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Proprioception and recurrent ankle inversion injuries: a narrative review.


This narrative literature review examined the evidence base concerning the relationship of impaired proprioception to the etiology and pathogenesis of functional instability of the ankle joint. This review conducted using the CINAHL, EMBASE, PUBMED, SCIENCE CITATION INDEX, and SPORTSDISCUS databases over the time periods 1966-2002 showed some support for the hypothesis that proprioception is impaired in persons with ankle joint instability. However, not all studies were affirmative, and whether the presence of a proprioceptive deficit has a significant bearing on the stability of either an injured or healthy ankle joint was not clearly discernible from the available literature. Stefanini L, Marks R. (2003) Proprioception and Recurrent Ankle Inversion Injuries--A Narrative Review. New Zealand Journal of Physiotherapy 31(1): 25-39.

Key words: ankle injury, proprioception, literature review.


According to Puffer (2002) roughly 25 per cent of all sports-related problems involve the ankle joint, with trauma to the lateral ligament complex (i.e. the anterior talofibular, calcaneofibular and posterior talofibular ligaments) being the most common site of injury (Hume and Gerrard 1998). Estimates by De Carlo and Talbot (1986), Gross (1987), Karlsson et al (1996) and Lentell et al (1990) suggest that approximately 25-40 per cent of cases who have sustained ligamentous ankle injuries will subsequently develop a residual disability, termed functional instability, a classical term introduced by Freeman et al. (1965) to describe 'a tendency for the foot to give way' after an ankle sprain.

To explain this phenomenon, some believe repeated ankle sprain injuries might occur because ankle joint proprioceptors, which encode sensory information, could become abnormal or cease their function altogether if the ankle joint tissues containing these are damaged or destroyed as a result of any momentary or repeated overstretching incident (Feuerbach et al 1994, Wilkerson and Nitz 1994). In addition, a pre-existing deficit in proprioception has been given as the explanation for causing both an acute, as well as repeated ankle inversion injuries (Freeman et al 1965, Glencross and Thornton 1981, Hintermann 1999, Lephart et al 1998, Robbins and Waked, 1997, 1998, Watson, 1999).

It has been hypothesised that without adequate sensory feedback from the ankle proprioceptors to the central nervous system (CNS) it might be difficult to produce precisely coordinated joint movements, thus potentially reducing joint protection mechanisms (Parkhurst and Burnett 1994). Ryan (1994) specifically suggested an impaired ability to generate adequate muscular forces in a timely manner consequent to poor proprioceptive feedback could impair an individual's ability to protect the ankle joint against any destabilising influences, for example those that might be experienced at the subtalar joint where a majority of lateral ankle sprain injuries occur.

Acute ankle sprains, recurrent ankle inversion injuries and persistent abnormalities in ankle joint function may foster persistent synovitis or tendinitis, fear of giving-way, ankle stiffness, persistent talar tilt, swelling, muscle weakness, range of motion limitations, premature ankle joint degeneration, cartilage damage and further joint injury, persistent pain and functional disability (Gross and Marti 1999, Hall et al 1999, Hintermann 1999, Hintermann et al 2002, Liu and Nguyen 1999, Lynch and Renstrom, 1999, Parkhurst and Burnett 1994, Safran et al 1999, Schultz and Stinus 1990, Verhagen et al 1995). The corroboration of this 'proprioceptive theory' in explaining acute and recurrent ankle inversion injuries could prove invaluable. In particular, interventions to improve proprioception such as co-ordination exercises (Bernier and Perrin 1998, Gauffin et al 1988, Renstrom and Konradsen 1997), balance exercises (Goldie et al 1994), ankle disk (Sheth et al 1997, Osborne et al 2001) or tilt board training (Lynch and Renstrom 1999), bracing (Vaes et al 1998), orthotics (Guskiewicz and Perrin 1996) and taping (Baquie 2000) might be especially effective in reducing the high incidence of recurrent ankle sprain injuries that occur (Verhagen et al 2000).

However, scientific support for the rationale underlying treatment such as exercise, taping, bracing or altering footwear design in preventing recurrent ankle sprain injuries remains equivocal. For example, in contrast to observations of a proprioceptive deficiency in those with acute and chronic ankle inversion injuries (Freeman 1965, Hertel et al 2001, Watson 1999), it remains unclear whether proprioception is actually impaired after an ankle sprain (Gross 1987, Isakov and Mizrachi 1997, Johnson and Johnson 1993, Refshauge et al 2000). Further, although ankle taping (Karlsson and Andreasson 1992, Refshauge et al 2000) and training to reduce peroneal muscle response times have been advocated for reducing or preventing functional instability of the ankle (Sheth et al 1997), neurophysiological responses to sudden ankle inversion movements are not necessarily improved by ankle taping (Allison et al 1999). In addition, the effectiveness of taping and bracing on balance has not been consistently demonstrated (Barkoukis et al 2002, Bennell and Goldie 1994).

It is also unclear whether deficient muscle response times are implicated at all in cases of acute ankle sprains (Beynnon et al 2001) or those experiencing recurrent ankle instability (Ebig et al 1997). As well, whether proprioceptive deficits in the periphery actually cause functional instability of the ankle joint, as recently implied by Richie (2001), is unclear, as concomitant findings of permanent damage to capsular, ligamentous and musculotendinous receptors have not been demonstrated in ankle sprain populations (Robbins and Waked 1998).

To establish a clearer perspective of the role of impaired proprioception in mediating ankle instability, literature was sourced from publications documented in the CINAHL, EMBASE, PubMED, Science Citation Index, and SportsDiscus databases over the time periods 1966-2002 using the keywords; ankle sprain injury, ankle joint, proprioception, joint position sense, functional instability. The findings were limited to those documented in the English language, and only data from full length studies published in the above data bases and related to ankle sprain injuries and ankle proprioception were reported. No other restrictions to the search strategy were applied.

There are four sections to this narrative review, which will firstly document the clinical features of lateral ankle sprains. Secondly, it will review current peripheral neural mechanisms believed to be involved in mediating ankle proprioception. Thirdly, the outcomes of the four different test modes used to evaluate the proprioceptive status of persons diagnosed as having functional instability of the ankle will be reviewed. Lastly, the results and the implications of the present findings will be discussed in light of the evidence supporting a role for the ankle joint proprioceptors in mediating ankle instability.

