P. NEYRET, G. LE BLAY, T. AIT SI SELMI Centre Livet, Department of Orthopaedic Surgery - F-69300 Caluire

We owe our knowledge in this field to Henri Dejour. Our grateful thanks are due to Matrise Orthopdique for providing us with the opportunity to translate what has so far been an oral tradition into a written record. This review article is intended to familiarize orthopaedic surgeons with the methodology required for a systematic and logical examination of the knee joint. The knee needs to be examined systematically, since so much can go wrong with the knee, and so many signs and symptoms may be produced, that only a systematic technique will ensure that nothing of importance is missed. Equally, a logical approach is required, since the best way to remember a technique is to know why it is being applied. We will, therefore, attempt to explain what the various signs and symptoms mean in terms of knee pathology or pathophysiology. The detailed examination of the knee will need to be preceded by taking the patient's history. This aspect of the clinical approach is vital, since it will often be found that a properly taken history will permit at least a presumptive diagnosis to be made. In fact, we might go so far as to say that good history-taking is "non-invasive arthroscopy." This article also presents the IKDC (International Knee Documentation Committee) Knee Evaluation Form, under the various headings, in order to allow the more junior surgeons to familiarize themselves with international rating systems. The IKDC form itself was explained by P. Chistel, in the Revue de Chirurgie Orthopdique (1993, 79:473). It is used mainly in anterior cruciate ligament (ACL) surgery, to facilitate comparisons of results obtained in different studies of knee ligament trauma, in Europe and in

the United States.

1 - HISTORY-TAKINGAfter establishing the nature of the principal complaint (or reason for consulting a doctor), a systematic history should be obtained, with questions grouped under three headings: History of present complaint; signs and symptoms; and life style (level of activity). No. 1 HISTORY OF PRESENT COMPLAINT As a rule, three questions should suffice to obtain all the information required under this heading. The first two concern the onset of the present complaint. 1.1 When? This first question allows the examiner to distinguish between two patterns - complaints with an identifiable starting point, a known accident (traumatic or post-traumatic knee disorders); and complaints that appear to have come on more insidiously, which would be more suggestive of inflammatory or degenerative disease. 1.2 How? The examiner should try to elicit the exact circumstances of how the disorder occurred - obtaining a description of how the accident happened or of how the problem has developed over time. Thus, in a trauma case, the examiner would seek to find out the nature of the contact (violent/non-violent; in valgus; in varus; in hyperextension) or whether the knee "went" after kicking a ball or "missing a kick." It would also be important to establish whether there was an audible "pop" in the joint, whether the knee swelled rapidly, and whether the athlete needed help to come off the pitch: - An affirmative answer to these questions would be highly suggestive of a torn ACL (Figs. 1-5).

Figure 2

Figure 3

Figure 4

Figure 1

Figure 5

1.3 What happened after that? This question needs to be asked in order to obtain information on any medical or surgical treatments already applied, on rehabilitation (if

any), and on the course of the condition up to the time of consultation. No. 2 SIGNS AND SYMPTOMS A complete picture of the patient's signs and symptoms should be obtained, since anything elicited under this heading may be of diagnostic value. There are four categories of cardinal signs and symptoms in the knee joint:2.1 Pain The examiner should establish the way in which the pain developed, its character, and its severity; the patient should be asked to point to the site of the pain. Pain at night suggests an inflammatory cause, while pain that gets worse towards evening, or during/after exercise, would be more likely to be mechanical in origin. Pain when going up or down stairs, or aching in positions where the knee is kept flexed for prolonged periods of time (car journeys, visits to the cinema), are indicative of patellar problems, while pain that occurs when the knee is hyperflexed is usually caused by meniscal pathology. The patient should also be questioned about pain in other parts of the body (low back pain, hip pain). Bar- or vice-like pain below the patella is highly suggestive of a low-riding patella. 2.2 Laxity A certain amount of confusion has occurred in the international literature, since the French use the term instabilit to denote what in English would be called laxity, and speak of laxit in the sense of the English term instability. "Going out": This is the term used by many lay persons to describe what will usually be found to be a torn ACL or a dislocation of the patella. "Giving way": This term is used to describe the sensation of the knee suddenly failing to provide proper support, especially when walking on uneven ground. The symptom may be due to three mechanisms:

- Interposition: If, during weight-bearing, a third structure (meniscus, synovial membrane, cartilage, etc.) is placed between the opposing cartilage surfaces of the joint, a protective reflex will be triggered. This reflex will make the quadriceps relax and unlock the knee, to allow the joint to clear itself. - Cartilage damage: If one or both of the cartilage surfaces are damaged, and the surfaces come into contact, the quadriceps may also be made to relax. - Muscle weakness: This may occur in quadriceps wasting, in polio, after surgery, etc. 2.3 Locking A proper knowledge of this clinical feature is vital, since patients have often been misdiagnosed because of the examining physician's imperfect understanding of this symptom. There are two types of locking, which must be carefully distinguished: Meniscal locking (true locking): This is what a physician would consider to be locking. It is the impossibility fully to extend the knee for an appreciable period of time (more than a few minutes). This "passive flexion deformity" is brought on by a mechanical obstacle which makes the knee stop short of full extension (Fig. 6). The cause may be a bucket-handle tear of the meniscus, or a bulky flap that has dislocated forwards in the joint; a loose body or an ACL stump may also be to blame. Patellar catching (false locking): This is what the patient would consider to be locking. It is a momentary "sticking" of the knee, during a flexion-extension movement, with the knee incapable of flexing or extending beyond that particular point. Catching is relieved as soon as weight is transferred to the other side (Fig. 7). Usually, patellar cartilage damage will be found to have caused this fleeting episode of "locking."

Figure 6

Figure 7

2.4 Effusion The knee swells up. Swelling of the knee is always indicative of a genuine lesion of the joint. Sometimes, its character will already have been established by aspirating the joint. The features of the aspirated fluid (colour, viscosity, protein content, cellularity) make it possible to ascertain whether the condition is mechanical or inflammatory; a search for microcrystals should always be made. Hydroarthrosis: The accumulation of clear, straw-coloured fluid is the result of irritation of the synovial membrane, which may be primary (inflammatory disease) or secondary to cartilage damage (osteoarthritis), meniscal lesions, or the presence of a loose body (osteochondritis dissecans; osteochondral fractures). Hydroarthrosis may also be seen following ligament lesions. Blood in the joint (haemarthrosis) without a history of trauma could mean two things: haemophilic arthropathy, or pigmented villonodular synovitis. In the latter condition, the fluid may be amber-coloured rather than frankly bloody (Fig. 8).

Figure 8

2.5 Other clinical features Subjective sensation of internal derangement: The patient feels that there is something moving in the knee (joint mouse); something "funny"; "a lump." This feature suggests a meniscal lesion or a loose body. Noises in the joint: Crepitus is a faintly audible and often palpable sensation of grating during flexion-extension. Clunks and clicks are much louder, and suggestive of meniscal lesions. For evaluation with the IKDC score, the patient will need to indicate the highest activity level that his or her knee will tolerate, even if (s)he does not practise the activities at that level. The levels are as follows:I - Strenuous activity (contact sports involving pivoting and cutting) II - Moderate activity (pivot sports without contact; manual work) III - Light activity (jogging, running)

IV - Sedentary activity Patients who report symptoms at level I but not at level II are rated B = "nearly normal." The lowest grade within a group determines whether the patient is group-graded A, B, C, or D in the last column in Table 1.

Table 1

No. 3 LEVEL OF ACTIVITY History-taking also involves obtaining information on the patient's present and desired levels of activity. This information is important for two reasons: Firstly, it gives an idea of the degree of disability produced by the knee disorder; and, secondly, it shows what the patient would like to be able to do with his or her knee. The questions to be asked will be a function of the patient's age: Young, active, or athletic patients should be questioned about the sports they practise, and about their ability to run, jump, or cut. Elderly or sedentary subjects should be asked about the use of walking aids, their walking distance, ability to go up and down stairs without holding on to a handrail, and whether they can get up from a sitting position without using their hands.

2 - EXAMINATIONThe patient should be examined standing up, walking, and lying supine. It is essential that a comparison be made throughout with the unaffected side. 1 - In the STANDING PATIENT, a study should be made of Lower limb pattern: The lower limb is said to be in normal alignment if, when seen head-on, with the patellae pointing forwards, the medial malleoli and the femoral condyles touch. Genu varum describes a condition in which the femoral condyles are apart when the feet are together, while in genu valgum the ankles are separated when the knees touch. The distances should be measured; they may be expressed in centimetres (or in fingerbreadths), with the knees in extension (Figs. 9-10). With the knees in hyperextension, a varus deformity may be seen to worsen. Genu varum and genu valgum are not, in themselves, abnormal conditions. This is why "normally aligned" is not synonymous with "normal."

Figure 9

Figure 10

Muscle wasting: With the patient standing "to attention",. the muscle bulk is checked. Quadriceps wasting shows up as wasting of the vastus medialis. Looking at the vastus medialis will give an immediate idea of whether the quadriceps is wasted. Wasting may be the result of under-use of the knee joint. It may be quantified by measuring the circumference of the thigh. 2 - In the WALKING PATIENT, the following features are checked:-

The toeing angle is the angle between the axis of the foot and the direction in which the subject is walking. Normally, the axis will be seen to point in a slightly lateral direction, enclosing an angle of 10 to 15. In the normal postural pattern, this angle will be the same on both sides. Tilting of the knee with single-leg stance: This is seen where bone wear has occurred as a result of osteoarthritis (OA). The feature does not manifest itself until several years have elapsed. Where the tilt is due to ligamentous problems, it will be seen early on. (a) With wear in the medial compartment, the tilt will chiefly be into varus, in a position of near-extension. It is best seen from behind the patient (Fig. 11).

