functional instability of the ankle joint: features and underlying causes

Physiotherapy August 2000/vol 86/no 8

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IntroductionAnkle sprain, injury of the lateral ligamentcomplex of the ankle joint, is one of themost common sports injuries (Smith andReischl, 1986) constituting up to 40% ofbasketball injuries, 31% of soccer injuries(Garrick, 1977) and 7% to 10% ofadmissions to accident and emergencydepartments of hospitals (Kannus andRenstrom, 1991).

A common sequel to an ankle sprain is thedevelopment of chronic functionalinstability at the ankle joint. Ryan (1994)cites three studies which reported thatfunctional instability complicates 10% to20% of all inversion injuries presenting for treatment (Moller-Larsen et al, 1988;

Niedermann et al, 1981; Prins, 1978). Peterset al (1991) report an incidence of 10% to30% following ankle sprain. Brand et al(1977) randomly surveyed 175 US NavalAcademy athletes and found a 17%incidence of instability in all subjects asevidenced by symptoms of frequent sprains,difficulty in jumping and cutting, anddifficulty on uneven surfaces.

Freeman et al (1965) have describedfunctional instability as a tendency for thefoot to sprain or give way repeatedly. It is adistinctly different phenomenon frommechanical instability, which refers to jointmotion beyond normal physiological limits, whereas in functional instability joint motion is beyond voluntary control yet within physiological limits (Tropp et al,1985). Excessive joint motion has beenproposed as a possible aetiological factor inthe development of functional instability(Ryan, 1994). The relationship between thetwo conditions is discussed below.

The primary aim of this literature review isto describe the features associated withfunctional instability and to examinepossible underlying mechanisms. Theimpairments associated with the conditionwill be addressed first. Numerous studieshave been carried out examining thefeatures associated with functional instabilityof the ankle joint. The findings from thesestudies form the basis for current anklerehabilitation practice.

Mechanical InstabilityClinical tests of mechanical instability suchas the anterior drawer test, maximal passiveinversion stress, and stress radiographs are aroutine component of patient evaluation inthe management of functional instability.External support to prevent excessive anklemotion in the form of braces and taping is acommon feature of treatment programmesfor patients who suffer recurrent anklesprains.

Functional Instability of theAnkle Joint Features and underlying causes

Summary Ankle sprain is one of the most common sports injuriesand residual functional instability complicates a large proportion ofcases. The mechanisms underlying the development of functionalinstability following acute sprain are poorly understood. Thisliterature review was carried out to shed light on the featuresassociated with this condition following ankle sprain, and toexamine possible underlying mechanisms.

Functional instability is a condition associated with disorderedmechanical output of ankle musculature, impaired balance abilitywhich appears to be central in origin, and decreased kinaestheticsensation. The interrelationships between these factors and theirinfluence on level of disability have yet to be adequately described.

Mechanisms underlying functional instability which have beenproposed in the literature include ligamentous laxity, nerve injuryand articular deafferentation. There may be a link between nerveinjury and functional instability, yet recent evidence suggests thatmechanical instability and articular deafferentation are not theprimary underlying mechanisms.

A motor programme for control of ankle stability duringfunctional activities has been demonstrated. Alteration of themotor programme controlling knee function occurs followinganterior cruciate ligament injury due to reflex inhibition and asimilar phenomenon may be the primary physiological mechanismunderlying functional instability.

Key WordsFunctional instability, reflex inhibition, motor control.

by Brian Caulfield

Caulfield, B (2000).‘Functional instability ofthe ankle joint: Featuresand underlying causes’,Physiotherapy, 86, 8, 401-411.


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Lentell et al (1995) report that a differenceof greater than 5˚ of talar tilt between anklesis frequently regarded as a necessaryrequirement for surgical management ofanatomical laxity of the ankle. Tropp et al (1985) found a very poor correlationbetween the presence of functional andmechanical instability. Only 42% of subjectswith functional instability exhibited signs ofligamentous laxity.