Ankle Sprain

In general, when the term 'ankle sprain' or 'ankle inversion injury' is used, this is essentially taken to indicate that the ligamenentous fibers associated with the lateral ligament complex of the ankle joint, including the anterior talofibular, the calcaneofibular and the posterior talofibular ligament have been stretched or torn during an unanticipated or unprovoked plantar flexion, supination and inversion movement of the fixed foot coupled with external rotation of the tibia (Safran et al 1999). However, it is important to note that damage to the lateral ligament complex of the ankle joint, which has the potential for loss of proprioception, seldom occurs in isolation. More typically, an injury to the lateral ligament complex of the ankle is likely to be accompanied by an injury to one or more ankle joint structures including the joint capsule, the subtalar joint ligaments (Lynch and Renstrom 1999), the tibio-fibular ligaments (Safran et al 1999), the muscle tissues surrounding the ankle complex (Hertel 2000) and the peroneal tendon sheaths and tendons (Boruta et al 1990, Liu and Nguyen 1999). As well, Reid (1992) reported that 17 per cent of grade II and a further 86 per cent of grade III ankle sprains involved injuries to either the peroneal nerve (currently termed the fibular nerve) or the tibial nerve. Nitz et al (1985) found a high incidence of peroneal nerve and posterior tibial neuropraxia in grade III ankle sprains and that 17 percent of grade II and 86 percent of grade III sprains had moderate denervation in the muscles supplied by the peroneal nerve. Moreover, alone or in combination, other problems that could impact upon neuronal function directly or indirectly, such as chronic effusion, abnormal scar formation, soft tissue and osseous impingement (Robinson and White 2002), pain and reflex sympathetic dystrophy could ensue following an ankle inversion injury.

Given that the sensory receptors believed to mediate ankle proprioception may be located not only in the ligamentous tissues, but also in the tendons, muscles and capsule of the ankle joint and that in addition to nerve conduction problems that may arise, all these structures may be vulnerable to damage as a result of an ankle sprain injury, the likelihood of detecting a proprioceptive deficit in the individual with an ankle inversion injury history could conceivably be quite high. However, although a single ankle inversion injury may affect dynamic stabilisation of the joint negatively (Hall et al 1999), it is not clear whether a) recurrent ankle injuries are definitively associated with the presence of a deficit in ankle joint proprioception and b) whether diminished ankle joint proprioception can cause chronic functional instability of the ankle joint.

Ankle Joint Proprioception

According to Grigg (1994), when the normal ankle joint is moved, its associated ligaments, joint capsule, muscles, tendons, and skin deform, thus activating populations of sensory neurons located in these tissues. Provided cortical pathways are intact, the ensuing sensory or proprioceptive inputs are implicated in mediating the cognitive experiences of ankle joint motion and/or joint position that influence joint function. The excitation of proprioceptors in the ankle joint tissues is also thought to evoke reflex responses at the brainstem and spinal cord levels, which protect the joint. Hence, an ankle injury, which may involve damage to one or more joint tissues and their sensory receptors, may not only have the potential for impairing the precision of joint motion and/or joint position sensibility, but also for influencing reflexly mediated protective neural responses (Freeman 1965).

Ligamentous and Capsular Receptors

According to Safran et al. (1999), joint ligaments as well as joint capsules serve as sources of proprioception information that influence joint function. The specific ligamentous sensory receptors found at the ankle joint are Ruffini endings and Pacinian corpuscles (Johansson et al 1991, Michelson and Hutchins 1995). While a proportion of joint afferents may be active in mid-range, or when a joint is immobilized, ligamentous tension increases their discharge rates, particularly at the extremes of joint movement (Grigg 1994). Data from animal studies of the biomechanical properties of the lateral ankle ligaments and their relationship to the distribution of mechanoreceptors in the ligaments suggests that mechanoreceptors in the lateral ligament may contribute to the stability of the joint by regulation of position and movement (Takebayashi et al 1997). In particular, the pole of the ligaments, may receive more mechanical stress compared with those in the center and may be effective in monitoring tension applied to the ligament (Takebayashi et al 2002). Although thought to be poor candidates for sensing movement in specific directions, when tensed (Grigg 1994), these ligamentous mechanoreceptors may thus impart sensory stimuli that mediate proprioceptive responses (Burke et al 1988, Boruta et al 1990, Nigg 1990, Wilkerson and Nitz 1994).

Other joint receptors that may play a role in mediating ankle proprioception are the Ruffini and Paciniform stretch receptors embedded in the joint capsule. The former, which are usually found on the flexor surface of the joint, are activated at the limit of joint extension (Grigg 1994, Marshall 1993) and the latter, which are widely distributed around the joint, are activated by tensile forces (Grigg 1994). In general, the activation of capsular receptors is thought to relay sensory messages both centrally and to gamma motoneurones within the spinal cord which influence reflex activity of the surrounding muscles (Wilkerson and Nitz 1994). The findings of Marshall (1993) supported this theory and suggested that damage to the ankle joint capsule, which could occur with an anterior talofibular ligament sprain, might cause a proprioceptive deficit as well as an impairment of joint protective reflexes. The findings of Bullock-Saxton (1995) of a deficit in vibration perception between the injured and non-injured sides of persons with severe ankle sprains, provided some support for the involvement of joint capsular receptors as one of the possible tissues other than muscle or tendon that might be affected by an ankle inversion sprain.

Muscle and Tendon Receptors

Strong evidence exists that in addition to ligamentous and capsular receptors, muscle spindles and possibly golgi tendon organs located in muscles, tendons and at musculotendinous junctions mediate joint positional and joint movement sense (Grigg 1994, Jami 1992, Jozsa et al, 1993, Wilkerson and Nitz 1994). As well, as indicated by Al-Falahe (1990) muscle spindles whose discharge rate is sensitive to stretch and the rate of muscle length changes can elicit graded muscular responses (Small et al 1994), which may be sufficient to enhance joint protection (Grigg 1994) and balance (Pyykko et al 1989).

In addition to diminishing foot position sense, a loss or decline in function of the ankle muscle sensory receptors could thus predispose the individual to postural instability, which results in destabilisation and potential injury of the ankle joint (Robbins and Waked 1997). Yet few ankle sprain studies to date have closely examined whether the stretch sensitivity of the ankle muscle or tendon afferents or their numbers are indeed compromised in cases of chronic ankle instability and these pathways have never been shown to be permanently damaged as a consequence of ankle sprains (Robbins and Waked 1998). Conversely, in 'simulated' ankle sprain studies, none have specifically targeted muscle to examine the possible role of abnormal muscle spindle or golgi tendon organ function in mediating ankle sprain injuries. Recent work also suggests that a central, rather than a peripheral program of control arising in the muscle spindle mediates ankle stiffness (Allum et al 1998, Gatev et al 1999). It is possible too that Golgi Tendon Organs (GTOs) found in tendons and musculotendinous junctions, which monitor muscle contractile force variations may mediate positional signals (Grigg 1994) in the absence of muscle spindle inputs.

Skin Receptors

Because they are activated during movement without any direct contact, recent studies have suggested skin receptors may perform a proprioceptive function (Cohen et al 1994, Collins and Prochazka 1996, Edin and Johansson 1995). The specific skin receptors implicated in mediating proprioceptive cues at the ankle are slowly adapting type 2 (SAII) afferents (Cohen et al 1994). Wooleem et al (1993) confirmed this in a study of the rat foot and additionally attributed greater significance of these receptors to the mediation of motion rather than position sense, a sensation that does seem of importance to ankle stability (see following section on motion sense).

