14]. However,
pertaining to modifiable risk factors, individuals with restricted
dorsiflexion ROM have been shown to have an increased risk
of sustaining a LAS when compared to individuals with normal
dorsiflexion ROM [15,16]. In terms of biomechanics, the dorsi-
flexion ROM risk factor makes sense given the fact that ade-
quate dorsiflexion (10° of passive ankle dorsiflexion) is
required for normal gait and descending stairs and that up
to 20–30° of active ankle dorsiflexion is required for running or
sprinting [17,18]. To be clear, individuals without the required
amount of dorsiflexion ROM for the previous functional tasks
are still able to complete the tasks; however, these individuals
must alter their biomechanics in order to account for the
limited motion available at the ankle, which in return may
place the foot in a more injury-prone position [15,17–19].
Immediately following a LAS, in the presence of pain and
inflammation [20], many patients are unable to reach a neutral
foot and ankle position and can only actively dorsiflex to 4–7° of
plantar flexion. During this same time frame, even with the
application of overpressure, patients are only able to achieve
7–8° of passive dorsiflexion [21]. After simple calf stretching,
regardless of the duration of stretch (30 s vs. 1 min vs. 2 min),
patients demonstrated the ability to improve to 7° and then 11°
of active dorsiflexion by weeks 2 and 4 post sprain [20].
Similarly, college athletes can regain 10° of sagittal plane
motion in the first two weeks following a LAS with progressive
rehabilitation [22]. Passive dorsiflexion ROM, however, may
actually improve up to 24° with just 2 weeks of conservative
management of rest, ice, compression, and elevation (RICE) [21].
Application of anterior–posterior joint mobilizations has
been shown to help patients achieve full passive dorsiflexion
ROM and normal dorsiflexion during gait faster than conser-
vative treatment alone [21]. If utilized in the early months of
rehabilitation following a LAS, Mulligan’s ankle mobilizations
with movement are able to increase weight-bearing dorsiflex-
ion ROM after a single session [23]. Even though dorsiflexion
ROM is limited acutely after a LAS, evidence suggests that
once athletes return to unrestricted athletic participation,
these deficits are unlikely to persist past 6 months. However,
even once dorsiflexion ROM returns to baseline levels when
compared bilaterally, there may still be restricted posterior
glide of the talocrural joint indicating a chronic alteration in
arthrokinematics following LAS [24].
Although the literature indicates that active and passive
dorsiflexion ROM is limited following an acute LAS, the
THE PHYSICIAN AND SPORTSMEDICINE 117
literature also suggests that multiple treatment approaches
are effective at restoring those ROM deficits. However, clini-
cians should be aware that limitations in arthrokinematic
motion may persist even after patients return to previous
levels of activity. This pattern of decreased dorsiflexion ROM,
restricted posterior talar glide, and improvement with rehabi-
litation is also observed in patients with CAI. The parallels
between patients with an acute LAS and CAI may suggest
that patients with a LAS did not perform rehabilitation after
their initial injury, did not return to previous levels of physical
activity, or perhaps the chronic alterations in arthrokinematics
may manifest as limited ROM years following the initial injury.
Regardless of the underlying link between LAS and CAI dorsi-
flexion ROM deficits, evidence suggests that both patients
with an acute LAS and CAI can be screened for decreased
ROM and treated for arthro- or osteokinematic restrictions as
suggested by Donovan and Hertel’s treatment paradigm for
patients with CAI.
Strength
The ability of skeletal muscle surrounding the ankle to pro-
vide dynamic support during joint decelerations and pertur-
bations is important for normal ankle function and injury
prevention [25]. Following an acute LAS, isometric eversion
strength is diminished when compared bilaterally for up to
3 weeks following injury [26]. Eversion strength deficits
would make intuitive sense given the inversion mechanism
could cause strain or injury to the peroneal musculature or
surrounding structures as they reflexively contract in an
effort to control the inversion perturbation. However, inver-
sion strength deficits have also been described in the first
few weeks following a LAS and thus both invertor and ever-
tor muscle strength may be equally important during early
phases of LAS rehabilitation [27]. Inversion weakness may be
a form of reciprocal inhibition in which musculature that
would generate the same movement as the injurious
mechanism would be inhibited from maximal contraction
during recovery [28].