Ryan (1994) performed standard talar tiltand anterior drawer tests for talocruralstability on 45 subjects with a history ofrecurrent ankle sprains. He used a five-pointscale to grade mechanical instability on thebasis of these tests, ranging from veryhypomobile to very hypermobile. Only 11(24%) of his subjects were classified asmechanically unstable, based on his gradingscale.

Karlsson et al (1992) performed stressradiographs on the ankles of 20 subjects withunilateral functional instability using theTelos® device -- a mechanical apparatuswhich can be used to apply an inversion oranterior drawer stress of known magnitudeto the ankle joint complex for the purposeof radiographic assessment. They foundhighly significant (p < 0.001) increases intalar tilt and anterior talar translation in theinvolved ankles compared to the uninvolvedankles. Interestingly, they reported thatnone of their subjects had clinical signs ofinstability, though they did not describe howthey came to this conclusion.

Lentell et al (1995) obtained stressinversion radiographs from 34 subjects withunilateral instability. Group mean talar tilt in the involved ankles was found to besignificantly (p < 0.05) higher than in theuninvolved ankles (5˚ versus 4˚). However,clinically symmetrical talar tilt values (lessthan 3˚ difference) were demonstrated bythe majority (59%) of subjects tested.

Birmingham et al (1997) examinedmaximum passive inversion range of motionand peak passive resistive torque in 30subjects with unilateral functional instability.They found no significant differencesbetween involved and uninvolved ankles.They concluded that functional instabilitycan exist in the absence of mechanicalinstability.

Overall, the studies cited above indicate apoor correlation between the presence offunctional and mechanical instability. OnlyKarlsson et al (1992) have demonstrated astrong relationship between the two in theirstudy population. Differences in results

obtained may arise from differences indisability levels in the subjects studied.

Wilkerson and Nitz (1994) report thatrotation of the talus in the transverse plane may be the most significantmanifestation of ligamentous laxity aboutthe ankle, and question the value ofassessing talar tilt and anterior talartranslation. They suggest that the lack of a demonstrable relationship betweenfunctional and mechanical instability may be due to a lack of methods for objectivequantification of rotatory instability of thetalus. Their hypothesis has yet to be tested.

In summary, there appears to be no clearand simple relationship between functionalinstability and excessive joint motion.Ligamentous laxity alone cannot explain thedisability suffered by those patients withfunctional instability, yet it can be a featurein some patients.

Altered Mechanical Output of Muscles Acting About the Ankle JointAnkle muscle strengthening, especiallyconcentrating on the peronei, is a centralcomponent of treatment of functionalinstability. This suggests that most cliniciansconsider evertor weakness to be a significantfactor in the development of functionalproblems following lateral ligament sprain.The first researchers to link peronealweakness and instability were Bosien et al (1955) who found manually detectedperoneal weakness in 22% of subjects with ahistory of ankle sprain and reported acorrelation between presence of weaknessand residual instability.

Tropp (1986) reported significantlyreduced evertor performance (in terms ofpeak torque) during isokinetic testing at30˚/sec and 120˚/sec in subjects withfunctional instability.

Ryan (1994) found invertor muscleweakness in subjects with functionalinstability when the involved extremity was compared to the uninvolved side (22.7 ± 8.4 NM versus 26.6 ± 8.5 NM, p < 0.001). However he found no significantevertor muscle deficits (18.8 ± 6.6 NM versus19.2 ± 5.8 NM, p = 0.49).

This finding is supported in part byWilkerson et al (1997) who found decreasedinvertor/evertor peak torque ratios on theinvolved ankle in subjects with ankleinstability.

Baumhauer et al (1995), in a prospectivestudy of ankle injury risk factors in 145college athletes, also found decreased


403Professional articles

invertor/evertor strength ratios in subjectswho subsequently sustained a lateralligament sprain.

Lentell et al (1995) reported no evertorpeak isokinetic torque deficits at 30˚, 90˚,150˚ and 210˚ per second in subjects withfunctional instability when the involvedankle was compared to the uninvolvedankle.