In an editorial piece by Grabiner (2000), this author concluded that ankle joint proprioception is definitively influenced by cutaneous receptors in the surrounding tissues. Alternately, Grigg (1994) argued that if cutaneous receptors are involved in proprioception, evidence suggests their role is only a minor one. There is considerable evidence though that impaired tactile responses from the plantar surface of the foot may be implicated in ankle inversion injuries (Robbins and Waked 1997, 1998).

In summary, several peripheral mechanisms may be involved in mediating ankle proprioception, and possibly in mediating initial and recurrent ankle sprain injuries, if damaged or impaired in some way. In this respect, an impairment in ankle proprioception in mediating recurrent ankle sprains seems likely, regardless of damage site.

Ankle Proprioception and Ankle Inversion Injuries

Examples of studies using one of the four methods described for assessing ankle proprioception as this relates to ankle sprain injuries are depicted in Tables 1-4. These assessment methods include the evaluation of joint position sense; joint movement sense; reflex response time; and static balance.

Joint Position Sense

Ankle joint position sense, defined operationally as the ability to replicate joint positions using active or passive movement cues, has usually been measured in an open-kinetic chain mode and in a uniplanar mid-range position, with the subject positioned either in supine (Konradsen et al 1998) or in a seated position (Eils and Rosenbaum 2001, Feuerbach et al 1994, Holme et al 1999, Konradsen and Magnusson, 2000). Active joint replication is believed to measure the muscular receptor contribution underlying this modality, while passive positioning is thought to invoke activity of receptors located in non-contractile structures.

Although muscle receptors and or joint and skin sensory receptors are thought to be possible mediators of joint position sense and these may frequently be damaged or impaired functionally in the ankle injured individual, position sense tests conducted by Holme et al (1999) and Gross (1987) with respect to the ankle injured individual (see Table 1) have indicated that, as with 'simulated' ankle sprains, authentic ankle sprains may not affect an individual's ability to match ankle positions, either actively or passively.

This was not the observation of Jerosch et al (1995) however, who observed that athletes with ankle instability demonstrated significant differences in positional sensitivity between their injured and the non-injured ankles. Other contrary findings, have been those of Boyle and Negus (1998), Glencross and Thornton (1981), Jerosch and Bischof (1996), Konradsen et al (1998) and Konradsen and Magnusson (2000), which support the view that ankle position sense is compromised in those with ankle sprains.

The former findings could imply either that neural pathways other than those residing in muscle, skin and ligamentous joint tissues might compensate for any deficit in ankle position sense attributable to impaired joint ligamentous or capsular, skin or muscular proprioceptive sources, for example central mechanisms. The findings of Bernier and Perrin (1998) who found ankle joint position sense was not improved after subjects with functional ankle instability underwent proprioceptive training, may also imply that ankle joint position sense is not necessarily impaired in the functionally unstable ankle. Although Eils and Rosenbaum (2001) argued to the contrary, their mean error scores of their control group were the same at the pretest as those of the exercised group posttest.

Alternately, the methods used to position the limb and the joint angles tested in the reported studies with negative outcomes may have been suboptimal. However, although Payne, Berg and Latin (1997) suggest a positional impairment at the ankle joint is predictive of future ankle inversion sprains, simulation results of Hertel et al (1996) and Konradsen et al (1993) using functional tests have implied an accurate sense of ankle position could prevail, regardless of any related ligamentous damage.

Joint Movement Sense

Operationally, joint movement sense is defined as the ability to detect the onset of passively imposed joint movements in a given plane and direction (Garn and Newton 1988, Parkhurst and Burnett 1994, Refshauge et al 2000) or to actively discriminate the onset or cessation of movement (Waddington and Adams 1999). Garn and Newton (1988) and Forkin et al (1996) who tested their subjects' ability to perceive ankle movements from a neutral position into 50 plantar flexion at a rate of 0.30/s, reported a significant difference between the injured and non-injured sides with the injured side performing more poorly. However, this finding did not concur with the more recent observations of Waddington and Adams (1999) and may reflect a result related to studying individual's with low, rather than high pain levels (Matre et al 2002). It can also not be assumed that the outcome of passive movement sense tests conducted slowly in a limited range into plantar flexion while seated is a valid indicator of joint movement sense as a whole, especially as this occurs functionally under variable velocity and weight-bearing conditions.

Lentell et al. (1995) concluded, however, that deficits in passive movement sense into inversion existed across their sample of functionally unstable ankle joints when compared with the contralateral controls. They felt their findings supported the view that an acute inversion sprain does cause trauma and loss of function of mechanoreceptors embedded in the anterior-lateral capsular structures of the ankle. In turn, they suggested that this diminished awareness of passive movement might be responsible for documented delays in muscle reflex activity about the joint in persons with functional instability. However, the fact that balance training, which probably involves central mechanisms was found by the authors to improve functional instability, suggests the observed deficit in passive motion sense may reflect an inherent or acquired centrally mediated neural deficit, rather than one implicating lateral ligamentous ankle mechanoreceptors. This view was also implied by findings of bilateral discrimination deficits in persons with unilateral ankle injuries by Waddington and Adams (1999). As well, the latter authors found that nearly one-half of the subjects studied did not present with any evidence of a clinical impairment of passive movement sense, a finding supported by Refshauge et al. (2000).

Reflex Response Time

Reflex response time, a neurophysiological construct, reflecting the time between the onset of a stimulus and its muscular response, has been applied in several studies of ankle injured and non-injured subjects as an objective indicator of proprioceptive sensibility (Beckman and Buchanan 1995, Brunt et al 1992, Ebig et al 1997, Fernandes et al 2000, Isakov et al 1986, Johnson and Johnson 1993, Karlsson and Andreasson 1992, Konradsen and Ravn 1991, Konradsen et al 1997, Larsen and Lund, 1991, Nawoczenski et al 1985). However, as a result of their negative findings, Isakov et al (1986) challenged the importance of peroneal reflex response time measures in mediating ankle sprain injuries, stating that ligamentous damage at the ankle probably occurs before the peroneal muscles can be recruited. Konradsen et al (1997) also support the view that both peripheral and central reactions to an ankle inversion stimulus seem too slow to afford ankle protection in the face of inversion perturbations.

In addition, given that afferent inputs at the hip and knee joints, may combine with those from load receptors to control stepping movements (Dietz et al 2002) in a compensatory way, it seems questionable whether findings by Karlsson and Andreasson (1992), Vaes et al (2001) and others of an increased peroneal or tibialis anterior latency among individual's with chronic ankle instability have a direct bearing on recurrent ankle instability mechanisms. This is especially so if the diminished functional control of unstable ankles is attributable to motor control processes that govern ankle supination speed, which may be faster in unstable ankles (Vaes et al 2001), or to other centrally mediated motor events as suggested by recent findings of Caulfield and Garnett (2002).

