What Actually Happens During an Ankle Sprain?

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Lateral ankle sprains are among the most common injuries in soccer and other field sports. From the sideline, they can look deceptively simple: a quick roll of the ankle, a few minutes on the ground, and then either a substitution or a taped‑up return to play. Underneath that moment, though, is a complex interaction between ligaments, tissue healing, sensory systems, and the brain.

A lateral ankle sprain begins as a local tissue injury, but recovery can involve a much larger system: ligament healing, sensory feedback, neuromuscular control, and movement behavior. Research increasingly suggests that these systems interact, even though scientists still cannot predict exactly why some athletes recover fully while others develop persistent instability.

This feature asks:

 

What happens to an athlete’s ankle, movement system, and nervous system after a lateral ankle sprain, and why can the consequences extend beyond the initial injury?

 

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Most lateral ankle sprains in sport involve the foot rolling inward (inversion) and pointing downward (plantarflexion) relative to the lower leg. This can happen when a soccer player lands on another player’s foot after a header, plants to cut and the foot slips, or lands awkwardly from a jump. The exact combination of forces and joint positions varies from play to play, but the common theme is that the load on the lateral ankle structures exceeds what those tissues can tolerate at that instant.

On the outside of the ankle, the main ligaments at risk are:

• Anterior talofibular ligament (ATFL) – commonly injured when the ankle is plantarflexed and inverted.

• Calcaneofibular ligament (CFL) – more involved when the ankle is closer to neutral or when inversion forces are larger.

• Posterior talofibular ligament (PTFL) – stronger and usually involved only in more severe injuries.

When the combination of body mass, speed, and joint position produces a torque that stretches these ligaments beyond their normal range, fibers can be strained or torn. Lower‑grade sprains may involve microscopic fiber damage and stretching; higher‑grade sprains involve more extensive disruption.

Not every ankle sprain follows the same script. Some involve more rotation, some occur in partial dorsiflexion, and some are contact while others are non‑contact. Two sprains that look similar on video can produce different patterns and severities of tissue injury.

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Once ligament tissue is injured, the body initiates a biological response that unfolds over days to weeks.

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Damaged fibers and small blood vessels release chemical signals that trigger inflammation. This early phase involves:

• increased blood flow

• movement of immune cells into the area

• release of inflammatory mediators

Fluid accumulates in and around the joint, leading to swelling. Swelling can increase joint pressure, change how the joint moves, and contribute to pain.

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Pain arises from both mechanical and chemical sources:

• mechanical: movement or loading of the injured tissue

• chemical: sensitization of local nerve endings by inflammatory mediators

Athletes often limit how much they move the ankle, especially into inversion and plantarflexion. This can reduce range of motion in the short term. Over time, stiffness can also be influenced by protective muscle activity and changes in the joint capsule and surrounding tissues.

Tissue Healing and Remodeling

Ligament healing is a gradual process:

1. Inflammatory phase – clearing damaged tissue and initiating repair.

2. Proliferative phase – new collagen is laid down, initially in a disorganized pattern.

3. Remodeling phase – collagen fibers gradually align more with the direction of stress, and the tissue’s mechanical properties evolve.

Even after an athlete feels “better,” the healing ligament may not have the same structure or mechanical behavior as before. That does not automatically mean the ankle will be unstable, but it is one factor in how the joint behaves after injury.

This section focuses on biology, not on specific treatments. Different rehabilitation approaches aim to influence these processes, but the underlying tissue response follows its own timeline.

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A lateral ankle sprain is not only a ligament event. It can influence how the entire lower limb and movement system behave.

Pain, Movement, and Function

Pain and swelling often lead athletes to change how they move. In the days and weeks after injury, players may:

• avoid loading the injured side

• shorten stance time on the affected leg

• reduce ankle motion during walking, jogging, or cutting

These changes can be protective in the short term. In some athletes, though, altered movement patterns persist longer than the acute pain and swelling.

Range of Motion, Strength, and Balance

After a sprain, some athletes show:

• reduced dorsiflexion range of motion

• decreased strength in muscles around the ankle, such as the evertors and plantarflexors

• differences in single‑leg balance and postural control

These changes can be influenced by pain, disuse, and neural factors (for example, how effectively the nervous system activates the muscles). They do not appear in every athlete to the same degree, but they are part of the broader picture of how an ankle sprain can affect function.