A summary of the available results ofstudies on isokinetic evertor muscle torquein subjects with and without recurrent anklesprains is presented in table 1. In the studiesperformed on subjects with functionalinstability, conclusions regarding strengthdeficits are based on comparisons bet-ween the involved and uninvolved sides.Unfortunately none of these studiesincluded an age and sex matched controlgroup, so comparison with normal subjectsis difficult. In addition, the studies did notgive separate results for males and females,so direct comparison with the normativedata supplied by Wong et al (1984) andLeslie et al (1990) is not possible. In spite ofthese limitations, a review of the datapresented in table 1 suggests that thesubjects with functional instability haveminimal or no deficits in peak evertortorque when the involved ankle is comparedto both the uninvolved side and tonormative data. Only Tropp (1986) hasdemonstrated significant evertor weakness.Differences in the findings between variousinvestigators could point to differences insubject inclusion criteria.

In summary, the main disorder ofmechanical output of the ankle musculatureassociated with functional instability seemsto involve altered invertor/evertor torqueratios and not simply evertor weakness as hasbeen proposed previously. Wilkerson andNitz (1994) have postulated that invertorweakness may have a significant role as itmay result in lateral displacement of thecentre of gravity of the body relative to the fixed forefoot on the ground, thusrendering the lateral border of the foot afulcrum for sudden inversion. The evidencepresented by Wilkerson et al (1997) appearsto support this postulate yet it has not beenclearly demonstrated so far. Other aspects ofmuscle performance such as endurancecapacity may have a role to play indetermination of residual symptomsfollowing ankle sprain yet they have not been investigated to date. Manyquestions regarding invertor/evertor anddorsiflexion/plantar flexion ratios and

endurance characteristics of ankle mus-culature in functional instability remainunanswered and warrant further attention.

Altered Postural ControlMany authors have demonstrated thataltered postural control, or impairedbalance ability, is associated with functionalinstability. This concept was first reported byFreeman et al (1965) using a modifiedRomberg test. Their methods of meas-urement of balance ability were largelysubjective yet this work laid the foundationfor much of current ankle rehabilitationpractice. They demonstrated that a regimeof ‘proprioceptive exercises’ using a wobbleboard could significantly reduce theincidence of functional instability followingankle sprain. The modified Romberg testemployed in their study is an essentialcomponent of a routine clinical ankleexamination today. Garn and Newton(1988), using similar methods, reportedbalance deficits on the side of injury in 20 subjects with unilateral instability.

More recently an objective stabilometrytechnique has been developed to record

Table 1: Peak isokinetic torque of ankle evertors at 30˚/sec in studiesinvolving subjects with functional instability (A) and normal controls (B).Values are means ± SD, ages in years

A. Injured versus uninjured ankles

Eversion peak torque at 30˚/sec (Nm) Level of Involved Uninvolved significance

Study extremity extremity

Ryan (1994) 18.8 ± 6.6 19.2 ± 5.8 P = 0.49 (NS)45 subjects with unilateral functional instability (12 M, 33 F; age 16-35)

Lentell et al (1995) 21.2 ± 5.6 20.7 ± 5.4 P > 0.05 (NS)42 subjects with unilateral functional instability (30 M, 12 F; age 18-27)

Baumhauer et al (1995) 30.8 ± 9.4 30.5 ± 10.4 P = 0.84 (NS)Prospective study on 15 subjects who subsequently sustained ankle sprain (8 M, 7 F)

Tropp (1986) 20.2 ± 4.7 23.0 ± 5.8 P < 0.01 (S)15 subjects with unilateral functional instability (12 M, 3 F; age 13-31)

B. Normal populations

Study Women Men

Leslie et al (1990) 23 ± 4 –16 normal subjects (16 F; age 20-33)

Wong et al (1984) 20 ± 3 28 ± 644 normal subjects (21 M, 23 F; age 20-37)

S = Significant difference. NS = No significant difference


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disturbances of standing equilbrium.Stabilometry involves measurement ofparameters of ground reaction force and co-ordinates of centre of pressure while asubject stands on one limb on a forceplatform. Tropp and co-workers (1984,1985) used stabilometry to demonstrateincreased postural sway and subsequentincreased risk of sustaining further injury insoccer players with functional instability ofthe ankle joint. Interestingly, they found thatpostural sway was worse in subjects withunilateral involvement when standing oneither limb when compared to a controlgroup, yet there were no differences whenthe injured and uninjured limbs werecompared. The fact that disordered posturalcontrol applied to both limbs and not justthe injured one suggests a central balancedisorder.

