Chronic lateral ankle instability Flashcards
(17 cards)
Definition
Chronic ankle instability (CAI) is considered present if the ankle still gives way easily six months after the first sprain
- Definition criteria for CAI: history of multiple ankle sprains, sensations of “giving way,” and a Cumberland Ankle Instability Tool (CAIT) score of ≤ 24.
o CAIT Interpretation:
28–30: Normal
25–27: Borderline
≤24: Positive for CAI
Epidemiology
10–20% of individuals with a severe ankle sprain develop chronic instability.
Up to 73% of individuals who have had an ankle sprain are likely to experience recurrent injuries.
Mechanism of Injury
- Typically involves excessive inversion with plantarflexion, damaging lateral ligaments.
- Injury often includes the anterior talofibular (ATF), calcaneofibular (CF), and posterior talofibular (PTF) ligaments.
- Lateral talocrural instability is the most common type; subtalar joint contributions should also be considered.
- Talocrural joint stability is highest in dorsiflexion (closed packed), and most unstable in plantarflexion.
ATFL is most commonly injured due to:
- Vulnerable Position:
The ATFL runs from the fibula to the talus and becomes taut in plantarflexion—a position where most ankle sprains occur (e.g., awkward landings or sudden twists). - Typical Injury Mechanism:
Inversion combined with plantarflexion places the greatest strain on the ATFL, making it the first to fail, ahead of other lateral ligaments like the CFL. - Weakest Structure:
The ATFL has low tensile strength (about half that of the CFL) and is thin and flat, making it structurally less robust. - Primary Role in Stability:
It limits anterior talar shift and resists inversion in plantarflexion—placing it under high demand in unstable positions. - Ankle Instability in Plantarflexion:
The ankle joint is least stable when plantarflexed, relying more on soft tissue support, especially the ATFL.
Talocrural Joint
Tibia & fibula articulate with the talus (plantar/dorsiflexion).
Lateral ligaments
ATFL - lateral malleolus of the fibula to the lateral side of the neck of the talus.
CFL - apex of the lateral malleolus of the fibula to tubercle on the lateral aspect of the calcaneus.
PTFL - fibula to the lateral tubercle of the talus.
Medial ligaments
Deltoid - (Splits into 4 - tibiocalcaneal, tibionavicular, tibiotalar A&P parts) - important to stabilise the ankle joint in eversion and prevent dislocations of the joint. Medial malleolus to the talus, calcaneus, and navicular bones.
Subtalar joint
- Talus and calcaneus (inversion/eversion)
- Ligaments:
o Intrinsic: Interosseus talocalcaneal, cervical
o Extrinsic: CF, tibiocalcaneal fascicle of the deltoid
Must be ruled out:
Ottawa Ankle Rules must be ruled out:
1. Inability to bear weight for 4 steps
2. Pain at posterior edge/tip of malleolus
3. Pain at base of the 5th metatarsal
Clinical assessment
- History: Recurrent giving way, previous sprains, pain location
- Major sprain more than 6 months ago in onset with a persistent weakness
- Tenderness over ATFL and sinus tarsi
- Muscle weakness in peroneal muscles, ankle dorsiflexors, and hip abductors in individuals
Tests
- Palpation: Tenderness at ATF, CF, sinus tarsi
- Anterior Drawer Test (ADT):
Indicates ATF compromise
Positive if excessive anterior movement or clunking; sensitivity 73–96%, specificity 84–97% - Talar Tilt Test:
10° inversion suggests instability - Subtalar Instability:
Difficult to assess; sinus tarsi tenderness + inversion laxity = suggestive
Neuromuscular and Proprioceptive Considerations
- Ankle instability leads to impaired muscle coordination, proprioception deficits, and prolonged peroneal reflex latency.
- Neuromuscular control includes:
1. Short-latency reflexes (~54 ms) – quick but weak, sent directly through the spinal cord
2. Long-latency responses (~176 ms) – stronger but too slow to prevent injury. involving higher brain centres. Here, information from the muscle spindles is sent to the brain, processed, and a descending motor command is sent back to the muscle.
Alpha-gamma co-activation
Enhances muscle spindle sensitivity, aiding joint stability without relying on passive structures.
- During voluntary muscle contraction, both alpha motor neurons (which activate the main muscle fibres) and gamma motor neurons (which activate the intrafusal fibres within muscle spindles) fire simultaneously. This co-activation keeps the muscle spindles responsive, even when the muscle is already contracted, allowing them to detect changes in length or stretch more accurately.
- By improving this neuromuscular control mechanism, muscles can respond more quickly and effectively to sudden joint movements or perturbations, helping to compensate for the lack of passive support from the ligaments or capsule.
- Studies show muscle reflexes are too slow to prevent injury without training.
Functional Deficits
- Muscle weakness in peroneals, dorsiflexors, and hip abductors
- Persistent dorsiflexion deficits due to soft tissue restrictions and altered arthrokinematics
- Knee and hip strength should be assessed in CAI patients
Rehabilitation & Management:
- Balance/postural training (wobble boards, single-leg stance)
o Enhances muscle/ligament strength more than proprioception - Strength training
o Targets peroneals, dorsiflexors (e.g., tibialis anterior), hips - Neuromuscular training: improves muscle coordination and compensates for ligamentous laxity
Note: Interventions may not prevent sprains from large/fast perturbations due to inherent speed limitations of neuromuscular responses.
Surgical options
- Brostrom Procedure: Tightens and reattaches ligaments
- Tenodesis: Uses tendon graft from hamstrings to recreate ligament support; for severe cases
Prognosis & Healing
- Ligament healing:
o Reparative phase: 3–6 weeks
o Remodeling: up to a year or more - Only 50–85% report full recovery after 3 years
- Athletes often return before healing completes, contributing to recurrence