After 4 weeks, clinically assessed muscle weakness (via
manual muscle testing) may be undetectable following stan-
dard RICE treatment protocols, but instrumented measures at
this time point have unveiled deficits in plantar flexion
strength [29]. Other instrumented studies [30] have demon-
strated deficits in plantarflexion, eversion, and inversion
strength up to 6 weeks following a LAS when measured iso-
metrically, whereas eccentric eversion strength appears to
return to baseline levels when compared bilaterally at this
same 6-week time point [26]. Interpreting the mechanism of
strength deficits in the acute setting is quite difficult. During
early healing, one could surmise that strength deficits are
related to prior insufficiencies present before the initial injury,
muscle inhibition associated with pain and swelling due to the
acute inflammatory process, or acute strain of surrounding
musculature. As functional status of the ankle improves,
patients often return to normal ambulation and sport [31]
before strength deficits are restored [26,30]. Clinicians should
be aware of persistent strength deficits in the first two months
118 T. M. MIKLOVIC ET AL.
following a LAS [26,30] even after most patients will return to
unrestricted activity [31].
In the general population, aforementioned deficits in four-
way ankle strength return to baseline levels at 4 months with
or without supervised rehabilitation [30]. However, in active
military soldiers that suffer a LAS, plantar flexor and evertor
muscle weakness may be present when compared bilaterally
to the uninjured limb 2 months following injury, and in more
severe injuries, plantarflexion deficits may even be present
6 months post-initial sprain [32]. When comparing the poten-
tially conflicting results of military personnel to the general
public, it appears that higher physical function prior to injury
(active military) may actually prolong the time it takes for
recovery when the standard for comparison is the contralat-
eral uninjured limb. While this is speculative, we believe it is
an extremely important consideration when translating these
results to LAS patients participating in athletics where it may
take even longer to recover symmetric strength profiles.
Strength deficits have been identified in numerous studies
[33–36] in patients with CAI, but other studies [37–39] have
shown conflicting results, suggesting strength deficits are likely
present in some but not all patients with CAI. This is interesting
considering that the current literature suggests strength deficits
often resolve in the first year following an acute LAS. This
collective body of evidence may suggest that the long-term
consequences of a LAS, including decreased physical activity,
reduced ankle ROM, and altered movement patterns, may con-
tribute to potentially re-emergent strength deficits in the subset
of patients that go on to develop CAI or perhaps that looking at
LAS cohorts as a whole neglects to consider the few LAS
patients hidden within the group means that never regain
normal strength. While we cannot be certain of the true expla-
nation for the obscure relationship between acute LAS strength
deficits and those deficits present in some patients with CAI,
rehabilitation following a LAS or in patients with CAI, should
involve screening for and treating potential deficits as well as
continued strength training even after clinically assessed defi-
cits appear to be resolved in the acute recovery of a LAS.
Postural control
Postural control has been defined as the act of maintaining,
achieving, or restoring a state of balance during any upright
stance [40]. Patients with an acute LAS or CAI are often eval-
uated utilizing some form of singe limb stance (static) or tasks
like the Star Excursion Balance Test (SEBT) (dynamic) to isolate
the injured limb during postural control testing.
Prospective assessment indicates that postural control def-
icits are present in both the injured and uninjured sides during
single-limb balance immediately following an acute LAS when
compared to pre-injury levels in collegiate athletes. After
1 week of supervised rehabilitation, postural control returns
to baseline values in the uninjured limb, whereas deficits in
the injured limb persist for 2 weeks [40]. From a general
population perspective, first time patients who sustain a LAS
also demonstrate bilateral impairments during eyes closed
single-limb-balancing tasks [41]. The uniform presence of
bilateral deficits across various patient populations may
indicate alterations in central somatosensory processing,
which may pose considerable risk for subsequent sprain if
patients return to activity too early during recovery. Altered
somatosensory processing may lead to compensatory strate-
gies in which patients utilize proximal musculature (hip) to
accommodate perturbations when trying to balance on one
limb [42]. It is intriguing to consider that central mechanisms
appear to alter somatosensory processing involved in the
reflexive restoration of balance manifesting in detectable bilat-
eral deficits, whereas the aforementioned strength deficits
(unilateral in nature) indicate that the contralateral (to the
injured ankle) corticospinal motor pathway appears to be
unaffected.