Another fundamental problem complicating conclusions reached as a result of testing reflex response time at the ankle joint muscles in the laboratory is that many reflex response time test procedures do not appear to simulate natural movements or those underlying an authentic ankle sprain at all adequately. This is because ankle sprains usually occur during abnormal loading of the ankle into inversion and plantar flexion, that is when weight is beginning to be put through the ankle (e.g., at heel contact, landing from a jump, Boruta et al 1990), and not while the ankle is fully loaded (Stormont et al 1985). However, the strategy used by Konradsen and Ravn (1990) for examining the reflex response time of the muscles of both normal and problematic ankles was for the test foot to fall into dorsiflexion and for the increased weight to be transferred through the stable leg while unloading the test leg. That used by Vaes et al. (2001) was measured in standing during 50[degrees] of supination and 40[degrees] plantar flexion in the standing position, while that used by Osborne et al (2001) had subjects stand so that 80 percent of his or her body weight was on the ankle to be tested when the hinged trapdoor beneath produced 20[degrees] of sudden lateral ankle inversion.

Further, although Brunt et al (1992) examined their subject's postural responses in the frontal plane, this motion had the effect of everting and loading one limb while inverting and unloading the contralateral limb. In addition, in the design by Lofvenberg et al (1995), one of the few reflex response time studies supporting the thesis of impaired response time as a significant mediator of ankle instability, subjects stood barefoot on 'trap doors' with equal weight on each foot and when the muscles were relaxed, one of the 'trap doors' was released and tilted 30[degrees]. Likewise, Johnson and Johnson (1993) and Fernandes et al (2000) who found no similar deficit in their study cohorts, assessed peroneal latency by tilting their subject's ankle joints into 35[degrees] of inversion, or 5[degrees], 10[degrees] and 15[degrees] in the frontal plane, whereas Hall et al (1999) performed their H-reflex tests of motoneuron excitability, a highly non-physiological stimulus (Hugon 1973), in a non-weight-bearing prone position.

Clearly, to establish whether an inability to contract the ankle muscles in a timely manner is truly a factor associated with ankle inversion injuries, an experimental design that tests the muscles of the ankle joint when it is being dynamically loaded by physiological stimuli into a plantar flexion/inversion position is required, as was recently attempted by Nieuwenhuijzen et al (2002). However, this latter method, which used surface electromyography to record the responses in six lower leg muscles, a methodology that may introduce non-physiological tactile stimuli around the ankle joint, relied on a treadmill, where subjects walked at a set cadence, and only ankle inversion movements of 25[degrees] were recorded during the controlled walking task.

Other evidence suggests, the peroneal muscular reflex interacts with a central reaction (a combination of reactions from other muscles at other joints) to decrease the magnitude of the vertical ground reaction force acting on the foot (Konradsen and Ravn 1990, Wilkerson and Nitz 1994) and that this central response is elicited much earlier than the peroneal response (20 msec compared to 64-84 msec). Given that evidence by Konradsen and Ravn (1990) established that the timing of this central response is similar in the normal and ankle injured population, the implications of finding any decrement in the peripheral response times of the ankle muscles of those with recurrent ankle sprains and functional instability may well be minor, rather than major, especially in individuals with intact central pathways.

Yet, even when unsupported by their findings, based on their reflex response data, Konradsen and Ravn (1990) plus others (e.g. Konradsen and Ravn 1991, Konradsen et al 1993, Nawoczenski et al 1985) have hypothesised that a partial deafferentation has occurred in those with ankle inversion injuries, resulting in a proprioceptive deficit. However, Jennings and Seedhom (1994) believe that reflex response time may not be a valid proprioceptive measure due to the many possible factors (i.e. biomechanical, neurophysiological) that can influence this, including speed of inversion moment and plantar flexion angle (Lynch et al 1996). Like Ebig et al (1997), Johnson and Johnson (1993) have argued strongly against any mechanoreceptor impairment in ankle sprain injuries on the basis of their reflex response time data.

Static Balance

Since 1965, the modified Romberg test used by Freeman et al to examine static balance has frequently been used in ankle sprain studies with a view to quantifying any accompanying proprioceptive deficit. In this test a subject commonly stands on one leg and an observer: 1) quantifies the amount of upper extremity and trunk movement required to maintain balance; 2) documents the number of times the subject loses balance (Garn and Newton 1988) or the time taken to loss of balance control (Bullock-Saxton 1995, Forkin et al 1996).

Although employed by several investigators with respect to the clinical investigation of persons with ankle sprains (for example, Garn and Newton 1988 and Lentell et al 1990), observation may not be an effective way to apply the modified Romberg test (Lentell et al 1990, Wilkerson and Nitz 1994). Due to its objectivity and sensitivity, Ryan (1994) thus proposed stabilometry as a quantitative alternative to observation when utilising the modified Romberg test for purposes of examining ankle sprain deficits. This method employs a force plate and measures the displacement of the foot's centre of pressure within a given time period (Cornwall and Murrell 1991, Tropp et al 1984, Wilkerson and Nitz 1994) or degrees of sway per second with eyes open and with eyes closed (McGuire et al 2000).

Yet, despite its discriminant validity and objectivity in differentiating between uninjured and injured ankle ligament injuries (Friden et al 1989) as well as its predictive validity in that higher postural sway scores correspond to increased ankle sprain injury rates (McGuire et al 2000), Gauffin et al (1988) argued against the validity of stabilometry in establishing that this observed deficiency in postural equilibrium was attributable to a deficiency in ankle proprioception. This is partly because central motor programs are likely to predominate over peripheral feedback mechanisms in the postural control of otherwise neurologically healthy persons (Wilkerson and Nitz 1994), as implicated by findings of De Carlo (1986) of improved average balance time scores following anaesthesia of the anterior talofibular ligament. Garn and Newton (1988) suggested an impairment in postural sway may also occur consequent to any mechanical instability of the joint caused by joint malalignment, or neuromuscular factors other than proprioception as suggested by findings of Friden et al (1989). Wilkerson and Nitz (1994) on the other hand, stressed the importance of the complex interaction that exists between cortical, cerebellar, spinal and peripheral afferent and efferent signals in controlling the position of the body's centre of gravity, which may affect postural control.

Further, Irrgang et al (1994) identified somatosensory input as only one of the 13 different systems required to maintain balance. Moreover, Ryan (1994) stated that these systems could not be isolated because the contribution of each was not fixed and an impairment in one might well be compensated for by an increased contribution from one or more of these intact pathways. As Forkin et al (1996) have also stated, balance test results which employ one-legged stance conditions are probably not well correlated with the mechanisms of proprioception occurring during complex movements. In light of compensatory effects, which may also mask the presence of any balance deficit between anaesthetized ankle joints and normal ankle joints (Konradsen et al 1993) and between injured and uninjured subjects (Tropp et al 1984, Jerosch et al 1995), plus limitations of single leg standing tests described above, the finding of Isakov and Mizrachi (1997) that the amount of postural sway incurred during single leg standing was similar in chronically sprained and uninjured ankle joints was not particularly surprising.

