Anterior Cruciate Ligament-Deficient

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Neuromuscular Performance in Normal andAnterior Cruciate Ligament-DeficientLower Extremities*

Edward M. Wojtys, MD, and Laura J. Huston, MS

From MedSport at the University of Michigan, Ann Arbor, Michigan


The neuromuscular function of the lower extremity in 40normal and 100 anterior cruciate ligament-deficient vol-unteers was evaluated by physical examination, KT-1000 arthrometer measurements, isokinetic strengthand endurance testing, subjective functional assess-ment, and an anterior tibial translation stress test. Aspecially designed apparatus delivered an anteriorly di-rected step force to the posterior aspect of the leg whileanterior tibial translation was monitored and electro-

myographic signals were recorded at the medial andlateral quadriceps, medial and lateral hamstrings, andgastrocnemius muscles. Testing was done at 30 ofknee flexion with the foot fixed to a scale to monitor

weightbearing, while the tibia remained unconstrained.Results indicate that muscle timing and recruitment or-der in response to anterior tibial translation are affectedby anterior cruciate ligament injury. These alterations inmuscle performance change with time from injury, cor-relate with an individuals physical activity level, affectsubjective functional parameters, and are directly re-lated to the degree of dynamic anterior tibial laxity seenwith stress testing.

Over the last 25 years, a tremendous research efforthas been focused on the biomechanics of theACL.13,15, 29, 30, 42, 46, 51-53, 76 The principles learned have beenapplied clinically in the hope of improving the natural his-tory of a knee with an injured ACL. In fact, impressivestrides in treatment have followed the course of ACL re-search. A torn ACL in an athlete is not necessarily the

&dquo;beginning of the end,&dquo; as it was once described.&dquo; The prog-nosis for an athletic individual with an ACL injury withproper care appears to be much improved, at least over theshort term. 16,56

Despite these clinical and biomechanical advances, ourcurrent information base does not explain the functionalstatus of several types of individuals with increased ante-rior laxity of the knee. One of these types is the athlete whohas excess anterior laxity but who functions at a very highlevel of activity without evidence of instability. 51,51,11 Someof these athletes have normal ligaments that are just notas tight as most, while a few represent asymptomatic ACL-deficient (ACL-D) extremities. Despite a lack of passive re-straint, no instability is apparent, and a high level of func-tion is maintained. Secondly, there is the individual whohas had an ACL reconstruction and has returned to a highlevel of activity without instability in spite of considerableresidual anterior laxity. Paradoxically, there are thosewhose laxities are within &dquo;normal parameters&dquo; yet in whomsymptoms of instability persist.22 These examples empha-size the dual nature of knee stability: the passive restraintsystem, which is composed primarily of ligaments and cap-sule, and the dynamic system, which is composed of theneuromuscular elements. The interaction between the dy-namic and static systems remains unclear. An improvedunderstanding of the neuromuscular component of stabi-lization is needed to augment our treatment of injuries tothe passive restraints of the knee.

This investigation was not performed to alter the currentstandards in decision-making regarding nonoperative ver-sus operative treatment of ACL tears. These decisionsshould be made based on the age and activity level of thesubject while keeping in mind the known risk factors fordegenerative disease. This research was designed to aug-ment both directions of treatment by maximizing the po-tential of the neuromuscular control system. This was at-tempted by studying the neuromuscular response toanterior tibial translation (ATT) in a specifically designedapparatus that allowed monitoring of spinal reflexes andcortical control activity. Unfortunately, at this time, we do

* Presented at the 18th annual meeting of the AOSSM, San Diego, Cali-forma, July 6, 1992

t Address correspondence and repnnt requests to: Edward M. Wojtys, MD,MedSport, POB 363, Ann Arbor, Mi 48106

No author or related mstitution has received any financial benefit from aproduct named or used in this study.


not fully understand the complexities of dynamic knee jointcontrol, which makes the interpretation of this data diffi-cult and subject to criticism.