It is not surprising that the presence of static balance deficits
in the initial two weeks following an acute LAS coincides with
dynamic postural control deficits during the same time frame
when patients reach in anterior, posteromedial, and postero-
lateral directions on the SEBT [43,44]. These bilateral deficits
again suggest the presence of local and global deficiencies that
may compromise the efficiency of the somatosensory system.
Fractal dimension (FD) analysis of center of pressure can be
used to assess how effectively patients can integrate somato-
sensory afferent information and utilize their base of support
when maintaining balance. This unique method allows for
assessment of postural control during traditionally ‘failed trials’
that are often excluded from analysis because a patient lost
balance during testing. FD analysis demonstrates that patients
with an acute LAS are unable to utilize their entire base of
support during eyes closed single limb stance [45] and during
dynamic [44] balance trials. While the aforementioned studies
highlight the presence of bilateral deficits in postural control,
other results underscore the expected reality that postural
control is impaired to a greater extent in the injured limb
compared to the uninjured limb, and with rehabilitation the
injured limb appears to recover slower than the uninjured limb
[46]. Supervised rehabilitation has the potential to restore pos-
tural control to pre-injury levels after 2 weeks [40]; however,
deficits persist much longer in untreated patients and deficits in
dynamic postural control have been identified at 1 month [47],
6 weeks [30], and even 6 months post injury [44].
Strength [48], proprioceptive [48], and balance training pro-
grams [49] have all demonstrated that rehabilitation can help
restore postural control following a LAS, whereas other results
have demonstrated that postural control is similar with or with-
out supervised rehabilitation at 6 weeks post injury if compared
bilaterally [30]. However, recent evidence suggests that bilateral
deficits may persist up to 6 months post LAS [50] and that the
aforementioned side-to-side percent differences used to com-
pare rehabilitation to no rehabilitation may have erroneously
concluded that there is no net benefit of rehabilitation.
Static and dynamic postural control is impaired bilaterally
following a LAS but only unilateral deficits have been reported
in patients with CAI [51]. These results suggest that the central
mechanisms influencing postural control within the first year
following a LAS may not persist and thus bilateral comparison
of postural control may only be sufficient when screening
patients with CAI but not patients with an acute LAS for
balance deficits. Furthermore, balance training is without a

doubt effective for bilateral restoration of balance in patients
with a LAS [40,49] and unilateral restoration of balance in
patients with CAI so clinicians should be aware of these
potential deficits and screen for these treatable insufficiencies
[12,25].
Functional tasks
‘Functional tasks’ with respect to the CAI impairment domains
include tasks such as walking, running, and jump-landing.
From a clinical perspective, restoration of normal gait is
often an early goal for the rehabilitation following a LAS
with progression to more functional tasks as patients return
to their previous level of physical activity. We have presented
evidence suggesting that dorsiflexion ROM, strength, and pos-
tural control are all impaired during the first few weeks to
months following an acute LAS and now we aim to demon-
strate how these functional insufficiencies may contribute to
altered movement strategies when completing functional
tasks. It is important to consider that while even though
these functional insufficiencies could intuitively contribute to
the following functional deficits, research has demonstrated
that simply treating ROM, strength, and postural control is
inadequate for restoring functional mechanics in patients
with CAI [52,53] and is likely the same story in patients with
an acute LAS, although the latter is speculative.
Walking
One of the most commonly reported biomechanic alterations
during walking observed in patients with CAI consists of
increased ankle inversion in the affected limb prior to, at,
and following initial contact, which is similar to the pattern
of increased inversion at initial contact that is seen in the first
few weeks following an acute LAS [54–57]. In patients with a
LAS or CAI, increased inversion during gait has been specu-
lated to be a risk factor for recurrent sprain and episodes of
instability as the inverted position places patients closer to the
mechanism of injury. Interestingly, patients with a LAS have
also been shown to have bilateral decreases in plantar flexion
at ground contact with concurrent increases in bilateral knee
flexion. Collectively, these results may be related to the afore-
mentioned limitations in sagittal ankle motion or central
mechanisms trying to maintain a ‘closed packed’ ankle posi-
tion leading to greater force attenuation at more proximal
joints. Furthermore, during force generation and propulsion
phases of gait, patients with a LAS demonstrate bilateral
increases in ankle inversion, bilateral decreases in ankle plan-
tar flexion, and ipsilateral decreases in hip extension [54].
