Anterior Cruciate Knee Ligament Injuries – The End Of The Affair For Most Sports Careers Despite The Injury Unlocking Exquisite Redundant Neuromuscular Protective Mechanisms

I was watching a rugby game recently and saw a player land wrongly in a tackle and immediately collapse to the ground clutching his knee joint, and heard later that he had suffered a ruptured anterior cruciate ligament injury that would require nine months post-injury before he would be able to return to his chosen sport. Many years ago in my student days, after a few too many beers at a party, I jumped off a low wall, landed wrongly, and tore the meniscus in my left knee. The next day it had swollen up, but I did not think much of it and tried to drive to University, and always remember the horror I felt when getting to the bottom of the road and I tried to push in the clutch with my left leg to allow use of the brake at the stop street, and my leg would not react at all, and I only avoided an accident by turning off the car while working the brake pedal with my right foot. It always puzzled me afterwards why my leg would not respond at all despite my ‘command’ for it to do so, as even with the injury, I expected, while perhaps it might be painful to do so, that I would still have reasonable control over my leg movements, which appeared okay when walking slowly to the car and taking my weight on my uninjured leg. Perhaps this triggered a ‘deep’ interest in what controlled our muscles and other body functions, and when I started a PhD degree with Professors Tim Noakes, Kathy Myburgh and Mike Lambert as my supervisors at the University of Cape Town in the early 1990’s, I chose to look at neural reflexes and brain control mechanisms regulating lower limb function after anterior cruciate ligament knee injury. So what happens when the knee joint suffers a major injury, and can one ever ‘come back’ from it?

The knee joint is one of the most precarious joints in the body, and as compared to the hip and shoulder joints, which have quite a degree of stability generated by their ‘ball and socket’ design, it is simply made up of three individual bones (the femur, tibia and patella) moving ‘over’ each other while being attached to each other with a number of ligaments and muscles, which are pretty much all that creates stability in and around the knee joint. The knee mostly moves in a backwards / forwards (in medical terms flexion and extension) plane, and has a small degree of rotation inwards and outwards, but is basically a ‘hinge’ type joint that moves in one plane only. The major ligaments of the knee joint preventing too much flexion and extension are the anterior cruciate ligament (ACL), which prevents hyper-extension (the lower limb calf region moving too far ‘forwards’ relative to the upper thigh) and the posterior cruciate ligament (PCL), which prevents hyper-flexion of the knee joint. There are also relatively strong ligaments on each side of the knee joint (the medial and lateral collateral ligaments), as well as several ligaments and tendons securing the patella in place in the front of the knee. Two large pieces of cartilage, the medial and lateral menisci, ‘sit’ on the tibia and allow smooth movement to occur across the entire range of movement between the two big bones (femur and tibia) of the knee joint and protect each of these from damage which would occur if they ‘rammed’ into each other each time the bone moved without the protection of the two menisci.

While these ligaments (and there are several others in the knee joint beyond those I have described above), tendons and menisci provide the majority of support to maintain the fidelity of the knee joint, the surrounding muscles – particularly the quadriceps and hamstrings muscles – also provide important secondary support to the knee joint during active movement such as walking or running, when a greater degree of dynamic stability beyond the static stability the ligaments and tendons supply, is needed. So muscles are not just creators of movement, they are also important stabilisers of the body’s joints, and there needs to be a high degree of dynamic control of them by the central nervous system during movement to ensure things work ‘just right’ with not too much and not too little force being applied to the joint at any one time during any movement. The hamstring muscles have been shown to be agonists (assistants) of the ACL, and when they fire they ‘pull back’ the lower part of the knee joint so as to reduce pressure on the ACL when the knee extends to its limits, while the quadriceps muscles similarly assist the PCL from having too much pressure on it associated with too much flexion of the knee joint (though only at certain angles of the knee joint and not through its entire range of movement). Interestingly, the quadriceps muscles are not just agonists of the PCL, but also are ‘antagonists’ of the ACL, and their activation can also increase hyper-extension pressure on the knee joint (and therefore on the ACL) when the quadriceps contracts particularly when the knee is in an extended position. So the quadriceps muscles can be the ‘friend’ of the ACL and knee joint, but can also be its ‘foe’.

What is fascinating in this process is the structure and function of the nerve pathways both from and to all of the knee joint, ACL and muscles around them, and how these nerve pathways act differently in an intact ACL as compared to the damaged ACL state. In the intact ACL are mechanoreceptors (receptors which pick up mechanical pressure) which fire when the ACL is put under pressure / moves, and they send information back via nerves to the spinal cord, and cause increased firing of the hamstring muscles, in order to protect both the ACL and integrity of the entire knee joint. When the ACL is ruptured, receptors called free nerve endings in the surrounding capsule of the knee joint fire in response to movement of the entire knee joint, which would happen to a greater degree in the absence of the ACL after it ruptures, and importantly, these injury associated capsular free nerve ending reflexes don’t just increase the firing to the hamstrings muscles, they at the same time reduce firing to the quadriceps muscle, in order to protect the knee from further damage which could occur if the quadriceps were active maximally in the absence of the ACL. This free nerve ending pathway is known as a redundant pathway, as it only ‘fires’ when the ACL is damaged, and does not do so normally. Interestingly, the redundant free nerve ending related pathway does not seem to stop working even if the ACL is repaired or replaced, which means that even if one fixes the ligament materially, one cannot ever completely repair the sensitive neuronal control pathways as part of the operation.