In 1944, Ivar Palmars2 wrote about the theory that liga-ments supply the central nervous system (CNS) input thatmakes neuromuscular control of knee joints possible. Sev-eral years later, in 1956, Cohen and Cohen&dquo; popularizedthe idea of an &dquo;arthrokinetic reflex.&dquo; Based on their workwith decerebrate cats, they suggested that the origin ofimportant protective afferent input was the knee joint cap-sule. Cohen and Cohen decided that a quadriceps-hamstrings tension balance was necessary for knee jointstability. Andersson and Stener concurred with Cohenand Cohens work after localizing important mechanore-ceptors in the anteromedial region of the cat knee jointcapsule. Subsequently, Petersen and Stener 63 suggestedthat these capsular receptors were not mechanoreceptorsbut merely nociceptors responding to large joint loads.These capsular receptors were later shown to be sensitiveto very low joint pressures and to tensile loads in the rangeof fractions of Newtons. 17,36

In hopes of isolating the origin of proprioceptive afferentinput, several neuroanatomic studies have focused directlyon the ACL. Kennedy et al. 41 isolated free nerve endings inGolgi-like receptors in the synovium covering the ACL.Schultz et al. 71 found these same receptors on the surfaceof the ACL beneath the synovial sheath. Schutte et al.2described an extensive network of sensory receptors in theACL, including Pacinian and Ruffini corpuscles and freenerve endings. Gomez-Barrena et aI,32 isolated direct neu-ral pathways from the ACL to spinal ganglia by using trac-ers to study axonal transport.Despite these anatomic advancements, the precise origin

of the afferent input needed to protect specific ligamentsand maintain joint stability is still not agreed on.2,3,25,6l.65, 73In 1987 Solomonow et al .73 reported a direct ligament-muscle reflex arc from their work with ACLs in cats andhumans. They suggested that ACL injury in humans in-terrupts this ligament-muscle reflex arc, triggering a sec-ond slower pathway needed to modulate the quadricepsand hamstrings muscles from muscle and capsular recep-tors. In a comparison of normal and ACL-D human ex-tremities, Solomonow et al. were able to show a substantialdifference in the EMG activity of the ACL agonist ham-string muscles when the ACL was severed. The meaning ofthese EMG changes remains in question.Electromyographic work by Draganich et al.20 with six

male subjects with ACL-D extremities also suggested thatthe hamstrings act synergistically with the ACL. Specifi-cally, they reported increased EMG activity in the bicepsfemoris muscle from 30 to 0, which is precisely whereACL force and strain increase. 14,15,70,76

In contrast, work done recently by Pope et al.s5 in 1990questioned the existence of a direct ligament-muscle reflexarc; they attributed the activity in the posterior articularnerve of cats after tugging on the ACL to receptors in theperiarticular tissues not in the ligament itself. Interest-

ingly, recent work by Pitman et al. 64 continues this debate.By using an arthroscope in vivo, they demonstratedsomatosensory-evoked potentials (SSEP) in the cerebralcortex after direct electrical stimulation of an intact ACLin nine patients. The SSEPs represent proprioceptive inputfrom peripheral nerves transmitted along the posterior col-umns.

While a direct ligament-muscle protection system maybe difficult to demonstrate in all animal and human modelsin all joint positions, there is increasing evidence that sup-ports a modulating system of knee joint afferent input onmotoneuron output. Alpha motoneurons are affected byboth high 14 and low34$ threshold joint afferents. Flexorreflex pathways,24 Ia interneurons,2s33 and Ib interneu-rons48 have all demonstrated the capability of modulatingdifferent efferent pathways.Even though a precise diagram of the neurocircuitry of

dynamic knee joint control is not yet agreed on by inves-tigators, there is no doubt that the neuromuscular systemis capable of altering the strains imposed on the passiverestraints of the knee.70 White and Raphael8 reported thata quadriceps contraction could reduce the strain producedin the medial collateral ligament when a valgus force wasapplied to the knee. Goldfuss et al.3l showed that the stiff-ness of the medial side of the knee could be increased up to

48% with contraction of the quadriceps and hamstringmuscles. Renstrbm et al. 70 used cadavers and a Hall effecttransducer to show that the hamstring muscles could de-crease ACL strain in all positions tested.Timely muscle contraction, or &dquo;dynamization&dquo; of the tib-

iofemoral joint, adds a new dimension to the concept ofknee joint stability. It is this juxtaposing of the joint sur-faces through muscle contraction or loadbearing that al-lows the geometry of the tibiofemoral joint to become anintegral part of joint stability.38 In the unloaded knee,which does not mimic most ligament injury situations, allexternally applied forces or moments are internally re-sisted by ligaments and capsule.15 When the knee joint issubjected to axial loading, joint contour becomes an im-portant stabilizing factor that is frequently underappreci-ated. Markolf et a1.5 tested axial joint loads up to 925 N at0 and 20 of knee fle