Friden et al (1989) performed stabilometrymeasurements on both the injured anduninjured limbs in 14 patients with acuteankle sprains (three to eight days afterinjury). Parameters used to describe posturalsway were significantly different in injuredand uninjured ankles (p < 0.01) and thuscould discriminate between the injured anduninjured limb. Use of an ankle brace(Aircast) on the injured side eliminated thedifferences. Isakov and Mizrahi (1997), in anuncontrolled study, examined variability ofground reaction force in the frontal plane in eight competitive female gymnasts with unilateral instability and found nosignificant differences between involved anduninvolved ankles. Kinsella and Harrison(1998) found no significant differencesbetween subjects with functional instabilityand a control group in measures of posturalsway. They point to greatly differingmethodologies in stabilometric measure-ment in published studies and postulate thatthis could underlie differences in results.

Ryan (1994), in another uncontrolledstudy, used a custom-made uni-axial balanceevaluator (UBE) to measure time spent outof balance when subjects with unilateralfunctional instability stood on one foot on asingle axis wobbleboard. During 30-secondtrials the subjects spent significantly greatertime out of balance when standing on theaffected leg compared to the sound leg (5.4sec versus 2.9 sec; p < 0.001).

The value of including wobble boardexercises in a rehabilitation programme toimprove balance ability has been wellestablished (Gauffin et al, 1989; Balogun etal, 1992) and there is general agreement in

the literature that subjects with functionalinstability do have a balance disorder. Whatis not clear is whether or not the degree ofimpairment of balance ability is related tothe level of disability experienced. Furtherwork is necessary to establish the relat-ionship between balance impairment anddisability and to validate stabilometrymeasurement protocols.

Proprioceptive DeficitsProprioception has been described byLephart et al (1997) as a sensory modalitythat encompasses the sensation of jointmovement (kinaesthesia) and joint position(joint position sense). Kinaesthesia has beenfound to be decreased in subjects withfunctional instability.

Garn and Newton (1988) reportedsignificantly decreased passive movementsensitivity on the involved side in subjectswith unilateral instability. Their subjectswere passively moved through 5˚ ofplantarflexion motion in a blinded pro-cedure at a rate of 0.3˚/sec and were askedto say whether or not joint movement hadactually taken place. There were significantlymore incorrect responses when the involvedankle was tested compared to the uninvolvedankle. This was associated with balanceimpairment as described above.

Lentell et al (1995) examined anotherdimension of kinaesthetic ability. Theirsubjects were passively moved into inversionat a rate of 0.3˚/sec, again in a blindedprocedure, and were asked to detect whenthey could actually feel movement takingplace. A significantly greater amount ofinversion was found in the involved anklescompared to the uninvolved ankles beforemotion was sensed. However they wereunable to find a relationship between theoccurrence of impaired passive movementsensitivity and the existence of impairedevertor performance or mechanical in-stability.

Glencross and Thornton (1981) examinedjoint position sense in subjects withinstability. Their subjects were passivelymoved into plantarflexion and were asked toreplicate this position actively, using thesame ankle. Significantly greater errors weremade in replication of the test position inthe involved ankles compared to theuninvolved ankles (p < 0.002).

There is agreement from the above threestudies that decreased proprioception isassociated with the presence of residualsymptoms following ankle sprain. What



exactly causes these proprioceptive deficits,and their relationship with level of disability,remains unclear.

The evidence presented above suggeststhat functional instability is a conditionassociated with varying degrees of lig-amentous laxity, disordered mechanicaloutput of ankle musculature, impairedbalance ability, and impaired proprioceptivefunction. The interrelationships betweenthem and their influence on level of disab-ility have yet to be adequately described. In the forthcoming sections, studies whichhave sought to explain the mechanismsunderlying the deficits associated withfunctional instability will be reviewed.