These biomechanical alterations manifest as a shorter stride
length, slower walking speeds, shorter single-leg support time,
and decreased maximum power during the first month follow-
ing an acute LAS [47]. Passive joint mobilization has proved to
be more effective at increasing stride speed and step length
symmetry during the first two weeks following a LAS when
compared to RICE protocol [21], which is likely related to
quicker recovery of dorsiflexion ROM. These findings are simi-
lar to those that demonstrate that once patients regain full
passive dorsiflexion ROM spatial and temporal gait parameters
also normalize [58]. Walking speed and step length at 4 weeks
THE PHYSICIAN AND SPORTSMEDICINE 119
are correlated with the patient’s level of pain, suggesting
resolution of the acute inflammatory process may also be
required for restoration of normal gait patterns [59].
As patients with a LAS approach 6 months post injury
without subsequent reinjury, most have returned to normal
activity and gait retraining is not likely a continued goal of
treatment in most clinical settings. Interestingly, at this time
point, there appears to be a mixed gait strategy that is similar
to both patients with an acute LAS and patients with CAI. At 6
months post LAS, patients exhibit bilateral increases in knee
flexion, which is consistent with the gait profile of a patient
with an acute LAS [7]. Interestingly, a subset of patients at this
6-month time point who report diminished levels of function
exhibit increased ankle frontal plane motion, which is consis-
tent with gait patterns observed in both patients with an
acute LAS and in patients with CAI [7]. These results are
particularly important because recent evidence has proven
that altered gait patterns in patients with CAI can be improved
with gait retraining [60] and now there is a clear link suggest-
ing these gait patterns (increased frontal plane ankle motion)
should be screened for and treated during recovery from an
acute LAS in a similar fashion to the recommended treatment
of CAI gait pathomechanics. This recommendation appears to
be particularly important for patients with decreased self-
reported function that persists for 6 months post-initial ankle
sprain.
Jump-landing
LAS occurs at a high rate during tasks that have a flight/
preparation phase and a loading phase such as landing from
a jump. Regarding patients with CAI, single-limb landing and
drop vertical jumps are often used to analyze the strategy
patients use to dissipate vertical ground reaction forces asso-
ciated with the landing. When analyzing patients 2 weeks after
their LAS, they demonstrate reduced plantar flexion on the
side of the injury during bipedal drop vertical jumping tasks
[61]. These patients also exhibit reduced flexor moments dur-
ing the loading phases compared to uninjured participants,
which is believed to represent a protective strategy to decele-
rate the body in a more controlled manner [61]. Unfortunately,
this protective mechanism results in asymmetry between
limbs as evidenced by increased extensor patterns in the
uninjured side, which may increase injury risk to the healthy
limb if these patients complete functional tasks or return to
sport before limb symmetry has been restored [61]. Similarly,
when landing on only the injured limb 2 weeks following
injury, patients exhibit increased hip flexion in an attempt to
decrease peak impact force and protect the injured ankle [62].
At 6 months post LAS, patients exhibit reduced plantar
flexion and increased inversion in the injured limb and
demonstrate bilateral increases in knee flexion during a drop
vertical jump task [42]. When completing a single-limb landing
task at this 6-month time frame, again there is increased
inversion around initial contact and increased hip flexion dur-
ing loading [42]. This landing profile at 6 months post LAS is
also (in a similar fashion to walking) a mix of characteristics
with features reminiscent of patients with an acute LAS and of
patients with CAI. Specifically, increased motion at the hip is
similar to patients with an acute LAS, whereas the increased
120 T. M. MIKLOVIC ET AL.

inversion [56] and knee flexion [63] is a landing profile that has deficits are shared between both patient populations the
been demonstrated in patients with CAI. Clinicians should be mechanism causing the deficit may differ depending on
aware of these emergent maladaptive strategies 6 months where in the acute inflammatory or recovery process a patient
after LAS that may be some of the earliest reported links to (LAS or CAI) is during assessment. Meaning, the specific inter-
CAI pathomechanics. vention required to resolve the deficit may also differ between
patient populations. For example, immediately following an
acute LAS, acute inflammation may be a primary cause of
Speculation, limitations, and future directions ROM, strength, balance, and functional movement deficits
but as previously outlined, these four impairments appear to
Currently, it has been shown that 70% of patients with an
remain well past the acute inflammation phase, which sug-
acute LAS return to their sport or activity within 3 days [31].
gests additional mechanisms of dysfunction (Figure 1).