To improve the validity of the modified Romberg test for assessing proprioceptive deficits in ankle sprain populations, an alternative method using a uniaxial balance evaluator (UBE) requires subjects to stand on one foot on a single axis wobble board. Here, the investigator measures the time spent 'out' of balance, using a method that places more specific demands on integrative ankle proprioceptive mechanisms than the modified Romberg test (Ryan 1994). Using this approach Ryan (1994) did indeed find that subjects with functionally unstable ankles had poorer UBE scores on the functionally unstable leg than the unaffected leg. However, while the use of an electronic wobble board may seem to have some face validity, the measured variable still does not account for the complex interaction of many biomechanical and neurological factors, other than proprioception, that may affect balance. As well, while Cornwall and Murrell (1991) found decreased stability in an ankle injured group compared to a control group using a similar strategy, they did not find sway frequency differences among the groups. This indicated that either proprioception is not lost as a result of an ankle sprain or that individual's studied had recovered their ankle joint proprioception sense. In their studies, De Carlo and Talbot (1986) and Konradsen et al (1993) noted postural stability could be maintained equally well, with or without ligamentous anaesthesia about the ankle as did Tropp et al (1986) and Rose et al (2000) for injured ankles. However, the platform used for testing balance in the injured ankle may have to be tilted to raise the stability index as noted by Testerman and Vander Griend (1999). That is, with a stable configuration of the platform, no difference is likely to be observed between previously injured and uninjured ankles unless the stable platform is tilted at least 20o in any plane.

Study results

The studies depicted in Tables 1-4 which have examined whether proprioception of the ankle joint is implicated in functional instability of the ankle joint provide no specific consensus as to whether proprioception is definitively impaired in ankle sprain injured individuals. These data are non-conclusive for the following reasons:

1) In position sense studies, results have ranged from the finding of no proprioceptive deficit, to a greater deficit in the unaffected ankle, to a definite deficit in position sense of the affected ankle;

2) Tests of movement sense are also somewhat equivocal, and those demonstrating an association between a movement sense impairment and functional instability of the ankle have usually tested movement sense in positions not often used during dynamic integrated functions;

3) In reflex response time studies, the results seem to point to ligamentous laxity, or a lack of ligamentous integrity or malalignment of the ankle joint with excessive range of motion as the cause of functional instability, rather than to any deficit in reflex response time (Johnson and Johnson, 1993);

4) Although postural sway seems to be impaired in ankle sprain populations, training, which reduces ankle injury rates does not have a measurable effect on postural sway (Holme et al 1999).

In addition, we believe, the cross-sectional nature of most of the published research designs on this topic, their small heterogeneous samples, the unknown reliability of the measures employed to assess proprioception, and unclear or questionable diagnostic strategies, makes it impossible to substantiate the potential role of proprioception as either a causative factor or a consequential outcome of either acute or recurrent ankle sprain injuries at the present time.


Proprioception is a complex sensory modality believed important for regulating fine movement, appropriate movement quality and/or timely motor responses to perturbations (Matre et al 2002). Thus it is possible that ligament deficiencies and joint damage, which could disrupt joint proprioception mechanisms and lead to local changes in motor patterns (Beckman and Buchanan 1995, Branch and Hunter 1990, Bullock-Saxton 1994, Parkhurst and Burnett 1994) may affect the ability of the individual to respond effectively to perturbations. At the ankle joint, a joint frequently susceptible to ligamentous sprain injuries, a concomitant loss of proprioceptive sensibility plus the presence of any abnormal movement pattern may place the individual at risk for recurrent ankle inversion injuries and possibly as well for the premature onset of osteoarthritic joint disease (Beckman and Buchanan 1995, Parkhurst and Burnett 1994). Other joints, too, may subsequently be overused and have abnormal stresses placed on them, or may be used less frequently or abnormally if the individual favours other joints, for example those of the uninvolved side or upper body segments (Tropp and Odenrick 1988).

Potential ankle sprain injury mechanisms and the serious results that could follow if abnormal stresses continue to be placed on an injured ankle joint thus merit a better understanding of the basis of this condition. In this sense, although proprioceptive deficits have been implicated in the mechanisms of functional instability (Caulfield 2000), deficits in ankle proprioception have not always been observed in all individuals with symptoms of recurrent ankle inversion injuries (Tropp and Odenrick 1988).

However, due to the complex interactions of all these potential mediating neural mechanisms, and the limitations of testing neuromotor function in only a few isolated positions of the ankle (see Table 1-4), the approach used in several studies to establish the presence and nature of any injury-related proprioceptive deficit at the functionally unstable ankle joint might have been inadequate, both for demonstrating the presence of a deficit or for discriminating the magnitude of the deficit. Further, afferents in other tissues might have reduced or even fully compensated for the deficit in the tested movement (LaRiviere and Osternig 1994, Vaes et al 1998).

It is also possible that although problems of recurrent ankle instability might be attributable to a loss of integrity in its supporting lateral ligamentous structures due to trauma (Freeman 1965, Watson, 1999, Wilkerson and Nitz 1994), that it is the intrinsic properties of the connective tissues of the joint, which affects their structural responses and viscoelastic properties (Nef and Gerber 1998), rather than any impairment of prevailing joint proprioception mechanisms. It is also possible that the anatomical arrangement of the bones such as a positional fault at the inferior tibiofibular joint (Kavanagh 1999), plus the nature of the origin and insertion of the muscles on the bone at a particular moment through the range of motion, along with the degree of relative flexibility and strength of the surrounding muscles (Beynnon et al, 2001, Hume and Gerrard 1998) affects frontal plane ankle joint stability to a greater extent than the status of its proprioceptive feedback mechanisms.

In addition, Ryan (1994), Caulfield (2000) and Richie (2001) have suggested that repeated incidents of instability of an ankle joint might be attributable to impaired motor control mechanisms, rather than any prevailing proprioceptive deficits at the joint. Other hypothesised ankle sprain mechanisms have included: mechanical hypermobility of the ankle joint (Richie 2001), subtalar instability (Karlsson et al 1997), neural transmission deficits (Pahor and Toppenberg 1996), nerve damage (Kleinrensink et al 1994), peroneal muscle weakness (Tropp 1986) or subluxation (Hintermann 1999), sinus tarsi syndrome (Renstrom and Konradsen 1997), defects of body mechanics (Watson 1995), increases in joint laxity (Cornwall and Murrell 1991), deficiencies in ankle invertor muscle function (Hall et al 1999, Wilkerson et al 1997), increased touchdown plantar flexion responses (Wright et al 2000), severe fatigue of peroneous longus (Gefen 2002), and muscle inversion-eversion and plantarflexion-dorsiflexion strength imbalances (Baumhauer et al 1995).