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To understand why an ankle sprain can have broader effects, it helps to look at proprioception—the sense of body position and movement.

Proprioception involves sensory information from:

• muscle spindles

• Golgi tendon organs

• joint and ligament receptors

• skin receptors

This information is integrated by the nervous system to create a sense of joint position and movement (kinesthesia). For the ankle, proprioception helps the brain know where the foot is in space and how it is moving, even without visual input.

Proprioception and Chronic Ankle Instability

A key question is whether ankle injuries are associated with longer‑term changes in proprioception. A systematic review and meta‑analysis by Xue et al. (2021) examined whether individuals with chronic ankle instability (CAI) show proprioceptive deficits compared with controls. Across multiple studies, people with CAI tended to demonstrate worse performance on measures such as joint‑position sense and kinesthesia than those without CAI.

The review also highlighted important limitations:

• studies used different tests and protocols

• definitions of CAI varied

• effect sizes were not identical across all tasks

Crucially, this evidence concerns chronic ankle instability, not every athlete immediately after a first sprain. The findings support an association between CAI and proprioceptive deficits; they do not prove that every ankle sprain automatically causes long‑term proprioceptive problems, or that proprioceptive deficits are the single cause of instability.

Brain and Sensorimotor Adaptations

Beyond local joint receptors, researchers have asked whether ankle injuries are associated with changes in the brain’s sensorimotor networks. A systematic review by Maricot et al. (2023) synthesized studies on brain neuroplasticity related to lateral ankle ligament injuries. The review included 20 studies, but only one involved participants with a recent lateral ankle sprain; the rest primarily examined individuals with CAI.

Many of these CAI studies reported differences in brain activation or connectivity in regions involved in sensorimotor control. At the same time, Maricot and colleagues emphasized that:

• most available evidence involves chronic conditions, not acute sprains

• study designs and tasks varied

• sample sizes were often modest

The review suggests that lateral ankle ligament injuries—particularly when instability becomes chronic—may be associated with brain‑level differences in sensorimotor processing. It does not establish that every ankle sprain “changes the brain” in a uniform way, or that these changes are the sole explanation for ongoing problems. The literature currently tells us considerably more about neuroplasticity in chronic ankle instability than about what happens in the brain immediately after a first lateral ankle sprain.

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For a soccer player, the ankle is involved in almost every movement: sprinting, decelerating, landing from a header, cutting to evade a defender, and balancing on one leg while controlling the ball.

Researchers use tools such as:

• kinematics – joint angles and movement patterns

• kinetics – ground‑reaction forces and joint moments

• dynamic postural stability tests – how well an athlete controls the body after landing

• muscle activity measures – such as EMG to examine timing and amplitude of muscle activation

A systematic review and meta‑analysis by Chan et al. (2022) examined how chronic ankle instability affects lower‑extremity kinematics, dynamic postural stability, and muscle activity during unilateral jump‑landing tasks. Across the included studies, individuals with CAI often demonstrated:

• altered joint angles at the ankle and knee during landing

• deficits in dynamic postural stability

• differences in muscle activation patterns compared with controls

Similarly, Simpson et al. (2019) reviewed studies on dynamic postural stability and unilateral landing biomechanics in people with CAI. They reported that individuals with CAI frequently showed:

• poorer dynamic stability after landing

• changes in landing mechanics, such as altered joint positions or loading patterns

These reviews primarily involved controlled jump‑landing tasks rather than full‑speed soccer match situations. Most participants were physically active adults, but not always soccer‑specific samples. Still, the findings suggest that, in some athletes with chronic problems after ankle sprain, landing and movement strategies differ from those of uninjured controls.

For soccer, this matters because landing from headers, cutting to change direction, and stabilizing on one leg are central to performance. If an athlete with a history of lateral ankle sprain and CAI lands with different joint angles or has reduced dynamic stability, that could influence both performance and how forces are distributed across the lower limb. The current evidence shows associations between CAI and altered mechanics; it does not define a single “correct” pattern or prove that one specific landing style prevents all future injuries.