Nerve InjuryNitz et al (1985) investigated function of theperipheral nerves in the leg in patients withacute grade II and grade III ankle sprains.The investigation was carried out becausepatients with severe ankle sprains were notable to push off in the stance phase ofwalking for weeks after injury and exhibitedmarked gastrocnemius atrophy. EMG studieswere performed two weeks after injury in 30patients with grade II sprain and 36 patientswith grade III sprain. EMG evaluationincluded analysis of distal motor latenciesand nerve conduction velocities of peronealand posterior tibial nerves. They found avery low rate of nerve injury in patients withgrade II sprains: 17% had injured theirperoneal nerve and 10% had injured theirposterior tibial nerve. In contrast 86% ofpatients with grade III sprains had injuredtheir peroneal nerves while 83% had injuredtheir posterior tibial nerves. Sensorydisturbance was noted in 54% of patientswith grade III sprains. Follow-up examin-ations at six months on 14 patients withgrade III sprains confirmed a return tonormal nerve function. They postulated thatthe disruption to nerve function might havebeen due to a mild traction injury to thenerve or an epineural haematoma sustainedat the time of the ankle sprain. Thereappeared to be no clear relationshipbetween the extent of the nerve injury andlong-term disability following the sprain,though such an analysis was not the focus ofthe investigation. Injury to peripheral nervesat the time of injury may lead to alteredmotor neurone recruitment and sensoryinput in the acute phase following injury.This could have a large influence onrehabilitation and, possibly, long-termdisability due to the sprain.

Altered Peripheral Control of Ankle Muscle FunctionFreeman et al (1965) proposed the theory ofarticular deafferentation to explain thedevelopment of functional instabilityfollowing ankle sprain. According to thistheory, dynamic ankle stability depends onthe evertors reacting quickly to any inversionstress and overcoming it to prevent ligamentor joint damage. Patients with instabilitycould have delayed reflex responses in theirperonei in reaction to an inversion stressdue to altered joint and ligament afferentinput.

Wilkerson and Nitz (1994) suggest that arelatively small increase in peronealresponse time may have highly significantconsequences in terms of risk of injury tothe lateral ligament complex.

Numerous studies have been carried outto put this theory to the test. The main focushas been on analysis of peroneal reactiontime in response to a sudden inversionstress, as examined by Isakov et al (1986).They used a uni-axial tilting platform toinduce sudden unexpected inversion whileEMG activity in the peronei was recorded.They found no significant differences in peroneal reaction times exhibited by acontrol group (n = 11) and a group ofpatients with recurrent ankle sprains (n = 11). They also found no significantdifferences in mean reaction times betweenthe involved and uninvolved ankles in the patient group (70.2 ± 7.4 ms versus 68.3 ± 6.5 ms).

Konradsen and Ravn (1990) used similarmethods to examine peroneal reaction timeand joint motion in response to suddeninversion in 15 subjects with functionalinstability and 15 age-matched controls.They reported that both groups respondedto the sudden inversion with similarkinematic patterns, ie ankle dorsiflexion of20˚, knee flexion of 30˚, hip flexion of 25˚,and hip abduction of 5˚ (median values).The patient group demonstrated sign-ificantly (p < 0.01) longer peroneus longus(median 82 ms versus 65 ms) and peroneusbrevis (median 84 ms versus 69 ms) reactiontimes to the inversion stress.

Karlsson and Andersson (1992) also foundsignificantly (p < 0.001) longer peroneuslongus (84.5 ± 4.0 ms versus 68.8 ± 4.5 ms)and peroneus brevis (81.6 ± 5.2 ms versus69.2 ± 4.1 ms) reaction times in the involvedlimbs of 20 subjects with unilateral instab-ility when compared to the uninvolved limb. They found a significant reduction

Author

Brian CaulfieldBSc(Physiotherapy)MMedSci is a lecturer atUniversity College DublinSchool of Physiotherapyand a PhD student at thesame university, workingon causes of functionalinstability.

This article was receivedon April 15, 1999, andaccepted on February 15,2000.

Address forCorrespondence

Brian Caulfield,University College DublinSchool of Physiotherapy,Mater Hospital, Dublin 7,Ireland.