The role of hip and trunk proprioceptive inputs, vestibular inputs, the spatial characteristics of muscle activation, as well as intermuscular timing may also be more important in triggering human balance corrections than proprioceptive input from the lower legs (Allum et al 1998). It is also possible that given the functional role proposed for the fusimotor system in providing spindle endings with a background discharge so they can initiate appropriate reflex correction (Burke et al 1978), that a preexisting central and/or peripheral muscle spindle or neural deficit might impair movement sensibility and reflex response mechanisms, or produce movement incoordination (Ernfors et al 1994), regardless of any ankle injury. The same argument can be applied to the presence of ankle pain, even in the absence of joint damage (Matre et al 2002).

Unfortunately, ankle injury simulation studies that have examined the effects of anaesthesia on ankle joint position sense and muscle reflex response times to provide insight into this question, have largely provided non-conclusive results. In particular, given that the evoked neural responses are unlikely to compare with those that occur naturally when walking on uneven terrains, or when landing with an unanticipated foot placement or during shoe slippage (De Carlo and Talbot 1986, Feuerbach et al 1994, Konradsen et al 1993), the use of unexpected perturbations applied in a static setting to explore whether proprioceptive deficits might cause ankle instability is highly questionable. Also ankle inversion injuries are often accompanied by a variety of physiological responses including bruising, oedema, haemarthrosis (Safran et al 1999), muscle inhibition and capsular distension (Wilkerson and Nitz 1994), and hence information gained by isolating and studying the causes of recurrent ankle sprains in simulation models that do not replicate injurious events or their associated discomfort levels adequately (e.g., Sheth et al 1997) may be of little value, especially if it is not possible to predict a priori which receptors might be implicated or redundant in any injurious sequence of events.

As well, in some authentic ankle sprain studies, the validity of the assessment methods utilised for detecting proprioceptive deficits remains open to question (Boruta et al 1990). For example, none of the ankle proprioception studies currently reviewed, adequately tested the anterior talofibular ligaments proprioceptive properties since only limited joint ranges of motion were studied. The proprioceptive properties of the calcaneofibular ligament were tested somewhat, although not adequately enough because the extremes of ankle motion were never reached. Also, it cannot be excluded that in some cases, it is not simply mechanical instability which is driving the recurrent instability and that those proprioceptive deficits that are observed are simply a consequence of joint effusion, muscle inhibition, aging processes, fatigue or injury related inactivity (Konradsen and Magnusson, 2000), rather than any direct proprioceptive deficit. Inadequate capsular, cutaneous or muscular stretching or the attenuation of tactile information caused by footwear (Robbins et al 1995) may also impair proprioceptive sensibility, inadvertently, regardless of any ankle sprain related injury. Also, individuals exposed to cumulative or repetitive stresses over an extended period might demonstrate impaired proprioception simply due to microtrauma effects. It might also be that subjects with asymmetrical movement patterns, for example those acquired through habitual activities, have impaired or asymmetrical proprioception (Parkhurst and Burnett 1994, Robbins and Waked, 1998), irrespective of whether they have an ankle injury or not.

Hence, because some individuals classified as having 'normally' stable ankle joints may actually have an inherent deficiency in ankle proprioception, it may be difficult to argue that proprioceptive acuity of ankle injured subject is of any relevance to their complaints of functional instability. Alternately, because healthy controls may display proprioceptive deficits for a variety of reasons, it may be difficult to detect differences in ankle proprioception between ankle injured subjects and healthy subjects in comparative studies addressing this question, unless this carefully controlled for.

In our view, therefore, the equivocal findings among published studies, and especially their failure to differentiate whether proprioception deficits that have been observed in some studies are inherent to the individual or specifically related to any recurrent ankle sprain injury, coupled with the failure to carefully examine and control other potential causes in mediating recurrent ankle sprains makes it difficult to support the conclusion that either acute or recurrent ankle sprain injuries are related to ankle proprioception deficiencies. The many research design limitations in this area, plus the many problems associated with the documented modes of testing ankle proprioception that have been conducted in various laboratories, especially the failure to test subjects under both physiologically and ecologically valid conditions, further complicates any meaningful consensus on this issue.


Due to the lack of a strong evidence base, we would argue that it is currently impossible to definitively support or refute the notion that a proprioception deficit is implicated in recurrent problems of functional instability of the ankle joint. Furthermore, a sound argument in favour of proprioceptive training for ameliorating this condition and which type of proprioceptive modalities and pathways are at fault, if any, cannot be clearly discerned from the present data base. Recent data also suggests that although lateral ankle sprains are the most common sports-related injury number, many lateral ankle injuries are often misdiagnosed as 'sprains', thereby resulting in misdirected therapy, delayed functional return and unresolved ankle pain (Vertullo 2002). Hence, while unlikely to do undue harm, it is our belief that a sound rationale for an effective treatment approach including proprioceptive training for ameliorating functional instability of the ankle joint cannot be formulated on the basis of such limited and equivocal evidence, especially if a careful history, differential clinical examination and investigative adjuncts such as bone scintigraphy have not been forthcoming. In addition, it is quite likely that non-proprioceptive sources of impairment contribute substantially towards producing a situation that favours a recurrent ankle sprain injury and if untreated or ignored could result in poor long-term outcomes for this population.


In light of the lack of strong empirical evidence to support the use of proprioceptive training in either the prevention of acute ankle inversion injuries or specifically in the rehabilitation of recurrent ankle instability incidents, we believe it seems reasonable to suggest that physiotherapists might best overcome the lack of definitive information in this area by conducting very careful assessments of their clients, especially those with recurrent ankle instability problems, to substantiate as adequately as possible whether proprioceptive or other mechanisms are potentially causing these injuries. Simply assuming a parallel between functional stability at the ankle and proprioception, and that improving proprioception through one or more related interventions will reverse this trend, could be expected to produce highly erratic and unsystematic results.

Although a comprehensive evaluative approach of clients with recurrent ankle sprains may not seem practical, because these injuries are extremely common and often have serious sequelae (Braun 1999, Gerber et al 1998), it would seem especially important to ascertain what the most likely causes of the individual's recurrent ankle instability problem are. Thereafter, it may be possible to establish more definitively how a particular case of ankle instability might best be ameliorated.

For this purpose, Lynch and Renstrom (1999) suggested the entire ankle, and foot complex must be examined to ensure there are no other injuries. In addition, because the results of a single proprioceptive test may be misleading, especially in light of the limitations of these tests, we advocate a detailed clinical examination involving a combination of sensory tests, which examines the individual's ability to detect joint motion, vibration, and position sense. As well, the Sensory Organisation Test (Wolfson et al 1992), which measures the sensory components of balance under a variety of altered visual and support surface conditions is recommended. Further, performance assessments conducted using the taxonomy of tasks as outlined by Gentile (1987) might help to more clearly identify the extent of any functionally related proprioceptive deficit of the unstable ankle.