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Not all athletes who sprain an ankle go on to develop chronic issues. Some recover with minimal long‑term differences, while others experience repeated sprains, ongoing pain, or a sense that the ankle is “giving way.”
 

A prospective cohort study by Doherty et al. (2016) followed 82 individuals after a first‑time lateral ankle sprain to examine recovery and predictors of chronic ankle instability. Participants were assessed at multiple time points for pain, function, and instability.

Doherty and colleagues reported that a substantial proportion of participants developed features consistent with CAI over the following year. Importantly, they also identified early functional and biomechanical measures that were associated with later outcomes.







 

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These numbers come from this specific cohort and represent how well the model classified participants within that study. They do not mean that clinicians can currently predict every athlete’s future with that level of accuracy, nor that these measures diagnose CAI on their own. They do, however, suggest that early functional performance and dynamic stability are meaningfully related to longer‑term outcomes.
 

A systematic review and meta‑analysis by Michels et al. (2022) examined the presence of persistent symptoms 12 months after a first lateral ankle sprain. Across multiple studies, they reported pooled estimates that at one year:

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These are pooled estimates across different studies and populations, and the exact values varied between individual studies. The key point is that:

• most people recover substantially after a first lateral ankle sprain

• a meaningful minority experience persistent symptoms or recurrent problems

• outcomes vary considerably between individuals

Together, Doherty et al. and Michels et al. show that recovery after a first sprain is not uniform. Some athletes return to play with few long‑term issues, while others develop patterns consistent with chronic ankle instability or ongoing symptoms.

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When the different lines of evidence are viewed together, a more integrated picture emerges.

Systematic reviews such as Xue et al. (2021) indicate that individuals with chronic ankle instability often demonstrate proprioceptive deficits compared with uninjured controls. Reviews by Chan et al. (2022) and Simpson et al. (2019) show that CAI is also associated with altered landing mechanics and dynamic postural stability during unilateral jump‑landing tasks. These findings suggest that, in chronic conditions, both sensory function and movement strategies can differ from those of uninjured athletes.

Prospective and longitudinal work adds another layer. Doherty et al. (2016) provide evidence that early functional performance and dynamic stability after a first‑time lateral ankle sprain are associated with who later develops features of CAI. Michels et al. (2022) show that, at a population level, a non‑trivial minority still report pain, recurrent sprains, or instability 12 months after an initial sprain.

Finally, Maricot et al. (2023) bring in a central‑nervous‑system perspective, synthesizing evidence that people with lateral ankle ligament injuries- especially those with CAI- can show brain‑level differences in sensorimotor networks. Although the evidence is still limited and heavily weighted toward chronic conditions, it raises the possibility that repeated injury and instability are associated with adaptations not only in the ankle but also in how the brain organizes movement.

Taken together, these studies do not outline a single pathway from ankle sprain to chronic instability. Instead, they point to several interconnected levels of change- mechanical, sensory, neuromuscular, and central. Persistent problems appear to emerge from interactions among these factors rather than from one isolated deficit.

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Even with multiple systematic reviews and a prospective cohort study, several important questions remain open.

• Why do some athletes recover fully while others develop chronic instability?
  Studies like Doherty et al. and Michels et al. show that persistent problems are common enough to matter, but they also show wide variability. Differences in tissue healing, neuromuscular control, proprioception, psychology, training environment, and exposure to further sprains likely all play roles. It is difficult to predict, at the time of the first injury, exactly which athlete will develop long‑term issues.

• Are proprioceptive deficits causes, consequences, or both?
  Xue et al. found that individuals with CAI often perform worse on proprioceptive tests. However, cross‑sectional data cannot fully separate whether sensory deficits are a primary driver of instability, a result of repeated sprains and altered loading, or part of a bidirectional relationship.

• How well do laboratory measures translate to actual soccer performance?
  Chan et al. and Simpson et al. focused on unilateral jump‑landing tasks in controlled settings. These tasks are useful for isolating mechanics and stability, but they do not fully capture the complexity of a 90‑minute match with fatigue, decision‑making, contact, and unpredictable surfaces.

• How much can jump‑landing studies tell us about match situations?
  Laboratory tasks often involve standardized jumps or cuts with clear instructions. In a game, players react to opponents, the ball, and tactical demands. The extent to which lab‑measured differences in joint angles or stability translate into injury risk or performance in real matches remains an active question.