E-mail: [email protected]


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(p < 0.05) in reaction time in the involvedlimb when tape was applied to the ankle.They suggested that tactile skin stimuluscould contribute to the shorter reactiontime.

Lofvenberg et al (1995) compared ipsi-lateral and contralateral peroneus longusand tibialis anterior reaction times tosudden inversion in subjects with functionalinstability and a control group. Significantlylonger ipsilateral reaction time (p < 0.0001)was recorded in the patients compared withthe control groups in peroneus longus(median 65 ms versus 49 ms) and tibialisanterior (median 68 ms versus 49 ms). Theyfound no significant differences in reactiontimes between the involved and uninvolvedankles in those patients with unilateralinstability.

Ebig et al (1997) examined reaction timesto sudden inversion and plantarflexionstress in 13 subjects with unilateralinvolvement. They reported shorter, yet non-significant, reaction times to theplantar flexion/inversion stress in theperonei and tibialis anterior of the involvedside compared to the uninvolved side. Theycite the work of Nawoczenski et al (1985)who also found no differences in peronealresponse time to inversion in injured anduninjured ankles.

Beckman and Buchanan (1995) examinedresponse in ipsi- and contralateral ankle andHIP muscles to sudden inversion in subjectswith ‘hypermobility’ and a control group.Inclusion in the hypermobile grouprequired that the subject had sustained aminimum of one inversion sprain in the pasttwo years and exhibited at least 10˚ increasein inversion range of motion on the involvedside compared to the uninvolved side. Theyfound decreased latency of gluteus mediusonset following perturbation in thehypermobile group. This suggested thataltered motor control of response toinversion had extended to other joints. Theauthors suggest that altered somatosensoryinput from the ankle might facilitatecompensatory reactions at more proximalsites. Interestingly, latency of hip muscleonset in the hypermobile group was of theorder of 100 msec, indicating that muscleactivation was due either to a polysynapticpathway or was according to a centrallyprogrammed pattern. The authors felt thatthe delay was polysynaptic as the latency wastoo long for a monosynaptic response andtoo short to allow for central integration andprocessing. They entertained the possibility

that the central nervous system, based onprevious experience of excessive inversion,might have increased gamma drive to thehip musculature in an attempt to reduce the load on the ankle.

Overall there appears to be littleagreement in the literature as to whetherthere really is a delayed response time in theankle musculature to inversion stress or not.A summary of the studies is presented intable 2.

The lack of clear agreement in the studiesoutlined above suggests that Freeman’stheory of articular deafferentation may notbe the main physiological mechanismunderlying the development of functionalinstability, at least in the way he suggestedthat it was. Two studies have recently beenpublished which add weight to this assertion.

First, Konradsen et al (1993) examinedperoneal reaction time in response tosudden inversion before and after regionalblock of the ankle and foot with localanaesthetic. This negated the effect of jointand ligament receptors on motor control.The subjects demonstrated impaired passiveposition sense with the blockade, yet theiractive position sense remained intact. Therewas no significant difference in peronealreaction time to sudden inversion beforeand after blockade. Articular deaffer-entation made no difference to responsetime. The authors suggested that afferentinput from the active peroneals, not thejoint and ligament mechanoreceptors, couldbe responsible for dynamic ankle inversioncontrol.

Konradsen et al (1997) subsequentlyexamined the role of the ankle musculaturein stabilisation of the ankle against suddenforced inversion. They recorded joint andmuscle reactions to sudden inversion indifferent standing and walking conditions in10 subjects with healthy ankles. PeronealEMG activity was apparent at a median of 54 ms following onset of inversion stress.The authors took onset of subtalar eversionto represent the time taken for sufficienttension to generate in the peronei toovercome the force of bodyweight and thusstabilise the ankle against further inversion.Subtalar eversion occurred at a median of176 ms after inversion stress. However,trapdoor inversion was occurring at a ratesufficient to cause ligament injury after only100 ms. Thus the authors concluded that theankle musculature cannot react fast enoughto protect an ankle from injury in the case ofsudden inversion stress. The reflex response,



even under normal conditions, is not fastenough to stabilise the ankle againstunexpected stress.