While these redundant neural firing pathways are protective and are designed to help the knee from incurring further damage, they are unfortunately not helpful in allowing athletes who suffer ACL injuries from getting back to their full strength and a return to sport with the one hundred percent function they had prior to suffering the injury. The quadriceps muscles inhibitory firing pathway is particularly a problem from a return to sport perspective, as it means that the quadriceps muscles will always be weaker than before the ACL injury, and this is born out from most studies of quadriceps strength after injury, which show a continued deficit of at least 5-10 percent injured limb compared to the unaffected limb, and that is when rehabilitation of the injured limb is done post-injury or operation, and is even higher when it is not. Furthermore, the altered firing synergies, even those of the increased hamstring firing, appear to be sub-optimal from a functional pattern of movement perspective, even if they are protective, and there even appears to be whole body / both limb firing pattern changes, with athletes favouring the injured leg and taking more weight on the uninjured limb even if they are unaware of themselves doing this (though some folk speculate that using crutches for a prolonged period of time after ACL injury may be in part a cause of these whole limb and gait changes). These changes surely are at least to a degree responsible for the high rate of re-injury of the damaged ACL observed in those athletes who return to competitive sport after ACL injury, and potentially the high rate of ACL or other knee joint injury in the unaffected limb which some folk suggest occurs with return to sport after ACL injury.

So therefore, sadly for those who suffer ACL (and other) knee injuries and want to return to competitive sport, or to their pre-injury level of sport, redundant neural mechanisms between the knee joint and the surrounding muscles, while functionally being designed to give a measure of protection to the knee joint in the case where the ACL is damaged or absent, paradoxically ensures by its very activity that the function of the surrounding muscles is attenuated, particularly in the quadriceps muscle, and they will never have ‘full’ functional activity of the knee joint after the injury, despite them having a brilliant surgeon who performs a perfect mechanical replacement of the ACL surgically, and despite the best rehabilitative efforts of either the athlete or those assisting them with their rehabilitation. An athlete has two choices after suffering an ACL injury (and other associated ligament injuries which worsen the prognosis even more). Firstly, they can attempt to return to their sport as they did it before their injury but with changing how they perform it by ‘compensating’ for their injury – if in team sports by improving other aspects of their game so that their reduced capacity for agility and speed after injury is not ‘noticed’, and in individual sports by altering pacing strategy or style of performing their sport (though particularly in individual sports this is not really an option and the loss of competitive capacity is ‘painfully obvious’), and with the awareness that that they have a good chance of re-injuring themselves. Secondly, they can downgrade their expectations and level of sport, either retiring from their sport if competitive or changing the level of intensity they routinely perform their sport to a lower level, as hard as it is for athletes to come to terms with having to do this. But there is no ‘going back’ to what life was like before the injury, and this creates a potential ethical dilemma for those involved in rehabilitating athletes after ACL injury – if one works on increasing for example their quadriceps strength, one is ‘going against’ a natural protective mechanisms ‘unlocked’ by the ACL injury, and one may be paradoxically increasing the chances of future damage to the athlete by the very rehabilitation one is trying to help them by doing it, and one should perhaps rather be ‘rehabilitating’ them by working on their psychological mindset so that they are able to come to terms with the concept of permanent loss of some function of their injured knee and the need to potentially look for alternative sporting outlets or methods of earning their salaries.

The wonderful period of my life as a PhD student back in the early 1990’s, learning about these exquisite neuromuscular protective mechanisms surrounding the knee joint that are ‘activated’ after knee ligament injury (and potentially meniscal injury too), started a lifelong work ‘love affair’ with the brain and the regulatory mechanisms controlling the different and varied functions of the body, that has lasted to this day, and ‘unlocked’ a magical world for me of neural pathways and complex control processes that has ensured for me a lifetime without boredom and never a moment when I don’t have something to ponder on, apart from initiating an amazing ‘journey’ trying to understand how ‘it all works’. But this scientific exploration has not helped me fix my knee joint after the injury all those years ago – my left leg has never been the same again after that injury which required a full meniscectomy eventually as treatment, and still swells up if I run at all and even if my cycle rides are too long, and the muscles around the affected knee have never been as strong as they were no matter how much gym I do for them. So by understanding more about the nature of the mechanisms of response to something as major as anterior cruciate ligament knee injury, I have also come to understand more about the concepts of fate and acceptance of things, and that a single bad landing (or indeed having one beer too many leading to that bad landing) can create consequences that there are no ‘going back’ from, and that will change one’s life forever. After a bad knee injury, nature has given us the capacity for a ‘second chance’ by having these redundant protective mechanisms, but that second chance is designed to work at a slower and more relaxed pace, and with the caution of experience and the conservatism the injury engenders, rather than with the freedom of expression that comes with youth and the feeling of invincibility associated with it. Rivers do not flow upstream, and we don’t get any younger as each day passes, and our knee joints sadly will never be the same again after major injury, despite the best surgery and rehabilitation that one gets and does for them. Nature ensures this ‘reduction in capacity’ happens paradoxically for our own ‘good’, and the biggest challenge for clinicians is to understand this and convey that message to the athletes they treat, and for athletes it is to accept this potential ‘truism’ too, and let go of their sporting ambitions and find a quieter, more sedate life sitting on the bank of the river they used to ride the flow of prior to suffering their knee injury. But please left knee, let me have a few more good bike rides in the cool morning air far from the madding crowd, before you pack up completely!

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About Alan (Zig) St Clair Gibson

Professor Alan (Zig) St Clair Gibson MBChB PhD MD - Associate Dean (Research), Faculty of Health and Science, , University of Essex, United Kingdom View all posts by Alan (Zig) St Clair Gibson

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