Figure 11

(b) With lateral compartment wear, on the other hand, the tilt will be into valgus and flexion; it is best appreciated from in front. (c)A tilt into recurvatum is rare; it is not well tolerated by the patient. 3 - EXAMINATION OF THE SUPINE PATIENT 3.1 General appearance There are two cardinal features with which the examiner has to be familiar, since they are as important in the examination of the knee joint as the temperature and pulse rate are in the general examination of a patient. They make it possible for a "spot diagnosis" of a genuine, organic knee lesion to be made by the examiner.

(a) Looking for an effusion: The examiner's hands are placed on either side of the patella, with the thumb and middle to little fingers stroking the synovial fluid towards the patella, while the index finger is used to elicit the patellar tap: The patella is at first pressed down and submerged under the synovial fluid, and will strike the trochlea, producing a tap. As the pressure is relieved, the patella will bob up like an ice cube in a drink (Fig. 12). (b) Looking for a fixed flexion deformity: The patient is positioned supine and made to relax. The examiner grasps both the patient's heels and supports them at a height of 10 cm above the examination couch. This is the best position for screening for a flexion deformity, which is a major feature of knee pathology. This sensitive and straightforward method is ideal for screening purposes. It does not, however, lend itself to a quantification (in degrees) of the deformity. Also, since the patient's feet are braced against the examiner's abdomen, the examiner may seek to reduce the flexion deformity by pressing down on the patient's knees (Fig. 13).

Figure 12

Figure 13

- Knee pattern in the supine patient: As the patient goes from two-legged stance into the supine position, the deformity may or may not correct itself. If a lower limb malalignment was found with the patient standing on both feet, the examiner should check whether the deformity can be reduced in the supine patient, which would suggest that the deformity is articular (rather than extra-articular and bony) in origin. Another way of checking for a flexion deformity consists in positioning the patient prone, on a firm table, with the knees supported on the table and the legs protruding beyond the table's edge. One heel is seen to be higher than the other. The distance between the two heels may be measured. It provides direct evidence of the flexion deformity. The test is reproducible, and the result is numerical (in cm). However, it requires a firm surface, and the patient must be positioned prone (Fig. 14).

Figure 14

In order to be able to tell whether a finding is abnormal, the affected side will have to be compared with the presumably healthy limb (the reference knee). This comparison will show whether there is a fixed flexion deformity or a genu recurvatum. - The range of movement (ROM) is tested at this stage of the examination (which also involves screening for quadriceps wasting). Three figures are used to denote the ROM. The first indicates flexion; the second, full extension; and the third, recurvatum. Thus, 140, 0, 5 means that flexion is 140; the knee can be extended fully; and there is 5 of recurvatum. 120, 5, 0 would mean that flexion is 120, there is a flexion deformity of 5; and no recurvatum. For evaluation with the IKDC score, the passive ROM is recorded in both knees. Values are given in 3-figure form: Extension/Flexion / Lack of extension (from 0) / Lack of flexion (Fig. 15) (Table 2).

Figure 15

Table 2

3.2 Extensor apparatus Inspection - The bayonet sign: This term describes the pattern produced by the patella, the patellar tendon, and the tibial tubercle. The line resembles a bayonet fixed to a rifle.

Pathophysiology: The bayonet results from a lateral position of the tibial tubercle. It was thought for a long time that this was an organic factor contributing to patellar instability. It is now known that it is the resultant of the forces produced by the lateral position of the tibial tubercle that tends to pull the patella sideways. Reliability: Not very good. A more reliable picture may be obtained from measuring the distance from the tibial tubercle to the inside of the trochlea on CT scans. - Squinting of the patella Palpation - Looking for tender points is particularly useful if the patient has also reported symptoms of pain (Fig. 16). * Tibial tubercle: In adolescents, the tibial tubercle may be affected by apophysitis, with fragmentation of the apophysis (the accessory ossification centre). The patient will complain of pain in the tibial tubercle, and the examiner will be able to elicit tenderness over that structure (Osgood-Schlatter disease). * Patellar tendon: This structure may be the site of repetitive strain injuries (jumper's knee); the patient will complain of pain in the patellar tendon, and extension against resistance will be painful. * Apex of the patella: In adolescents, inflammation of the distal pole of the patella may occur as a very rare condition (Sinding-LarsenJohansson syndrome). * Medial facet of the patella (Fig. 17a): The medial facet of the patella may be tender to palpation, and the patient may report pain at that site. The feature is usually part of an anterior knee pain syndrome. * Lateral facet of the patella (Fig. 17b): The examiner pushes the patella in a lateral direction, and palpates the lateral facet. Patellofemoral dysplasia will produce lateral impingement and pain and tenderness along the lateral border.

Figure 16

Figure 17

* A search should also be made for a mediopatellar plica, which appears as a tender cord that rolls under the palpating finger, on the medial femoral condyle. It sweeps along the condyle during flexion, and may give rise to pain symptoms. * Patellar tilt: The examiner holds the edges of the patella between the thumb and index finger, thereby establishing the axis of the patella, which should differ only slightly (10 lateral tilt) from the horizontal plane of the knee seen head-on. The patella may be said to squint (convergent or divergent squint) (Fig. 18). Broadly speaking, a convergent squint tends to occur in anterior knee pain syndrome, while a divergent squint would be more likely in recurrent dislocation.

Figure 18

Patellar tests - Apprehension sign The patient is positioned supine, with the knee flexed between 0 and 30. The examiner firmly pushes the patella in a lateral direction. The patient, who knows and apprehends the dislocation that will be produced by this manoeuvre, will stop the examiner. Results are recorded as + or 0. Pathophysiology: Between 0 and 30 of flexion, the patella is at its highest point in the trochlea. Pressure from the medial side will push the patella in a lateral direction, causing it to dislocate from the trochlear groove. This will cause not only pain, but apprehension on the part of the patient (Fig. 19). This sign may be elicited in recurrent dislocation; it is highly suggestive, and particularly useful in patella alta. As Henri Dejour puts it, "You can't get near their kneecaps." (Fig. 20)

Figure 19

Figure 20

The test must be stringently performed and analyzed. - Patellar grind test The examiner's hand is placed on the front of the knee. The patient performs flexion-extension. The examiner will feel a crepitus, and may even notice the patella catching. The crepitus is difficult to interpret. If there is nothing more than a positive grind test, a diagnosis of OA or of cartilage damage cannot be made. Patellofemoral joint crepitus should be sought over the entire ROM from flexion to extension, against slight resistance. Crepitus in the tibiofemoral compartments is sought from flexion to extension, against resistance, as well as in valgus-flexion-external rotation (to test the lateral compartment) and in varus-flexion-internal rotation (to elicit medial compartment crepitus). Gradation depends on the loudness of the crepitus and on the pain produced by the manoeuvre (Table 3).

Table 3

3.3 The menisci Broadly speaking, the menisci should be examined with the knee in flexion. There must be tenderness (i.e. the patient must respond to palpation with pain). There are various ways in which the sensitivity of the tests can be enhanced. However, all the tests for meniscal lesions rely on the same principle: Stressing an injured medial or lateral meniscus will cause pain. Tenderness to palpation is elicited with the knee flexed 90 and the patient's foot resting on the table. The examiner's index finger probes the meniscus along the joint line. The most frequently encountered sites of tenderness are over or behind the medial collateral ligament, at the medial meniscal tender point (Fig. 21). Less often the tender point will be anterior, in which case the phenomenon may be part of a patellar disorder, a bucket-handle tear of the medial meniscus, or a lesion of the anterior horn of the lateral meniscus. The lateral meniscal tender point may be anywhere along the joint line (Fig. 22).

Figure 21

Figure 22

Meniscal tenderness on mobilization: Compression of the different parts of the meniscus by the femoral condyle occurs as the meniscus glides backwards on the condyle during flexion, and forwards during extension.

This means that the posterior horn will be compressed when the knee is in hyperflexion (Fig. 23); while the anterior horn will be compressed in hyperextension. The diagnostic accuracy of the tests is improved by adding a component of tibial rotation to the simple flexion-extension manoeuvres. This rotation tends to bring the posterior horns forward. Medial pain will be elicited in external rotation, and lateral pain in internal rotation. - McMurray's test: Forced flexion and external rotation with compression of the medial joint line will elicit pain in the medial meniscus. The hand pressed over the joint line will feel a click. The test may be reversed, to examine the lateral meniscus. - Apley's grinding test: For this test, the patient is positioned prone, with his or her knee flexed. Compression and external or internal rotation may be painful, showing that the medial or the lateral meniscus are torn. This test is always checked, by performing rotation without compression. This manoeuvre should not cause discomfort, unless the collateral ligaments are affected (Fig. 24).