In summary, functional instability does notappear to result simply from a disorder ofperipheral reflex control of ankle stability.There must be a higher level of control ofankle muscle function to provide anklestability during functional activities.

Higher Control of Ankle Musculature During Functional ActivitiesArmstrong (1988) has proposed the idea ofcentrally developed motor programmesbeing the driving force behind motorcontrol in functional activities. Theseblueprints for movement, mediated bycentral pattern generators, are quite robustin nature as evidenced by T G Brown’s

Table 2: Summary of studies examining lower limb musculature reaction times in response toinversion stress

Study Test group Reaction times in response to inversion stress (ms) Values

Peroneus Peroneus Tibialis (median

longus brevis anterior (range) ormean ± SD)

Isakov et al (1986) Unstable group:11 subjects with Stable ankles 68.3 ± 6.5 Mean ± SDrecurrent sprains and 11 control subjects Unstable ankles 70.2 ± 7.4 Mean ± SD

Stable group:Left ankle 69.3 ± 6.4 Mean ± SD

Right ankle 67.0 ± 5.4 Mean ± SD

Level of > 0.05significance (p value)

Konradsen and Stable ankles 65 (55-78) 69 (60-80) Mean ± SDRavn (1990)15 subjects with Unstable ankles 82 (70-90) 84 (70-94) Mean ± SDfunctional instability and 15 age matched Level of 0.01 0.01controls. significance Age 21-32 (p value)

Karlsson and Stable ankles 68.8 ± 4.5 69.2 ± 4.1 Mean ± SDAndreasson (1992)20 subjects (10 M,10 F) Unstable ankles 84.5 ± 4.0 81.6 ± 5.2 Mean ± SDwith unilateralinstability. Level of 0.001 0.001Age 19-28. significance No control group (p value)

Lofvenberg et al(1995)

A.15 unstable ankles Stable ankles 49 (41-64) 49 (43-62) Median (range)and 15 age, sex and side matched controls Unstable ankles 65 (53-89) 68 (53-83) Median (range)Age 24-49

Level of 0.0001 0.0001significance (p value)

B. 13 subjects from Stable ankles 65 (55-80) 66 (58-80) Median (range)above study withunilateral symptoms. Unstable ankles 66 (53-89) 68 (53-83) Median (range)Within-group comparison Level of 0.2411 0.7989

significance (p value)

Ebig et al (1997) Stable ankles 65.3 ± 17 67.9 ± 14 Mean ± SD13 subjects (5 M, 8 F) with unilateral Unstable ankles 58.6 ± 11 71.6 ± 14 Mean ± SDfunctional instability. Age 19.2 ± 1.5. Level of 0.238 0.467No control group significance

(p value)


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early experiments on cats (Brown, 1914).Feedback from the periphery can be used tomodify and refine the blueprint from thepattern generator (Dietz, 1992). So, we canexpect a motor programme to be in place togovern ankle stability during functionalactivities. If the theory of articulardeafferentiation proposed by Freeman et al(1965) holds true, its mechanism of actionmay be via alteration of a central motorprogramme due to decreased afferentfeedback, not by means of decreased reflexstabilisation.

Reber et al (1993) examined muscularcontrol of the ankle joint during running at various speeds using fine wire electro-myography in 15 runners without injuries.Results indicated increased activity in boththe peroneus brevis and tibialis anteriormuscles towards the end of the swing phase of the running cycle. Presumably this reflected a preprogrammed muscleactivation to ready the ankle for theimpending forces which would be actingupon it at heel strike, a frequent time forankle injury. This pattern of activationappeared to be related to functionaldemands as there were significant increasesin peroneus brevis activity throughout thecycle when the subjects increased theirspeed from jogging to race pace. Theseincreases were very evident in late swing and early stance, suggesting increased needfor ankle stabilisation against inversion athigher speeds.