Also advocated for deriving a sound rationale for utilising proprioceptive enhancing strategies in the armoury of preventive treatments proposed for recurrent ankle sprain injuries are: referrals for stress radiographs plus stress examinations using a stress testing device (Rijke et al 1986); magnetic resonance imaging to facilitate a more precise diagnosis of the extent of damage of the lateral ligamentous components and ligamentous damage in those with severe sprains (Shahabpour et al 1992); and well-defined instrumented stability tests to determine the extent of any ligamentous disruption.

In terms of future research, more extensive longitudinal studies of well-defined samples of uninjured ankles, as well as injured ankle joints measured under different static and dynamic conditions are especially indicated. Measurement tools advocated in this respect include those that assess neuromuscular function, joint kinematics, and joint kinetics interactively (Branch and Hunter 1990, Rijke 1986, Siegler et al 1994). To establish whether abnormalities in gait and electromyographic measures are caused by a direct loss of mechanoreceptors, or by altered stimulation of remaining receptors, or by both, as this pertains to improving the outcomes of rehabilitation strategies for preventing recurrent ankle sprain injuries, it may prove helpful to implement nerve conduction tests, assess the amount of prevailing joint laxity, and to scan the injured ankle using computed tomography (Robinson and White 2002).


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L Stefanini, BScPT, Formerly: University of Toronto, Department of Physical Therapy Research Associate, Osteoarthritis Research Centre Toronto, Canada

R Marks, PT Columbia University, Teachers College Adjunct Assistant Professor, Department of Health and Behavior Studies Director Osteoarthritis Research Centre Toronto, Canada
Table 1. Summary of studies of joint position sense conducted in
relation to ankle sprain injury.

Authors Act Pass Design Plane

Boyle and X X 25 subjects with 42[degrees]
Negus (1998) recurrent ankle sprains plantar
 between the ages of 19 flex.
 and 25 and a similarly inv
 aged group of 67
 uninjured subjects were

Glencross and X 24 subjects under 25 yr flex/ext
Thornton with history ankle injury
(1981) of at least 8 m duration
 allocated to 3 groups on
 basis of severity were
 compared to 9 healthy

Gross (1987) X X 14 subjects with inv/ev
 unilateral ankle sprain compared
 were to subjects with
 'normal' ankles

Holme et al. X 92 subjects without prior inv
(1999) complaints of ankle
 instability who had
 sustained acute sprains
 of the ankle

Konradsen et al X 44 subjects, 32 men and inv/ev
(1998) 12 women, median age 28
 yr with grade II or III
 instability were studied
 at 6 weeks and 3 m post
 ankle sprain

Konradsen and X X 23 subjects, median age inv/
Magnusson, 29 years, range 22-37
2000 scheduled for ankle
 stabilising operations
 were studied and compared
 to non injured controls

Payne et al X 31 F and 11 M basketball inv/ev
(1997) players ages 18-22 with
 no ankle injury history dorsi/pl
 were studied flex

Feuerbach X 12 subjects with no ankle pl/dorsi
et al (1994) sprain history were flex
 measured before and after patterns
 anaesthesia of 1) inv/ev
 Anterior talofibular
 ligament 2) Anterior
 talofibular and
 calcaneofibular ligament

Konradsen X X 7 subjects with no ankle inv/ev
(1993) sprain history were
 measured before and after 25[degrees]
 anaesthesia on same ankle inv

 Joint angles
Authors tested Device Results

Boyle and 30, 60, Pedal Greater errors
Negus (1998) and 90 goniometer occurred in passive
 percent of position sense for
 range the injured group.
 Active position sense
 at 30 per cent
 position was worse in
 injured group.

Glencross and 105[degrees], Clinical There was a linear
Thornton 120[degrees] goniometer trend between the
(1981) 130[degrees], degree of error and
 140[degrees] range of motion. The
 injured group showed
 better position sense
 on the unaffected
 side. The error was
 greatest for the most
 severely injured

Gross (1987) 10[degrees] ev Cybex II No significant side
 10[degrees] inv isokinetic differences were
 20[degrees] inv dynamometer identified.

Holme et al. 10[degrees] inv Electrical Position sense at 6
(1999) 15[degrees] inv torsiometer weeks was the same
 20[degrees] inv (Biometrics between the injured
 Ltd, Gwent, and uninjured sides,
 UK) regardless of whether
 subjects received
 rehabilitation or

Konradsen et al 10[degrees], Goniometer Mean position sense
(1998) 15[degrees] footplate over all test
 20[degrees] occasions was greater
 starting for injured ankles.
 from 0[degrees]
 and 40[degrees] Mean errors decreased
 pl. flex for 5 over time for the
 sec at injured group but
 2[degrees]/sec were still greater at
 12 weeks than the
 uninjured group.

Konradsen and 10[degrees] Torsion The absolute error
Magnusson, 15[degrees] goniometer was significantly
2000 20[degrees] greater for the
 affected ankle in the
 unstable group, and
 when compared to the
 control group,
 although numerically
 this difference was
 less than 1 degree.

Payne et al 15[degrees] inv Biodex Ankle position sense
(1997) 20[degrees] ev isokinetic deficits predicted
 1[degrees] pl dynamometer ankle injury.
 Right inversion
 proprioception was
 better in the injured
 than the uninjured

Feuerbach 9 diff 3-D Motion No significant
et al (1994) movement analysis difference observed

Konradsen 5[degrees], Goniometric Significant
(1993) 10[degrees], footplate difference et al in
 15[degrees], passive position
 20[degrees], sense after

ab--abduction; A--active; ad.--adduction; ank.--ankle;
df.--dorsiflexion; ev.--eversion; inv.--inversion; jt.--joint;
m--months; ms--meters per sec; norm.--normal; P.--passive; pl.
flex.--plantarflexion; p.s.--position sense; RT--reaction time; sig.
diff.--significant difference; spr.--sprains; s--seconds; yr--year.

Table 2. Summary of studies employing movement sense in relation to
ankle sprain injury.

Authors Subjects Movement Instrument

Forkin et 11 gymnasts with Passive pl. Kinesthesiometer
al (1996) unilateral ankle flex

Garn and 30 athletes 18-24 yr with Passive pl. Kinesthesiometer
Newton multiple ankle sprains flex

Lentell et 42 subjects with chronic Passive Box with
al (1995) ankle instability 18-27 ankle inv moveable
 yr platform

Authors Protocol Conclusion

Forkin et 30 trials Movement detection
al (1996) 15:with movement ability was worse
 15:without movement in injured ankles.