Figure 23

Figure 24

- Cabot's manoeuvre: The heel is placed on the tibial crest of the opposite leg. The knee is gradually flexed, while the heel runs along the tibial crest. This movement may produce lateral pain, when the knee is in 90 of flexion with the heel resting on the other leg (Cabot's position). The lateral compartment is distracted by pressure on the medial side of the knee; this, too, may be painful. Cysts of the lateral meniscus will be seen in extension, and disappear in flexion. They are on or near the lateral joint line. They are best seen in semiflexion. The cysts will disappear in hyperflexion, and reappear as the knee is gradually extended; in full extension, they will

once again be out of sight. (In children, a malformation of the lateral meniscus may give rise to snapping when the knee is taken through flexion and extension. This abnormal movement is associated with a clicking noise, which may be very pronounced.) 3.4 Stability testing 3.4.1. Medial/lateral instability in extension (a) Medial instability in extension The examiner grasps the patient's heel (not the ankle or the leg) with one hand, while the other hand is placed against the lateral aspect of the patient's knee. A brisk valgus stress is imparted and immediately released. Medial instability is demonstrated if the medial joint line opens up (Fig. 25). Sometimes the most characteristic phenomenon is a little click as the knee reduces after the stress test. Sometimes, it is difficult to decide whether there is instability.

Figure 25

Several points need to be borne in mind: The abnormal feature is the asymmetrical pattern of the instability. The examiner may also ask the patient, "Do you think your right knee

is different from your left knee?" The leg may be supported halfway between the knee and the ankle, by pressing it against the examiner's body. That way, a greater valgus thrust may be applied. The third point of support produces better leverage. The instability will be due to a lesion of the ligaments on the medial side and/or to medial tibiofemoral compartment wear. (b) Lateral instability in extension The examiner grasps the patient's heel with one hand, while exerting pressure against the inside of the knee with the other hand. The varus stress applied will cause lateral gaping in the laterally unstable knee. Lateral joint gaping is physiological. It is the asymmetry of the gaping that constitutes the abnormal finding. 3.4.2. Medial/lateral instability in 30 flexion Description: The leg is held as described above, but the knee is unlocked by putting it in 20-30 flexion. (a) Medial instability The movement imparted is one of valgus-flexion rather than valgus-flexion-external rotation. Instability in valgus-flexion-external rotation would be a sign of an injured medial collateral ligament. (b) Lateral instability Varus-flexion-internal rotation is used to investigate the lateral collateral ligaments. Once again, asymmetry would have to be demonstrated to qualify the result as abnormal (Fig. 26).

Figure 26

In the United States, examiners prefer to sit on the couch, between the patient's knees, for the performance of this test (Fig. 27). The lateral collateral ligament is palpated with the knee in Cabot's position (see above), where it will be felt as a tense band. It is possible to explore both knees simultaneously, with the patient in the "frog position" described by Henri Dejour (Fig. 28).

Figure 27

Figure 28

3.4.3. Anterior instability (a) Lachman-Trillat test It is important to ensure that the patient is relaxed. This is all the more vital in recent trauma cases. In order to obtain relaxation, the patient is made to rest his or her head on the couch. It may be useful to roll the thigh in and out, to get the muscles to relax (Fig. 29). For the test, the knee is unlocked in 20 flexion. The patient's heel rests on the couch. The examiner holds the patient's tibia, with the thumb on the tibial tubercle. The examiner's other hand is placed on the patient's thigh, a few centimetres above the patella. The hand on the tibia applies a brisk anteriorly directed force to the tibia (Fig. 30).

Figure 29

Figure 30

The quality of the endpoint at the end of the movement is described as either "firm" or "soft." Grading depends on the quality of the endpoint observed, and on whether there is a difference of 3-5 mm between the affected and the unaffected knee. A soft endpoint will make the grading "abnormal" rather than "nearly normal." If the movement of the tibia on the femur comes to a sudden stop, this is described as a firm endpoint. If it does not, the endpoint is described as soft. A soft endpoint is pathognomonic of a torn ACL. It is easier to demonstrate a firm endpoint, which is also recognized by the patient. If the ACL is torn in one knee, the patient will be perfectly aware of the difference between the firm endpoint in the healthy, and the soft endpoint in the cruciate-deficient knee. Sometimes, the endpoint will be firm, but translation will be seen to be asymmetrical. This is known as a "delayed firm endpoint" (increased excursion and a good endpoint). It is indicative of a torn and partially healed ACL (ACL adherent to PCL), of a stretched ACL graft, or a torn PCL (changing the "starting point" of the test). A firm endpoint results from the sudden tensioning of the ACL (Fig. 31). The test is of lesser value in knees affected by OA, with a large number of osteophytes.

Figure 31

Lachman used to perform the test with the thumb of the distal hand on the medial joint line, so as to feel the displacement of the tibia on the femur. In Trillat's modification of the test, the thumb is placed on the tibial tubercle, so as to get visual evidence of the translation. In our practice, we prefer Trillat's method. The Lachman-Trillat test, the drawer test in 70 flexion, and the medial and lateral joint opening tests may be performed manually or using an arthrometer (KT-1000, KT-2000) or stress radiography. If an arthrometer is used, a force of 134 N (30 lbs.) will need to be applied. Measurements are performed on both sides. The difference between the affected side and the opposite side is recorded. Usually, only one value is recorded. The absolute value is also of interest, and should be recorded for prospective study purposes. If, after ACL surgery, the operated side is found to be tighter than the healthy side, the graft will be at increased risk of failure. Active resisted extension In obese patients or subjects with bulky muscles, it may be difficult for the examiner to encircle the patient's thigh with his or her hand. In such cases, the examiner may place a fist under the knee, hold the ankle against the couch with the other hand, and ask the patient to lift the leg against resistance (Fig. 31b). This resisted quad setting will move the tibial tubercle forward. This is a useful screening test, which will not, however, be positive unless there is major instability. It would be preferable to obtain stress radiographs (134 N stress) on which to base the diagnosis.

Figure 31b

(c) Pivot shifts Tests screening for pivot shift were first described by M. Lemaire, in 1968. Since then, many such tests have been devised, of which we shall only list the main ones. According to Noyes, the phenomenon is potentiated when the hip is abducted. At present, attempts are being made to substantiate the diagnostic value of these tests. However, they should not be expected to provide more than they can: A shift means that the ACL has gone. Sometimes, though, the ACL may be deficient without a pivot shift occurring during the relevant tests. Screening for pivot shift must be done systematically, using the customary techniques. The IKDC form records only the greatest shift found. The scoring system is conventional: + = glide; ++ = clunk; +++ = gross. - Pivot shift in extension (Dejour's test) (1978) Description: (1) The patient's foot is wedged between the body and the elbow of the examiner. The examiner places one hand flat under the patient's tibia, pushing it forwards (force applied in an anterior direction), with the knee in extension. The other hand is placed against the patient's thigh, pushing the other way (force applied in a posterior direction) (Fig. 32).

Figure 32

(2) The lower limb is taken into slight abduction, by the examiner's elbow, with the examiner's body acting as a fulcrum to produce the valgus. (3) The examiner maintains the anterior tibial translation and the valgus, and imparts flexion. At 20-30 flexion, pivot shifting will occur, with a clunk as the lateral tibial plateau suddenly reduces (Fig. 33).

Figure 33

Significance: The valgus stress associated with the anterior tibial drawer makes the lateral tibial plateau sublux on the lateral femoral condyle and compresses the structures. The sudden reduction of the convex lateral tibial plateau compressed under the lateral condyle is responsible for the clunk. Sometimes, a clunk may be elicited with compression, rather than any major valgus stress. The pivot shift is easy to produce, and causes no discomfort. It is a mixture of shift and Lachman, and provides evidence of ACL tears and damage to posteromedial structures. - The glide pivot shift test described by Henri Dejour is the equivalent of Noyes' test. It produces a glide (a minor form of shift) rather than a proper clunk. The patient is unaware of the slip of the plateaus on the femoral condyles. The valgus component is less pronounced than are the compression and anterior drawer applied by the examiner. It produces joint play rather than a pivot shift. It can be seen in patients with a torn and partially healed ACL, as well as after ACL grafts or other ACL surgery (Fig. 34).

Figure 34

- The pivot shift test of MacIntosh "When I pivot, my knee shifts." This is how a hockey player described his symptoms - hence the name of the test. MacIntosh realized that the sensation of shifting or slipping was related to rupture of the ACL. He devised a test to reproduce the sensation reported by patients, involving stress applied to the knee in valgus and flexion, with or without internal rotation (Fig. 35).

Figure 35

Description of the test: The patient is positioned supine, with the examiner standing on the affected side. The examiner uses one hand to hold the patient's foot in very slight internal rotation. With the other hand, (s)he applies a valgus stress to the posterolateral aspect of the proximal calf. At this point, flexion is started. The lateral tibial plateau will be seen to sublux forwards during the first degrees of flexion. As flexion progresses, the anterolaterally subluxed tibia will suddenly reduce, at 30 of flexion. This reduction is associated with a characteristic clunk, which the patient will readily recognize. - Hughston's jerk test The patient is positioned supine, with the examiner holding the lower limb in such a way as to have the hip flexed 45, the knee flexed 90, and the leg in internal rotation. The distal hand grasps the foot and places it in internal rotation, while the left hand applies valgus stress to the upper end of the leg. A jerk is defined as a sudden change in the relationship between the joint surfaces. The phenomenon occurs as the subluxation reduces near full extension. Hughston thought that rotational phenomena were more important (hence his defence of the concept of rotary instability). - Slocum's ALRI test (1976) The patient is placed in a semilateral position, with the knee unsupported, and the lower limb resting only on its heel. This allows internal rotation of the foot, to produce translation of the lateral tibial plateau. The examiner stands behind the patient's back, with the distal hand holding the upper end of the leg, and the proximal hand around the lower end of the thigh. The test is started in extension, using vertical

pressure. Next, flexion is commenced. Translation occurs at 20, and the pivot shifts at 40 (Fig. 36).