One theory for this relatively early return is that the acute
Therefore, as acute inflammation subsides, although all four
inflammation phase of tissue healing only lasts for approxi-
of the reported impairments will have significantly improved,
mately 3 days [64]. During the acute inflammation phase, the
it appears these impairments are not fully restored and new
ankle joint is often characterized as painful due to the chemi-
mechanisms of impairment should be sought and resolved.
cal reactions and swelling associated with tissue healing [64].
Stated differently, clinicians must be able to not only assess for
We theorize that once the patient moves out of the acute
impairments, but also be able to ascertain the primary driving
inflammation phase the reduction in pain stemming from a
force for each limitation and implement an intervention strat-
cessation of chemical processes provides patients with a false
egy that targets the mechanism of impairment.
sense of healing. At this time, treatments such as non-steroidal
Although we provide these recommendations, we recog-
anti-inflammatory drugs and external ankle support devices
nize that many of the previously mentioned studies are cross-
(braces and tape) allow patients to participate in their previous
sectional in nature and that longitudinal studies are needed to
sport or activity relatively pain-free. Consequently, these
truly understand the progression of impairments over time. In
patients have a 30% chance of reinjuring their previously
addition, although the focus of this paper was to review the
sprained ankle [65]. We believe the high recurrence rate of
literature and demonstrate that an impairment-based model
LAS is most likely due to the injured tissue not being fully
may be an appropriate treatment strategy for both patients
healed prior to return to sport and many of the aforemen-
with an acute LAS and for patients with CAI, this approach
tioned impairments.
may be appropriate when completing a general injury risk
Based on our review of the literature, patients with acute
assessment and implementing preventative exercises based
LAS often exhibit similar deficits within the same four impair-
on the impairments observed during the assessment prior to
ment domains (ROM, strength, postural control, and functional
athletic participation in clinical and research settings.
activity) that have been identified in patients with CAI. As a
result, we speculate that the rehabilitation paradigm for
patients with CAI proposed by Donovan and Hertel [12,52]
Conclusion
may also be an appropriate rehabilitation paradigm for
patients with acute LAS. Therefore, we propose that clinicians We aimed to describe patients with an acute LAS in terms of the
and researchers utilize an assess–treat–reassess treatment four impairment domains established for the evidence-based
model that is comprised of the same four impairment domains treatment of patients with CAI so that parallels could be drawn
[12,52]. However, we must recognize that although similar between the two populations during the rehabilitation of LAS and

Figure 1. Summary and time course for lateral ankle sprain and chronic ankle instability domains in relation to the initial injury and natural healing process.
Individuals with acute lateral ankle sprain, sub-acute lateral ankle sprain and chronic ankle instability often share the same impairments.

for future research geared toward the link between LAS to CAI
development. While this narrative review is not intended to be a
comprehensive review of all the available LAS and CAI literature,
we believe it provides a unique perspective for clinicians involved
in the care of patients following a LAS and should encourage
clinicians to be hyperaware of potential clinical characteristics
that are shared between patients with an acute LAS or CAI. The
current definition for CAI is based upon duration of symptoms that
persist for at least 12 months post-initial LAS. This is a fundamental
characteristic for researchers when enrolling patients with CAI so
that results can be compared and contrasted across various stu-
dies. However, we have now provided a brief synopsis highlighting
how it is prudent from a clinical perspective to think of patients
during the entire first year after a LAS as patients that may have
identifiable and treatable impairments suggesting chronic impair-
ment even though they do not meet inclusion criteria as a patient
with CAI from a research perspective.
Funding
None.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial conflict with
the subject matter or materials discussed in the manuscript. This includes
employment, consultancies, honoraria, stock ownership or options, expert
testimony, grants or patents received or pending, or royalties.
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