• What evidence exists for brain adaptations, and what remains unknown?
  Maricot et al. reported differences in brain activation and connectivity in people with lateral ankle ligament injuries, especially CAI. But with only one study involving acute sprain and considerable variation in methods, it is not yet clear how these findings relate to individual symptoms, performance, or recovery decisions.

Recognizing these uncertainties is not about making the science sound vague for its own sake. It is part of taking the evidence seriously- separating relatively well‑supported findings from associations, hypotheses, and areas where data are still limited.

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From a research perspective, a lateral ankle sprain is not only a short‑term ligament problem. It can:

• trigger a structured biological healing process in the injured tissues

• influence how the ankle moves and how much range of motion is available

• be associated, in some athletes, with changes in strength, balance, and dynamic stability

• be linked to differences in proprioception and neuromuscular control, especially in chronic ankle instability

• coincide with altered landing and movement strategies during tasks that resemble soccer actions

• in chronic cases, be associated with differences in how the brain organizes sensorimotor control

For soccer players, this means that the ankle is part of a broader movement and control system. Researchers study not only whether the ligament heals, but also how the injury affects movement strategies, sensory function, and neuromuscular control over time.

This article is educational, not prescriptive. It does not provide rehabilitation plans, exercises, diagnoses, or return‑to‑play timelines. Instead, it aims to give a clearer picture of why scientists take ankle sprains seriously and why they continue to investigate their long‑term effects.

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• A lateral ankle sprain is both a mechanical and biological event, involving ligament overload, tissue damage, and a structured healing response.

• In some athletes, the consequences extend beyond the ligament, with associations reported between chronic ankle instability and changes in proprioception, dynamic stability, and landing mechanics.

• Recovery after a first sprain is highly variable: most people improve substantially, but systematic‑review evidence shows that a meaningful minority still report pain, recurrent sprains, or instability at 12 months.

• Current research supports a multifactorial view of chronic ankle instability, involving mechanical, sensory, neuromuscular, and contextual factors rather than a single cause.

• Laboratory and neuroimaging studies provide important insights but have limitations, and translating their findings to real‑world soccer performance and individual outcomes requires caution.

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Chan LYT, Sim YTN, Gan FK, Rahmatullah Bin Abd Razak H. Effect of chronic ankle instability on lower extremity kinematics, dynamic postural stability, and muscle activity during unilateral jump-landing tasks: A systematic review and meta-analysis. Physical Therapy in Sport. 2022;55:176–188. PubMed: https://pubmed.ncbi.nlm.nih.gov/35462322/

Doherty C, Bleakley C, Hertel J, et al. Recovery From a First-Time Lateral Ankle Sprain and the Predictors of Chronic Ankle Instability: A Prospective Cohort Analysis. American Journal of Sports Medicine. 2016;44(4):995–1003. PubMed: https://pubmed.ncbi.nlm.nih.gov/26912285/

Maricot A, Dick E, Walravens A, et al. Brain Neuroplasticity Related to Lateral Ankle Ligamentous Injuries: A Systematic Review. Sports Medicine. 2023;53(7):1423–1443. PubMed: https://pubmed.ncbi.nlm.nih.gov/37155129/

Michels F, Wastyn H, Pottel H, et al. The presence of persistent symptoms 12 months following a first lateral ankle sprain: A systematic review and meta-analysis. Foot and Ankle Surgery. 2022;28(7):817–826. PubMed: https://pubmed.ncbi.nlm.nih.gov/34961654/

Simpson JD, Stewart EM, Macias DM, Chander H, Knight AC. Individuals with chronic ankle instability exhibit dynamic postural stability deficits and altered unilateral landing biomechanics: A systematic review. Physical Therapy in Sport. 2019;37:210–219. PubMed: https://pubmed.ncbi.nlm.nih.gov/29914742/

Xue X, Ma T, Li Q, Song Y, Hua Y. Chronic ankle instability is associated with proprioception deficits: A systematic review and meta-analysis. Journal of Sport and Health Science. 2021;10(2):182–191. PubMed: https://pubmed.ncbi.nlm.nih.gov/33017672/