Figure 36

- Losee's test (1969) Over the years, Losee has described five tests: The first is identical with the MacIntosh test; the second uses external rotation of the tibia to elicit the pivot shift; the third (deceleration test) uses the quadriceps slingshot effect; while the fourth and the fifth test the anti-pivot shift effect of extra-articular ligament reconstructions. (c) Anterior drawer in 90 flexion, or direct anterior drawer The examiner sits on the patient's foot, which has been placed in neutral position. The knee is in 90 flexion. The index fingers are used to check that the hamstrings are relaxed, while the other fingers encircle the upper end of the tibia and push the tibia forwards (Fig. 37).

Figure 37

If a direct anterior drawer is obtained, the ACL will be torn. However, for this sign to be elicited, peripheral structures such as the medial meniscus or the meniscotibial ligament must also be damaged. This ligament forms a wedge, in 90 flexion, preventing anterior tibial translation. The finding of an anterior drawer is conclusive evidence of an ACL tear. However, not every ACL tear will be associated with a positive anterior drawer test. Drawer in external rotation (foot in external rotation). This test examines the posteromedial structures (posteromedial corner, posterior horn of medial meniscus). The results are recorded as +++/0. Drawer in internal rotation (foot in internal rotation). The diagnostic value of this test is less well established.

Table 4

One-leg hop functional test (Dale Daniel) This test investigates the greatest distance the patient can hop on one leg. The test is performed three times, and the mean value achieved is recorded. It is a comparative test, the result of which is expressed as a percentage of the value achieved on the healthy side.

Table 5

3.4.4. Posterior instability - Posterior tibial sag in 90 flexion In the IKDC form, the posterior tibial sag is recorded in 70 flexion; a comparison is made with the opposite side, looking sideways at the knees to establish the amount by which the tibial tubercle has dropped backwards. Posterior tibial translation may be confirmed if it is seen

that quadriceps contraction pulls the tibia forward. - Straight posterior drawer With the patient supine, the test is performed with the knee in 70-90 flexion and the foot in neutral rotation. The examiner sits on the patient's foot, placing both thumbs on the tibial tubercle, and pushing the tibia backwards. A positive test (i.e. one in which the tibial plateau moves in a posterior direction) means that the PCL is torn. Oddly enough, this is a difficult test to perform, since the patient's tibia may often sag spontaneously, requiring this posterior translation to be reduced before the test is started, since otherwise the result may be erroneously given as an anterior drawer. The quality of the endpoint (firm or soft) is of no significance in the posterior drawer test. To check the knee pattern, the knees should be inspected side-on, to see whether the tibial tubercle has sagged backwards. The knees should be in 90 flexion, with the patient's feet resting on the couch. It is preferable to use Godfrey's drop back test. There are three tests that can be used to demonstrate a posterior drawer, and which may be resorted to in case of doubt: - Godfrey's drop back test: The patient is supine, with the thighs and knees flexed 90, legs horizontal, and heels held by the examiner in such a way as to have the legs parallel to the table. The test is positive if the upper end of the tibia on the affected side is seen to drop backwards (Fig. 38).

Figure 38

- Muller's test: Patient positioning is identical to that for the posterior drawer test in 90 flexion. Tibial sag is observed. The patient is asked to set his or her quadriceps: Before the heel will have had time to lift off the couch, the posterior displacement of the tibia will have reduced. - Active extension against resistance: This is the same as Muller's test, but in 20 of flexion. This test is of lesser practical value. - Posterior drawer in external rotation The foot is placed in external rotation. This test is equivalent to the straight posterior drawer test in patients with PCL deficiency. The result is more pronounced in cases of posterolateral lesions. - Posterior drawer in internal rotation The foot is placed in internal rotation. Translation is usually 4 mm less than in the straight posterior drawer test. If the same value is obtained, this would be indicative of a lesion of the medial meniscofemoral or even the medial collateral ligament. - Whipple's test: In order to rule out tibial translation as a result of gravitational sag, the patient should preferably be examined prone. "This test is difficult. It has not yet gained wide acceptance." (B. Moyen). The information provided is the same as that obtained with the conventional posterior drawer test performed with the patient supine, feet resting on the couch. Apart from the fact that sag is eliminated, this test is completely unconstrained. - Posterior translation in 20 flexion: Posterior displacement may be observed with the knee in 20 of flexion. If the result is the same as that of the straight posterior drawer test, there will be associated posterolateral lesions. 3.4.5. Posterolateral instability (a) External rotation recurvatum test Description: The patient is supine. The examiner stands at the foot of the couch, and grasps the patient's big toes, lifting the feet off the couch. The affected knee will go into varum-plus-recurvatum (Fig. 39).

Figure 39

According to Hughston, this test provides information on major disabling peripheral instabilities; it cannot be positive unless the PCL is also torn: A positive recurvatum test shows that at least one cruciate is torn and that there is a posterolateral lesion. Of the cruciates, the ACL is more often involved than the PCL. (b) Jakob test (reverse pivot shift test) The patient lies supine. The examiner stands at the patient's feet, and places his or her distal hand on the patient's ankle, with the patient's leg braced against the examiner's pelvis. The proximal hand supports the upper third of the calf on the lateral side, and imparts a valgus force so as to compress the lateral compartment. The lateral tibial plateau will drop back under its own weight, with the foot in external rotation. This test starts with the knee in flexion. The joint is gradually taken into extension by its own weight. At a given point, the subluxation will reduce with a snap, and the foot will go into neutral rotation. The test involves a pivot shift manoeuvre, but since it starts from a subluxed position of the lateral tibial plateau, with reduction in extension, it is known as a reverse test. The jolt is produced by the reduction of the posterior subluxation through the action of the lateral head of the gastrocnemius, the capsule, and the pull of the iliotibial band, which, past 40 of flexion, moves from a flexor to an extensor function. All these factors will tend to pull the tibial plateau forward, out of its posteriorly subluxed position. Since there cannot be any rolling-sliding, the plateau will snap back into reduction.

Significance: This test provides evidence of a posterolateral instability which may or may not be associated with a lesion of the PCL. The test is not very specific. Posterior subluxation of the lateral tibial plateau may occur without any PCL deficiency, since, in external rotation, the PCL is relaxed and will allow a certain amount of posterior displacement of the tibial plateau. However, where the PCL is torn, the pivot shift will be very much more pronounced. (c) Increased external rotation It is indicative of lateral lesions. The test is performed as a side-to-side comparison: External rotation in 20 flexion: The examiner stands at the foot of the couch, and looks for unequal rotation. The difference found may be expressed in degrees (Fig. 40).

Figure 40

External rotation in 90 flexion. (d) Lateral hypermobility This test has been described by Gilles Bousquet. It is performed with the knee flexed at 90, with the examiner's hands around the top of the tibia (tibial tubercle), applying external rotation (Fig. 41). A positive test shows that the posterolateral structures have been injured. To complete the test, the examiner should

Look for stiffness of the hamstrings,. With the hip flexed at 90, the popliteal angle is measured (Fig. 42). The examiner tries to take the knee into extension, maintaining the foot in dorsiflexion.

Figure 41

Figure 42

Look for stiffness of the rectus femoris. For this, the patient is positioned prone. The heel is brought towards the buttock, with the hip in extension. The heel-to-buttock distance is measured (Fig. 43). While the patient is supine, a check should also be made for popliteal (Baker's) cysts. This test should always form part of the general examination of a knee patient; in particular, it must always be borne in mind that knee pain may be due to problems in the hip or the spine.

Figure 43

3 - FURTHER INVESTIGATIONSThe following techniques are available for the further workup of knee patients: 1 - Scout radiographs A.p. single-leg stance; lateral in 30 of flexion; axial views in 30 of flexion. Instability should be investigated using the radiological Lachman test. For the instrumented test, a Telos device may be used (varus, medial/lateral instability, a.p. instability). Long films may be used to measure limb length and study the axes of the lower limb. Rosenberg views (p.a. weight-bearing views in flexion) may be used to detect incipient OA or to screen for osteochondritis dissecans of the medial femoral condyle. 2 - Other imaging techniques

Arthrography: This is a useful technique in peripheral meniscal detachment, or when there is a suspicion of recurrent meniscal lesions. CT is essential in cases of patellar instability and of bone disease (tumour, trauma). MRI shows meniscal lesions, injuries of the cruciates, villonodular synovitis, and necrosis of the femoral condyles. Radionuclide bone scans should be requested if it is thought that the patient may be suffering from a tumour, from incipient avascular necrosis of a femoral condyle, or from reflex sympathetic dystrophy; or if an infection is suspected. 3 - Blood tests Sed rate, blood count, CRP, and rheumatological tests (latex fixation, Rose-Waaler, complement, ANA, antimitochondrial antibodies, Lyme serology, etc.) should be ordered in inflammatory knee conditions. 5 - Arthroscopy and biopsy These modalities are rarely indicated in the diagnostic workup of knee patients. They may occasionally be used in inflammatory conditions. The various signs observed may be grouped together to distinguish a number of knee disorder patterns:- Complete isolated anterior instability = Lachman-Trillat +; pivot shift + - Incomplete isolated anterior instability = Lachman-Trillat: Delayed firm endpoint +; glide pivot shift + - Advanced anterior instability = Lachman-Trillat +; pivot shift +, straight anterior drawer + - Posterior instability = Lachman-Trillat: Delayed firm endpoint +; posterior drawer +, tibial sag +, pivot shift 0 - Organic patellar instability = Apprehension + - Anterior knee pain syndrome = Medial facet tenderness + (quad/hamstring stiffness ) - Medial meniscus lesions = Effusion +, medial joint line tenderness +, McMurray +, Grinding + - Lateral meniscus lesions = Effusion +, lateral joint line tenderness +, Grinding +, Cabot +