 Tested randomly on both
 injured and uninjured

Garn and 30 trials Subjects had greater
Newton performed bilat. difficulty detecting
(1988) 15:with no movement 15: passive movement in
 with movements from their injured ankle.
 neutral-5[degrees] at a
 rate of .3[degrees]/s

Lentell et From a starting position of The correlation between
al (1995) 0[degrees] foot was rotated 3 tests on the injured
 into inversion. side was .78; and .71 for
 The position at which the uninvolved side.
 subject sensed movement was
 recorded. Significantly greater
 motion was found in the
 involved ankles.


ab--abduction; A--active; ad.--adduction; ank.--ankle;
df.--dorsiflexion; ev.--eversion; inv.--inversion; jt.--joint;
m--months; ms--meters per sec; norm.--normal; P.--passive; pl.
flex.--plantarflexion; p.s.--position sense; RT--reaction time; sig.
diff.--significant difference; spr.--sprains; s--seconds; yr--year.

Table 3. Summary of studies employing reflex response time measures in
relation to ankle sprain injury.

Authors Design Muscle Dep. variable

Fernandes et al. 34 male athletes, Peroneus Mean peroneal
(2000) ages 18-30 yr with longus. 97.23 ms-left
 and without a latencies
 history of ankle
 injury received 4
 random tilts to
 their left ankles at
 10[degrees], and
 15[degrees] in the
 frontal plane on a
 dual platform
 trapdoor in a single
 blinded, quasi-
 experimental trial.

Johnson and Subjects with non Peroneus Mean latency
Johnson (1993) surgically treated longus time for
 ankle sprains, and brevis peroneal
 sprains muscle
 rehabilitated activity
 following surgery
 and injury free
 ankles were studied.

Konradsen et al 7 'normal' subjects Peroneus Median R.T.
(1993) were assessed before longus
 and after
 anaesthesia on same

Konradsen and 15 subjects with Peroneus Median R.T.
Ravn (1991) functionally longus
 ankles Peroneus
 15 controls brevis

Konradsen and 15 subjects with Peroneus Median R.T.
Ravn (1990) functionally longus
 ankles Peroneus
 15 controls brevis

Lofvenberg et al. 13 patients, 4 men, Peroneus Contralateral
(1995) 9, women with longus and ipsilateral
 chronic lateral R. T.
 instability of
 the ankle for at Tibialis 68.3 ms
 least 12 months anterior
 (range, 12-288),
 mean age 37 years
 (range 24-49)
 15-control group
 members matched for
 sex, age with no
 trauma or
 instability history

Nawoczenski et al 15 controls Peroneus Mean R.T.
(1985) 15 subjects with an longus difference
 inv. sprain 1 ankle

Authors Normal Problem Conclusion
 ankle ankle
Fernandes et al. 5[degrees]: No sig. diff.
(2000) 93.21 93.21

 98.91 ms 93.21



Johnson and 75.2 ms 70.8 ms No sig. diff
Johnson (1993) (surgical)


Konradsen et al 80 ms 83 ms No sig. diff.

Konradsen and 69 ms 84 ms No sig. diff.
Ravn (1991)

 65 ms 82 ms

Konradsen and 69 ms 84 ms No sig. diff.
Ravn (1990)

 65 ms 82 MS

Lofvenberg et al. 68.3 ms 65 ms No sig. diff.


Nawoczenski et al 9.4 ms 13.6 ms No sig. diff.


ab--abduction; A--active; ad.--adduction; ank.--ankle;
df.--dorsiflexion; ev.--eversion; inv.--inversion; jt.--joint;
m--months; ms--meters per sec; norm.--normal; P.--passive; pl.
flex.--plantarflexion; p.s.--position sense; RT--reaction time; sig.
diff.--significant difference; spr.--sprains; s--seconds; yr--year.

Table 4. Summary of studies employing static balance measures in
relation to ankle sprain injury.

Authors Subjects Dependent variable

Bullock-Saxton 20 men with Time
(1995) unilateral ankle

 11 healthy men

De Carlo and 14 subjects with no Time
Talbot (1986) ankle problems who
 had their anterior talo
 fibular ligament

Forkin et al 11 gymnasts with Question responses
(1996) unilateral ankle sprain concerning "which
 side yielded better
 balance perception"

Hertel et al. 17 adults, age Centre of pressure
(2001) 21.8 [+ or -] 5.9 excursion length,
 years, 9 men, 8 women root mean square
 with unilateral acute velocity of excursions,
 mild or moderate range of excursions
 lateral ankle sprains

Holme et al. 92 subjects with first Postural sway using a
(1999) time ankle sprains force platform (Amti,
 who were receiving Newton, MA, USA)
 supervised physical
 therapy or no therapy

Isakov and 8 female gymnasts Postural sway using a
Mizrahi (1997) mean age 16.2 year force plate
 with history inversion
 injuries and positive
 anterior drawer sign

Leanderson Basketball players Sway area
et al (1993) with no ankle injury;
 injured players; and a
 control group

Rose et al. Patients with acute Mean sway index
(2000) ankle sprain and with eyes open and
 uninjured controls closed

Authors Instrument Finding

Bullock-Saxton No specific Side to side differences
(1995) instrument in balance were recorded
 Subjects simply stood on for the injured group.
 one leg with vision
 occluded for as long The stance time on the
 as possible injured leg was 5.7 s
 less on the injured side
 than on the uninjured

De Carlo and Multiaxial balance There was a significant
Talbot (1986) evaluator increase or improvement
 in balance time after

Forkin et al One legged standing Subjects reported better
(1996) for 30 s performed balance when standing on
 bilaterally with no the uninjured ankle.

Hertel et al. Measures were calculated Postural control was
(2001) separately in the significantly impaired
 frontal and sagittal in the injured limbs at
 planes during 5-s trials day 1 and 2 weeks after
 of static single-leg injury, but not during
 stance week 4.

Holme et al. One legged standing for Postural sway differed
(1999) 1 min with eyes open and between the injured and
 arms folded across the uninjured sides in both
 chest, with sides groups at 6 weeks, but
 assessed in random order there were no side to
 side differences for
 either group at 4

Isakov and One legged standing on The amount of postural
Mizrahi (1997) each leg for 35 s with sway during single leg
 eyes open and closed standing was similar in
 the chronically sprained
 and the uninjured ankle

Leanderson Computer-assisted Players with previous
et al (1993) forceplate was used for injury differed
 60 s unilateral standing significantly from
 tests controls. Uninjured
 players did not

Rose et al. A Chattanooga balance There were no
(2000) machine (Chattanooga significant group
 Group Ltd, Bicester, differences in
 Oxfordshire, UK) was stability, although
 used patients appeared less
 stable than controls in
 all balance tests.


ab--abduction; A--active; ad.--adduction; ank.--ankle;
df.--dorsiflexion; ev.--eversion; inv.--inversion; jt.--joint;
m--months; ms--meters per sec; norm.--normal; P.--passive; pl.
flex.--plantarflexion; p.s.--position sense; RT--reaction time; sig.
diff.--significant difference; spr.--sprains; s--seconds; yr--year.
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Author:Stefanini, L.; Marks, R.
Publication:New Zealand Journal of Physiotherapy
Geographic Code:8NEWZ
Date:Mar 1, 2003
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