Further evidence for pre-programmedcontrol of ankle stability during functionalactivities has been provided by Dyhre-Poulsen et al (1991). They demonstratedpre-innervation of ankle musculature whenlanding from a jump. Electrical activitystarted before landing in both soleus (150 ms) and tibialis anterior (170 ms).Interestingly, the time-order of the pre-innervation corresponds very well with thelatency between trapdoor opening and onsetof eversion in the Konradsen et al (1997)study described earlier. Similar findingsregarding pre-innervation of soleus inlanding have been reported by Duncan andMcDonough (1997). We have found similarpatterns of pre-innervation in the peronealmuscles during landing while performingunpublished laboratory studies.

Alteration to the programme for motorcontrol could lead to disordered control of forces acting upon the joints. Gauffin andTropp (1992) have reported alteredmovement and muscle activation patterns

during functional activities in patients withold anterior cruciate ligament tears. It ispossible that a disorder in the pattern ofactivation of ankle musculature duringfunctional activities could contribute to thedevelopment of functional instabilityfollowing an ankle sprain. Patterns of anklemuscle activation during functional activitieshave not been investigated to date insubjects with functional instability.

Reflex InhibitionThis leads us to question of whichmechanisms could underlie any disorder ofmotor control about the ankle in subjectswith functional instability, if such aphenomenon exists. Reflex inhibition of thequadriceps following knee ligament injuryhas been widely reported in the literature(DeAndrade et al, 1965; Spencer et al, 1984;Stokes and Young, 1984; Elmqvist et al, 1988;Fahrer et al, 1988; Snyder-Mackler et al,1994). Damage to the knee joint can disruptthe central nervous system drive to the kneemusculature because of a change in afferentinput from joint receptors. This alteredmotor unit activation by the CNS maybecome a permanent feature of the motorprogramme as evidenced by the work ofGauffin and Tropp (1992) described above.

The principle of reflex inhibition may alsoextend to the ankle musculature followingankle ligament injury.

Altered afferent input from joint,ligament, muscle and nociceptive receptorsmay occur at the time of injury due to jointeffusion, capsular distension, ligamentdamage, nerve injury, and pain sensation.Petrik et al (1996) demonstrated a significant(p < 0.05) increase in gastrocnemius H-reflex amplitude brought about by isolatedankle joint effusion. This suggests that ankleeffusion can have an influence on neuralcontrol. Altered afferent input in the acutephase following injury may lead to an alteredmotor unit activation pattern. This may havea profound effect on future central andperipheral ankle control mechanisms.

ConclusionFunctional instability may occur without anyobjective signs of mechanical instability ofthe ankle complex. It is associated with anill-defined disorder of mechanical output ofankle musculature, balance deficits whichappear to be central in origin, anddecreased kinesthetic sensation. Thephysiological mechanisms underlying thesedeficits do not appear to be peripherally



mediated. The work of Konradsen et al(1993, 1997) indicates that dynamic anklestability is controlled by the CNS. Evidencefrom research into knee injuries suggeststhat the motor programme provided by theCNS may be altered in subjects withfunctional instability. This may be caused byafferent input at the time of initial injury.

Future ResearchIn light of the possibility of altered motorcontrol due to reflex inhibition beingimportant in the development of functionalinstability, a research programme examining

motor control in subjects with this conditionis currently under way in University CollegeDublin. We are analysing joint movement,ground reaction forces and electrical activityin ankle musculature before and afterlanding in jumping and hopping movementsin subjects with and without instability.

If altered motor control is identified it willhave significant effects for rehabilitation ofpatients with acute ankle sprains. Modalitiessuch as electrical stimulation of anklemusculature may be employed to min-imise the effects of reflex inhibition and subsequent disability.

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Key Messages

� Functional instability of the ankle andankle joint laxity are independentphenomena. Functional instability refersto a tendency of the ankle to give wayrepeatedly.

� Functional instability is associated withdisorders of ankle muscle strengthratios, impaired postural control andproprioceptive deficits.

� Recent evidence suggests that articulardeafferentation may not be the majorcausative factor in development offunctional instability.

� Alteration to the motor programme laiddown by the CNS may be more likely tolead to development of functionalinstability.

functional instability of the ankle joint: features and underlying causes

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