- Isolated peripheral lesions: Medial collateral ligament = Instability in valgus-flexion-external rotation - Associated peripheral lesions: Medial triad (ACL + MCL + IM ) Lachman-Trillat +, direct anterior drawer +, valgus-flexion-external rotation +, instability in extension-valgus + - Posterolateral lesions: Posterior drawer +, reverse pivot shift + - Pentads: Posterior drawer +, straight anterior drawer +, Lachman-Trillat +, pivot shift +, external rotation recurvatum + (in lateral pentad); Medial instability in extension, valgus-flexion-external rotation, varus-flexion-internal rotation + (in medial pentad)

PS: The authors would appreciate hearing from other colleagues, in order to expand and augment the present list of tests. Please send your suggestions, descriptions of tests, etc. to Prof. Philippe Neyret Centre Livet 8, rue de Margnolles F-69300 Caluire France

CHRONIC ANTERIOR INSTABILITY OF THE SHOULDERPathophysiology and clinical examination The third parameterO. GAGEYDepartment of Orthopaedics, Bictre University Hospital

INTRODUCTIONOur knowledge of the mechanisms underlying instability has been greatly enhanced in recent years, mainly as a result of the consideration of a new parameter - ligamentous laxity. In the work-up of instability, the clinical examination is of paramount importance: in the overwhelming majority of the cases, it will allow a diagnosis to be made; further investigations will only provide confirmation. The clinical examination will allow the physician to recognize an associated inherent multidirectional laxity.(10,20,34) In some, very rare cases, examination under general anaesthesia will be required. Sometimes, the definitive diagnosis can only be made in the light of the arthroscopic findings

SHOULDER ANATOMY AND PHYSIOLOGYAnatomyFive anatomical features of the shoulder are crucial to an understanding of the problem: 1) The shoulder joint is not congruous. 2) There are no discrete ligaments. 3) No one ligamentous structure is taut in all positions of the joint. 4) All the ligaments of the shoulder are slack in the resting position. 5) There is a weak point. The ligaments of the glenohumeral joint are not discrete structures. The joint is surrounded by a sheet of fibrous tissue, which

constitutes both the capsule and the ligaments. This sheet inserts all around the glenoid, except for the rotator interval, and on the humerus. Back in the 19th century, Schlemm described the structure as the "broad ligament of the shoulder."(30) In this paper, the term inferior glenohumeral ligament (IGHL) will be used to denote the ligamentous structure inserted on the glenoid between 2 o'clock and 6 o'clock, which is the zone involved in instability. This zone includes the middle glenohumeral ligament and the anterior band of the inferior glenohumeral ligament, as described in anatomical studies of the shoulder.(7,22) The shape of this capsuloligamentous apparatus changes with the position of the glenohumeral joint; this is why the physiology of this structure is much more difficult to understand than is that of a linear ligament that extends between two "point" attachments. The kinematic analysis of the joint is made difficult by the fact that no one ligament is taut in all positions. This fact also accounts for the difficulty encountered in trying to devise a simple and specific ligament test that would show abnormal ligamentous laxity; in other words, there is nothing in the examination of the shoulder that would equate to the Lachman test, or to varus/valgus stress testing, of the knee. The relaxed condition of the ligaments at rest was demonstrated by Kumar and Balasubramaniam,(19) who showed that puncturing the capsule resulted in a downward displacement of the humeral head by more than 1 cm. When the arm is in 90 of abduction and in external rotation, the subscapularis muscle is pulled cranially, leaving the head of the humerus covered anteroinferiorly only by the IGHL, without any other muscle providing a check to anterior displacement.(33) This is the weak point through which the head may dislocate.

Mechanisms of glenohumeral joint stabilizationThere are many and complex ways in which the glenohumeral joint is stabilized. The fibrous labrum adds some depth to the glenoid socket; however, its role in the stabilization of the joint is very limited. The rotator cuff used to be considered the only significant stabilizer of the shoulder. Recent research (7,8,22,23) has redressed the balance by showing the importance of the ligaments. Between the resting position (with the arm hanging at the side) and maximum scapular-plane abduction, the articular ligaments go from complete relaxation to a state of uniform tension. Thus, it could be said that the stabilization of the joint gradually increases throughout abduction. The rotator cuff, in turn, has a very important role to play at the start of elevation, becoming progressively less important as the movement continues. This discrete involvement of the two anatomical structures is very clearly reflected in the clinical pattern: shoulder instability is virtually only seen at the extremes of abduction and external rotation, i.e. when the ligaments have come into play. Conversely, destabilization of the humeral head in rotator cuff lesions occurs chiefly at the start of abduction. This instability can be demonstrated by Leclercq's resisted-abduction manoeuvre. The vacuum phenomenon described by Kumar & Balasubramaniam (19) and by Habermeyer et al (13) is virtually unique in the human body. In the cadaver shoulder, all the muscles stabilizing the glenohumeral joint may be cut without affecting the position of the humeral head within the glenoid, providing that the joint capsule has not been breached,. As soon as the capsule is punctured,

the head will translate downwards by more than 1 cm. This shows that the shoulder depends to a considerable extent on negative pressure for the maintenance of the humeral head in the glenoid fossa. It is difficult to assess the importance of this mechanism in the prevention of shoulder instability.

3 PATHOPHYSIOLOGY: THE SEARCH FOR THE "THIRD PARAMETER"Findings at surgeryIn order to understand the mechanisms of instability, it is useful to consider the main findings at surgery using the Bankart technique, i.e. with separation of the subscapularis from the capsule, to provide a detailed and comprehensive picture of the ligamentous lesions. In the overwhelming majority of cases, the ligamentous apparatus will be continuous, and inserted on, or at a distance of less than 1 cm medial to, the glenoid rim. The labral lesion1 will vary from a complete disappearance of the structure and bone wear, through greater or lesser detachment, to discreet surface damage. In some patients, there will be evidence of a glenoid rim fracture. These findings allow several conclusions to be drawn: a) a Broca-Hartmann pouch, in the strict sense of the term, is extremely rare; b) the initial ligamentous lesion will heal, regardless of its shape and site; c) lesions of the anterior rim vary greatly in size. Their significance in the production of chronic instability is difficult to assess, since the movement of the humeral head forward of the glenoid rim during repeated episodes of instability must progressively change and aggravate the lesional pattern.

Fig. 1a-c : 1a Dislocation following a direct blow to the back of the shoulder 1b Formation of a Broca-Hartmann pouch. The persistence of this pouch is thought to be the main factor responsible for recurrent dislocation. 1c Mechanism of indirect dislocation

A "historical misunderstanding"In France, the mechanism underlying recurrent shoulder dislocation is still explained in terms of the formation of a Broca-Hartmann pouch.4 Broca and

Hartmann published the first description of the stripping of the capsule and the periosteum from the anterior aspect of the scapula, in 1889. The persistence of this detachment leaves an anterior pouch, which accounts for recurrent dislocation: the humeral head will "drop" into the pouch (Fig. 1b). That publication attracted general attention. However, the authors' second paper,3 published one month later, went unnoticed. In that paper, the authors stated that the lesion described previously was produced by a direct blow from behind (Fig. 1a), and had nothing to do with the very much more frequently observed so-called indirect dislocations (Fig. 1c). Thus, the Broca-Hartmann pouch should be seen for what it is: a very rare injury mechanism, which cannot account for recurrent anterior dislocation. (The rarity of the lesion is shown in our clinical material, where, in a consecutive series of 100 cases, there was only one pouch.)

Experimental studiesMany papers published in the international literature over the past few years have allowed us to formulate a more coherent concept of how chronic instability of the shoulder is produced. In order to dislocate a shoulder, at least the anteroinferior portion of the capsuloligamentous apparatus must be divided. (In the right shoulder, the division should extend from 3 o'clock to 6 o'clock.) The division of the capsuloligamentous apparatus is not enough to cause dislocation.9,33 The rotator cuff must also be damaged. Some authors have obtained dislocation following division of the supraspinatus tendon. We have shown that the lesion required may consist in a partial detachment of the deep portion of the cuff insertion. The anti-dislocation role of the rotator cuff can also be shown the other way round, by looking at the rate of cuff lesions found in shoulder dislocation in patients over the age of 40 years.21 It is thus clear that the rotator cuff provides a second line of defence to protect the shoulder from dislocating. The experimental creation of an isolated Bankart lesion32 has also been found to be insufficient for the production of shoulder instability.

La lsion de BankartIl est actuellement couramment admis que la lsion typique de l'instabilit chronique de l'paule est la lsion de Bankart. Elle associe une lsion du bourrelet qui peut tre us, dsinsr, voire presque entirement dtruit, un dcollement capsulo-priost antrieur d'importance variable. Nous avons vu que le dcollement antrieur tait le plus souvent trs limit. Il parat douteux que la lsion du bourrelet entrane une perte importante de stabilit. De plus on sait maintenant que les lsions antrieures s'aggravent progressivement avec le nombre de rcidives (12) ce qui peut laisser un doute quant l'importance des lsions initiales et fait que la question est pose : la lsion de Bankart suffit elle expliquer l'instabilit chronique ?

The Bankart lesionThe Bankart lesion is nowadays accepted as the typical pattern in chronic instability of the shoulder. This lesion combines damage to the glenoid labrum, which may be worn, avulsed, or almost entirely destroyed, and anterior soft-tissue stripping, of varying extent. We have found this anterior detachment to be usually very limited. It is doubtful that the labral lesion will lead to a major loss of stability. It is also now known that anterior lesions tend to get worse with recurrences.(12) Thus, the importance of the initial lesion may not be as great as hitherto assumed; and the real question is whether the Bankart lesion as such can account for chronic instability.

The Hill-Sachs lesionUnlike the reverse Hill-Sachs lesion, which plays a major role in recurrent posterior dislocation, the implication of the Hill-Sachs lesion15 (known in French as the Malgaigne notch) in the generation of recurrent anterior instability has never been conclusively demonstrated.

Laxity of the inferior glenohumeral ligament (IGHL) complexOver the years, several publications have stressed the importance of ligamentous laxity in shoulder instability. Neer and Foster(20) showed that some subjects have extremely hypermobile shoulders, which could cause multidirectional instability, in a context of inherent, non-trauma-related laxity of the shoulder capsule. Other authors have stressed the presence of ligamentous laxity in some cases of atraumatic shoulder instability.(31) Others found that, in traumatic dislocation, the ligament could undergo plastic deformation at the time of the traumatic event, and remain permanently stretched, with further stretching caused by repeated episodes of instability.(2) In a paper to be published soon, we have shown that IGHL laxity is also consistently seen in traumatic dislocation.

OveruseThis is an interesting concept, since it shows how shoulder laxity can be acquired without a discrete macrotraumatic event. Repeated stress (cumulative microtrauma) from sports involving extremes of abduction and external rotation (throwing, pitching) may result in gradual stretching of the capsuloligamentous apparatus of the shoulder. (25) In the position required by these sports, the ligament is tented and stretched over the unyielding convexity of the humeral head.

Arthroscopic repair of chronic anterior instabilityMajor progress in the arthroscopic management of chronic anterior instability came with the advent of devices for the fixation of sutures in bone. This has resulted in a simplification of the technique, and in a reduction of the recurrence rate, from 30% following the Caspari procedure,(5) to a level of 10-15%.(14,17,18) However, this rate is still well above the 3-5% rate seen after conventional surgery. The other major advance is the recognition of the importance of IGHL laxity, which is seen as a factor adversely affecting the outcome of arthroscopic repair.(29) Thus, developments in arthroscopic shoulder surgery have served to under line the role played by IGHL laxity.

Fig. 2 The ligament complex restricts glenohumeral abduction to 85

.

Voluntary instability

Voluntary subluxation or dislocation should be considered as a separate entity. While, obviously, the patients concerned will have generalized ligamentous laxity, voluntary instability also involves an element of volitional control of muscle forces. We wish to emphasize that surgery is absolutely contra-indicated in this subset of patients.

Fig. 3 Cutting the ligament provides an additional 10-15 of abduction. The tuberosities are not involved in restraining this movement.

4

CHRONIC SHOULDER INSTABILITYThe different forms of chronic instability of the shoulder can be brought together in an overall picture. On the one hand, there is instability with laxity brought on by trauma and made progressively worse by recurrent episodes of instability, and instability with laxity resulting secondarily from gradual stretching of the capsule (overuse); on the other hand, there is instability in the context of congenital excessive laxity.

Chronic anterior instability of the shoulderis, thus, characterized by three main parameters: - ligamentous laxity, which is a consistent feature, regardless of whether it is congenital or acquired; - a labral lesion, which may vary greatly in size, and which will worsen with every dislocation of the humeral head; - anterior soft-tissue stripping, which will often be very slight. This suggests that anterior instability of the shoulder is an instance of joint instability resulting from ligamentous laxity. What distinguishes the pattern from that seen in other joints is the lack of bony constraints in the glenohumeral joint, and the fact that stabilization is provided by one single ligament. The "labrum syndrome" may be accounted for by the fact that the laxity is great enough to allow the humeral head to ride up the glenoid slope, without being great enough to allow it to ride over the rim.

Fig 4 : Clinical measurement of passive abduction. The examiner stands behind the patient, and gradually lifts the upper limb, strictly in the coronal plane, while pushing down on the top of the shoulder. The patient's elbow is flexed to 90, while the forearm is held horizontal. The patient must be fully relaxed throughout the test.

A constant physiological valueCan ligamentous laxity of the shoulder be directly analyzed?

In order to analyze laxity directly, one would need a test performed in a position where the IGHL is taut. This is the only way in which the presence of stretching can be assessed. In an anatomical study, it was shown that glenohumeral abduction is consistently limited to 85 by the IGHL, with no other restraints involved (Fig. 2). The tuberosities have nothing whatsoever to do with restricting the range of this movement (Fig. 3): dividing the ligament allows an additional 15 of abduction to be obtained. The clinical measurement of passive abduction may be performed as shown in Figure 4. The examiner stands behind the patient, and exerts firm downward pressure on the top of the shoulder. The examiner's other hand is used to gently lift the patient's upper limb in the strict coronal plane, with the elbow flexed to 90 and the forearm held horizontal. The patient must, of course, be completely relaxed throughout the test. A study in 100 healthy volunteers showed that the range of abduction never exceeded 90, in 95% of the patients. This finding was bilateral. In 5% of the subjects, passive abduction was greater than 105, bilaterally; this suggested generalized ligamentous laxity. Radiographic checks showed that the scapula did not rotate by more than 5 during the

test. Thus, scapular rotation during the test would account for at most 6% of the range of movement. It follows that the measurement of passive abduction will show only the movement that occurs in the glenohumeral joint. This movement is limited by the IGHL, and has a constant range. We therefore hypothesized that IGHL laxity should lead to an increased range of passive abduction. In the light of the results obtained in that study, we wish to propose a test for the direct assessment of IGHL laxity, which will be described in the section concerning the clinical examination.

PRESENT-DAY CLASSIFICATION OF ANTERIOR SHOULDER INSTABILITYThis classification is important from the point of view of prognosis and of the management policy to be adopted. Instability may be traumatic or atraumatic. It may occur with or without evidence of excessive ligamentous laxity. Instability may take the form of recurrent dislocation (in which case, reduction may be performed by the patient himself or herself, or may require the assistance of a third party). Equally, it may manifest itself as a brief sensation of painful instability (the condition described by Patte et al(24) as a "painful and unstable shoulder," and by Rowe(28) as "recurrent transient anterior subluxation). Also, each patient should be checked to see whether the instability is voluntary or involuntary. The two parameters combine to form a spectrum of instability, as in the classification proposed by Silliman and Hawkins:(31) instability following initial trauma, without any prior laxity; instability following initial trauma and laxity acquired from overuse; instability following trauma, with prior laxity; and instability without a history of trauma, with prior laxity.

CLINICAL EXAMINATIONIn patients with typical dislocation and radiographic evidence (radiographs showing the shoulder in the dislocated position), the diagnosis is fairly straightforward; the only pitfall being an associated hyperlaxity that may be missed. As more and more people practise sports intensively, an increasing proportion of clinic patients will present with a less well-defined pattern. In these patients, a methodical examination will be of the utmost importance.

HistoryOften, the patient will spontaneously report the initial traumatic event. The index event should always be carefully elicited. Sometimes, the first episode of dislocation would appear to have been atraumatic; however, detailed history taking may reveal fairly major shoulder trauma in the past, which must be taken into account. There are situations where trauma may cause all the lesions required for instability, without any dislocation occurring. In other patients, a history of intensive sports practice involving abduction and forced external rotation will provide useful clues. On the other hand, the existence of an initial trauma should not stop the physician from searching for an associated multidirectional hyperlaxity. The nature of the trauma is not always easy to identify. The only important pattern is a direct posterior blow to the shoulder, or indirect trauma (a blow or fall on the elbow or on the outstretched, externally rotated arm). Indirect trauma is by far the most frequent cause involved. In this analysis of the first parameter, there is much that is not clear-cut.

It is important to obtain a description of the episodes of instability, trying to ascertain how many there have been, and how easily they tend to occur. If there have been many episodes of instability after very minor trauma, surgery should, obviously, be considered. Equally, though, a diver or a mountaineer with a first recurrence may be a candidate, given the risk involved in his or her sport.

Physical examinationThis examination is performed in three stages, and involves a search for three broad patterns: apprehension, during dynamic manoeuvres designed to reveal instability; laxity, which will be discussed in greater detail below; and evidence of associated multidirectional hyperlaxity.

Apprehension testsAll apprehension tests are designed to place the humeral head in a position of imminent subluxation or dislocation, which makes the patient recognize the familiar pattern of instability, and react with anticipated fear.

Crank test and fulcrum testThis test is designed to reproduce the position of instability. It is the oldest of the apprehension tests. The examiner places the arm in extreme abduction and external rotation, which may cause apprehension (Fig. 5). This is the most commonly used test. It has a high specificity. A negative test does not rule out shoulder instability. The test may be performed in the sitting or standing patient (crank test), or with the patient supine (fulcrum test).Fig 5 Crank test. This test serves to place the shoulder in a position of maximal instability (extremes of abduction and external rotation). The test is positive if the patient expresses pain or apprehension.

Relocation test

This is a more sensitive variant of the test described above. The patient is positioned supine. The first part of the test is a classic fulcrum test, in which the humeral head is pushed forward to elicit apprehension. In the second part of the test, a posteriorly directed force is applied to the humeral head. This prevents anterior subluxation, and produces a negative apprehension test (Fig. 6a and b).

Inferior apprehension testThis test was initially described by Feagin, and further refined by Itoi et al,16 who suggested the name ABIS (abduction inferior stability). For this test, the upper limb is held in abduction, with the patient's forearm resting on the examiner's shoulder. The examiner exerts downward pressure over the neck of the humerus. If the shoulder is unstable, the head will be pushed down, and a groove will appear; also, the patient may show apprehension (Fig. 7).

Fig 6 : Relocation test. This test is performed with the patient supine. 6a Pressure over the back of the humeral head causes apprehension, while 6b pressure over the front of the humeral head prevents the head suluxating anteriorly, and does not cause apprehension.

Tests for overall laxityThese tests are designed to show abnormal mobility of the humeral head. Since none of the articular ligaments is taut in the position used for these tests, the procedures should not be looked upon as ligamentous laxity tests. What is provided is global, and difficult-to-interpret, information on excessive joint mobility, covering not only laxity of the capsuloligamentous apparatus, but also the control of muscle tone. These procedures are tests of excessive mobility.

Sulcus testFig 7 : Abduction inferior stability (ABIS) test. The patient's arm is in abduction, with the forearm resting on the examiner's shoulder. The examiner exerts pressure on the arm, gradually pushing the humeral head downwards. The test is positive if there is downward displacement of the head, or if the patient shows apprehension.

The patient is told to relax, while the examiner exerts gentle downward traction on the patient's arm (Fig. 8). The test is positive if traction makes the humeral head move down; this distal movement of the humeral head manifests itself as a groove or sulcus below the lateral border of the acromion.(20) The amount of downward movement of the humeral head may be measured and graded.

Drawer tests

These tests, too, should be performed in a relaxed patient. The patient is asked to lean forward slightly, with both arms hanging down. The examiner holds the patient's shoulder girdle with one hand, while cupping the other around the humeral head, and sliding the head backwards and forwards to detect any abnormal mobility(27) (Fig. 9). This test may be performed with the patient sitting(26) or supine.(11)

Fig 8 : Sulcus test. In the relaxed patient, the examiner gently pulls the humerus downwards. The test is positive if the humeral head descends, with formation of a groove or sulcus under the lateral border of the acromion. The amount of downward movement can be measured. A positive test is indicative of abnormal mobility.

Fig 9 : Drawer test. The patient is made to relax and slightly lean forward. The examiner holds the humeral head between his or her thumb and index finger, and tries to make the head slide backwards and forwards. This test demonstrates overall hyperlaxity (without being specific of any particular ligament), and may provide information on the direction of the instability.

Is there a specific test for laxity?Since passive abduction has a constant range, and since the range is controlled by the IGHL, we suggest that laxity of the IGHL will be associated with an increase in the range of abduction. The passive abduction test was performed in patients with post-traumatic shoulder instability without any associated hyperlaxity. In 85% of the cases, the range of passive abduction was at least 105, while, on the healthy side, it was limited to 90. In 15% of the cases, the test caused acute apprehension, making it impossible to measure passive abduction. In such cases, the test works as an apprehension test, along the lines of the procedure initially devised by Feagin, and proposed by Itoi et al as the ABIS test. The test was performed under general anaesthesia, immediately prior to surgery. In all the cases, passive abduction was at least 105, while, on the contralateral side, it was restricted to 90. Providing that the test is performed strictly in the coronal plane, it furnishes objective evidence of excessive IGHL length, and gives a direct demonstration of the laxity of the ligament. Thus, this test of passive hyperabduction is positive if the range on the affected side is greater than 105 (Fig. 10). This is the first test that allows shoulder ligament laxity to be directly assessed; however, it will need to be used more widely, in a prospective study, to establish its specificity and sensitivity.

Neurological examinationThis part of the general work-up must not be overlooked: in almost 15% of cases of chronic shoulder instability, the axillary nerve is affected.

Looking for evidence of generalized ligamentous laxityMultidirectional hyperlaxity affects the outcome of instability treatments.(29) On examination, there will be a groove of more than 2 cm in the sulcus test, as well as major anterior and posterior drawer movements. External rotation of the upper limb of more than 90 is also considered to be a sign of abnormal laxity. The wrists should be examined for increased palmar flexion, as should the elbow for marked hyperextension, the knees for a recurvatum deformity, and the trunk for enhanced forward bending (palms of hands to floor). In patients with generalized ligamentous laxity, the passive hyperabduction test will be bilaterally positive.

Fig 10 : Positive hyperabduction test. Marked asymmetry between the affected and the healthy side is characteristic of laxity of the ligament complex.

Where these tests are positive, the diagnosis will be one of instability associated with multidirectional hyperlaxity. Evidence of true multidirectional instability should be carefully sought. The most important feature is episodes of posterior instability when the arm is in forward elevation and internal rotation. The patient should be questioned about episodes of posterior instability of the shoulder. Special attention should be devoted to eliciting previous incidents of voluntary shoulder dislocation. In some of the more difficult cases, especially when trying to confirm or exclude multidirectional instability, CT arthrography may be helpful. Arthroscopy may be indicated, to obtain objective evidence of laxity, as described by Detrisac and Johnson.(6). REFERENCES 1. BANKART A.S.B. : The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg 23, 1938.(Abstract) 2. BIGLIANI,LU., POLLOCK,R., SOSLOWSKY, L., FLATOW, EL., PAWLUK, R., and MOW, V. : Tensile properties of the inferior glenohumeal ligament. J Orthop Res 10:187, 1992. 3. BROCA, A. and HARTMANN, H. : Contribution l'tude des luxations de l'paule (luxations anciennes et luxations rcidivantes). Bull Soc Anat 416, 1890. 4. BROCA, A. and HARTMANN, H. : Contribution l'tude des luxations de l'paule (luxations dites incompltes, dcollements priostiques, luxations directes et luxations indirectes). Bull Soc Anat 312, 1890. 5. CASPARI, R.B.: Reconstruction for anterior shoulder instablity. Tech Orthop 3:59, 1988. 6. DETRISAC, D.A. and JOHNSON, L.L.: Arthroscopic shoulder capsulorrhaphy

using metal staples. Orthop Clin North Am. 24:71, 1993. 7. FERRARI, D.A.: Capsular ligaments on the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sport Med 18:219, 1990. 8. GAGEY,O.J., BONFAIT, H., GILLOT, C., and MAZAS, F.: Anatomie fonctionnelle et mcanique de l'lvation du bras. Rev Chir Orthop 74:209, 1988. 9. GAGEY, O.J., GAGEY, N.F., BOISRENOULT, P., HUE, E., and MAZAS, F.: Etude exprimentale des luxations antro-internes et recta de l'articulation scapulohumrale. Rev Chir Orthop 79:13, 1993. 10. GERBER, C.: Les instabilits de l'paule. Paris, L'Expansion Scientifique Franaise, 1989, 11. GERBER, C. and GANZ, R.: Clinical assessment of instability of the shoulder with special reference to anterior and posterior drawer tests. J Bone Joint Surg 66-B:551, 1984. 12. HABERMEYER, P., GLEYZE, P., and RICKERT, M.: Evolution of lesions of the labrum-ligament complex in posttraumatic anterior shoulder instability : a prospective study. J Shoulder. Elbow.Surg 8:66, 1999. 13. HABERMEYER, P., SCHULLER, U., and WIEDEMANN, E.: The intra-articular pressure of the shoulder : an experimental study on te role of the glenoid labrum in stabilizing the joint. Arthroscopy 8:166, 1992. 14. HAYASHIDA, K., YONEDA, M., NAKAGAWA, S., OKAMURA, K., and FUKUSHIMA, S.: Arthroscopic Bankart suture repair for traumatic anterior shoulder instability: analysis of the causes of a recurrence [see comments]. Arthroscopy. 14:295, 1998. 15. HILL, H.A. and SACHS, M.D.: The grooved defect of the humeral head. A frequently unrecognized complication of dislocation of the shoulder joint. Radiology 35:690, 1940. 16. ITOI, E., MOTZKIN, N., MORREY, B., and AN, K.: Scapular inclination and inferior stability of the shoulder. J Shoulder Elbow Surg 1:131, 1992. 17. KAGAYA, K., YONEDA, M., HAYASHIDA, K., WAKITANI, S., NAKAGAWA, S., MAEDA, A., and IZAWA, K.: Modified Caspari technique for traumatic anterior shoulder instability: comparison of absorbable sutures versus absorbable plus nonabsorbable sutures. Arthroscopy. 15:400, 1999. 18. KARLSSON, J., KARTUS, J., EJERHED, L., GUNNARSSON, A.C., LUNDIN, O., and SWARD, L.: Bioabsorbable tacks for arthroscopic treatment of recurrent anterior shoulder dislocation. Scand.J Med. Sci. Sports 8:411, 1998. 19. KUMAR, V.P. and BALASUBRAMANIAN, P.: The role of atmospheric pressure in stabilizing the shoulder. J Bone Joint Surg 67B:719, 1985. 20. NEER, C.S. and FOSTER, C.R.: Inferior capsular shift for involuntary and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg 62A:897, 1980. 21. NEVIASER, R.J., NEVIASER, T.J., and NEVIASER, J.S.: Concurrent rupture of

the rotator cuff and anterior dislocation of the shoulder in the older patients. J Bone Joint Surg 44A:523, 1996. 22. O'BRIEN, S.J., NEVES, M.C., ARNOCZKY, S.P., and ROZBRUCK, S.R.: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am. J. Sport Med. 18:449, 1990. 23. O'CONNEL, P.W., NUBER, G.W., MILESKI, R.A., and LAUTENSCHLAGER, E.: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am.J.Sport Med. 18:449, 1990. 24. PATTE, D., BERNAGEAU, J., and GARDES, P.: Epaules douloureuses et instables. Rev.Chir.Orthop. 66:157, 1980. 25. PERRY, J.: Anatomy and biomechanics of the Shoulder in throwing, swimming, gymnastics and tennis. Clin Sport Med 2:247, 1983. 26. ROCKWOOD, C.: Fractures. Tome 1 Rockwood and Green Ed, Lipincott, Philadelphie, 1984. 27. RODINEAU, J., COURROY, J., and KUMAR, A.: Epaules douloureuses et instables par lsion du bourrelet et du rebord glnodiens. Mdecine du sport 54:343, 1980. 28. ROWE, C.R.: Recurrent transient anterior subluxation of the shoulder. The dead arm syndrome. Clin Orthop 11, 1987. 29. SCHENK, T.J. and BREMS, J.J.: Multidirectional instability of the shoulder: pathophysiology, diagnosis, and management. J Am Acad.Orthop Surg 6:65, 1998. 30. SCHLEMM, F.: Uber die Verstarkungbander am Shultergelenk. Arch Anat 48, 1835. 31. SILLIMAN, J. and HAWKINS, R.: Classification and physical diagnosis of instability of the shoulder. Clin Orthop 291, 1993. 32. SPEER, K.P., DENG, X., BORRERRO, S., TORZILLI, P.A., ALTCHEK, D.A., and WARREN, R.F.: Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am 76:1819, 1994. 33. TURKEL, S.J., PANIO, I.M., MARSHALL, J.L., and GIRGIS, R.G.: Stabilizing mechanisms preventing anterior dislocation of the gleno-humeral joint. J Bone Joint Surg 63A:1208, 1981. 34. WALCH, G., AGOSTINI, J., LEVIGNE, C., and NOVE-JOSSERAND, L.: Instabilit antrieure rcidivante avec hyperlaxit multidirectionnelle de l'paule. Rev Chir Orthop 81:682, 1995.

Clinical Examination of the ElbowC. Dumontier Hpital St-Antoine, 184 rue du faubourg St-Antoine, F-75012 Paris Institut de la Main, 6 square Jouvenet, F-75016 Paris

INTRODUCTION The elbow complex is made up of three separate articulations, the humero-ulnar joint, the humeroradial (radiocapitellar) joint, and the superior radio-ulnar joint. These joints are covered by the same capsule. The elbow allows flexion and extension, as well as pronation and supination, and thus enables the hand to be placed in a variety of positions in space. Elbow flexion brings the hand to the chest, the mouth, or the face, thereby allowing the performance of most of the activities associated with feeding, dressing, and body care; elbow extension, on the other hand, takes the hand away from the body, and enables it to grasp objects. Elbow injuries are rare; however, they may be difficult to diagnose. This problem may be resolved to some extent or simplified by a full and systematic clinical examination. The joint is superficial, and hence readily accessible to clinical examination. As with other structures in the body, the examiner must be thoroughly familiar with the anatomy of the joint and with the abnormal conditions that may be encountered. This article deals with the broad principles of clinical examination, and will highlight only some of the disorders of the elbow. ANATOMY AND PATHOPHYSIOLOGY ANATOMICAL STRUCTURES The anatomy of the elbow joint and the surrounding structures has been the subject of much research. In this article, only the main points that have emerged from recent studies will be summarized.

The bones (Figs. 1-4 )

Figure 1 Diagrammatic AP view of elbow joint Figure 2 Diagrammatic lateral view of elbow joint. Note that the elbow is slightly twisted in respect of the axis of the ulna.

The trochlea is shaped like a pulley; its medial lip is more prominent than the lateral one. The groove of the pulley runs obliquely downwards and outwards; it courses in a helical manner, forming an arch of about 330. The distal joint surface of the humerus is in about 30 anterior rotation with respect to the long axis of the humerus, in the sagittal plane; the condyles have 3-8 of internal rotation with respect to a line joining the epicondyles, in the axial plane; while, in the frontal plane there is a 6-8 valgus tilt of the condyles with respect to the long axis of the humerus(32, 34, 42). Elbow rotation is virtually around a single centre, which coincides with the condylotrochlear axis(48). On a true lateral radiograph of the elbow, the flexion-extension axis is at the centre of three concentric circles formed, respectively, by the projection of the edges of the condyles, the ulnar groove at the back of the medial epicondyle, and the medial lip of the trochlea (Fig. 4b). This flexion-extension axis is on a vertical line drawn down from the anterior cortex of the humeral shaft. It is an essential landmark for the implantation of a total elbow joint replacement (TEJR).Figure 3 AP radiograph of the elbow Figure 4a: Radiograph of the elbow taken at right angles to the axis of the forearm. Note medial rotation of the humerus, as shown in the diagram in Figure 2. Figure 4b: True lateral radiograph of the humerus. The centres of the three circles formed by the edge of the condyle, the ulnar groove, and the medial lip of the trochlea coincide; this point is the flexionextension axis of the elbow. The axis is on a vertical line drawn down from the anterior cortex of the humeral shaft.

There is a valgus angle of about 4 between the trochlear (greater sigmoid) notch of the ulna and the ulnar shaft (32, 34). The opening of the trochlear notch is angled ca. 30 posteriorly with respect to the long axis of the ulna; this allows better approximation in flexion to the 30 anterior rotation of the humeral articular condyles (34). The joint surface of the trochlear notch forms an arc of about 180; however, it is not entirely covered with cartilage: in over 90% of individuals, a bare area covered by fibro-adipose tissue extends transversely across the mid-portion of the trochlear notch; this feature accounts for the frequency of fractures at this site, and permits a trans-olecranon approach to the joint (34). The radial head is covered with cartilage over four fifths of its circumference. The 15 angulation between the neck and the shaft of the radius leaves an excursion of 180 for forearm rotation(34).

The joint capsule

The capsule is attached around the articular surfaces, and blends with the annular ligament. It covers the tip of the olecranon, the coronoid process, and the radial fossa. The fibres are arranged in such a way as to provide stabilization in flexion and in full extension(23). When the

elbow is stiff, the capsular capacity will be reduced by more than 50%; equally, the capsular compliance of the stiff elbow will be very poor, which shows that the capsule itself has been compromised(14). The position of minimum intracapsular pressure ("resting position") is around 60-70 of flexion, which means that prolonged immobilization of the elbow in this position - as practised since the days of Ambroise Par - will increase the risk of capsular contraction(14).

The ligaments

The medial collateral ligament is a strong and well-demarcated structure that consists of three bundles (Fig. 5):Figure 5 Diagrammatic view of the medial collateral ligament, with its three bundles. The anterior bundle is the most important functionally, since it provides valgus and anteroposterior stability.

Figure 6 Diagrammatic view of the lateral ligament complex. It would appear that the most import structure is the lateral collateral ligament, which blends with the annular ligament. The lateral ulnar collateral ligament is indissociable from the lateral collateral ligament, at its attachment to the lateral epicondyle. Distally, it branches off, and attaches to the supinator crest. The role of the accessory lateral collateral ligament is poorly understood.

Figure 7 Diagrammatic view of the origin and insertion of anconeus, which covers the capsule and collateral ligaments on the

lateral side.

x The oblique anterior bundle is wide (5 mm) and thick. Its apex is attached to the front and the medial aspect of the medial epicondyle, of which it covers two thirds, and its base to the medial aspect of the ulna, just below the coronoid process(9, 32). This bundle is taut in flexion and in extension; its mean length is 27 mm(31, 32). x The oblique posterior bundle is less well defined. This broader structure is also attached low on the medial epicondyle, and inserts in a fan-shaped pattern over virtually the entire margin of the trochlear notch of the olecranon. It is one of the structures that make up the cubital tunnel floor(9). This bundle is taut in flexion only; it is absent in many primates, which suggests that it is not a main stabilizer of the elbow(31, 53). The two bundles of the medial collateral ligament insert slightly posterior to the centre of rotation, which accounts for the fact that they are tauter in flexion than in extension(23). x The oblique transverse ligament (sometimes referred to as the ligament of Cooper) is short, and does not appear to have a stabilizing role(31, 32). It extends from the posterosuperior portion of the trochlear notch to the coronoid process; its origin blends together with that of the anterior bundle(9). Like the posterior bundle, it contributes to the floor of the cubital tunnel.

On the lateral side, there is no discrete collateral ligament in the strict sense of the term. Anatomical patterns vary widely, which is why the description of the structures involved has been difficult, and why disorders of the lateral collateral complex may be hard to understand(31, 32, 42, 43). There are five ligamentous structures involved in the lateral stabilization of the elbow joint (Figs. 6, 7):

x The lateral (radial) collateral ligament attaches to the medial aspect of the lateral epicondyle and inserts into the annular ligament(31). Its origin overlies the centre of rotation of the elbow, which means that the ligament will be taut throughout flexion and extension(23, 32). Its mean length is 21 mm(31). The fan-shaped base of the ligament blends with the fibres of the annular ligament(43). x The annular ligament is a thick structure that attaches to the anterior and posterior margin of the radial (lesser