Demarcus Cousins’ on-court future: Is his body fundamentally compromised?

Hey everyone, it’s Raj from 3CB Performance. Demarcus Cousins picked up another serious
injury – a complete anterior cruciate ligament, ACL, rupture – in his left knee playing in
a pick-up game while trying to get back to 100% fitness after an achilles rupture in
late January 2018 while playing for the Pelicans and a partial left quad tear in the first
round of last seasons’ playoffs while playing for the Warriors. Obviously another major injury – his third
within eighteen months – on the same leg is clearly a major cause for concern, especially
as he’ll now have another 7+ months of rehab, lost fitness, and even more residual deficits. However, my focus in this video is to take
the injury analysis multiple levels deeper by explaining how the series of injuries are
all connected and why the way he tore his left ACL – aka the mechanism of injury – is
the reddest of red flags and may indicate that Cousins is fundamentally physically compromised. When a player gets hurt, of course the diagnosis
is very important because it informs you of severity, timetable and risks. However, what
I also look at is how the injury happened, known as the mechanism of injury. I’ll ask questions like: Was it contact
or non-contact? Does the injury make sense based off the specific movement during which
it happened? What other factors could be in play? These questions and answers provide a wealth
of information on potential root causes and underlying deficits that may have caused the
injury. In Demarcus’ case, his first two injuries
made sense but his ACL rupture hints at something far more nefarious and compromising. Lets
take a look at each. Demarcus’ left achilles rupture occurred
while he was doing a quick double jump on a rebound. This movement puts a huge stress
on the achilles tendon as it first has to elongate while contracting – known as eccentric
contraction and then like a spring to push off the ground. That’s a common
mechanism of injury for the achilles tendon. Further, in the lead up to the rupture, Demarcus’
game minutes had jumped up significantly which is another risk factor because increasing
week to week activity by over 10% has been found to increase muscle and tendon injury
risk by as much as 7x. This is known as the acute to chronic workload ratio. Additionally, that jump in minutes can lead
to increased fatigue which is another known risk factor for soft tissue injury. Demarcus’ left partial quad tear – like
his achilles tendon rupture – also made sense based on the MOI. He was chasing after a loose
ball and decelerating to gather it. This movement created a triple stress on the quads – specifically
the rectus femoris muscle – as it’s actively involved in flexing the hip AND eccentrically
controlling knee flexion (bending) to slow down the front leg and create a stable base
of support, all on the dead run. That’s a massive stress on the rectus femoris
which was potentially already weakened from residual muscle atrophy that’s been shown
to occur for up to two years on the injured leg after an achilles rupture. Additionally, the quads were likely taking
on more stress than usual for three reasons: Firstly, a weakened achilles and calf complex
– again from the achilles rupture – means a larger force shockwave into and above the
knee. Secondly, the playoffs are a higher intensity
setting which leads to increased physical exertion and load through the body. To that
point, the research shows a positive relationship between match intensity and injury risk. Thirdly, all the muscles in his left leg – including
the quads which are major stabilizers and movers – were compensating for the recovering
achilles tendon and taking on more stress. Demarcus’ ACL rupture doesn’t make much
sense based on the MOI as he injured the knee while loading up his left leg to finish a
right handed layup. This movement typically stresses the quads to control knee flexion
(bending) and stresses the hamstrings and calf complex to control the tibia (shin bone) as it translates forwards. And yet, Demarcus – who had also lost considerable
weight to decrease the amount of load and force he was putting through his body – ended
up fully rupturing the ACL. This sequence places very mild stress on the anterior cruciate
ligament but nothing that comes close to even moderately tensioning it, let alone completely
rupturing it. It’s a complete mismatch of movement and
injury which immediately led me to believe that Cousins’ left leg has been fundamentally
compromised. A key component of biomechanical function
and physical viability is a concept known as “active vs passive stabilization”. Active stabilization refers to the body’s
muscles and tendons actively contracting during movement to stabilize joints and attenuate
stress. They’re the body’s main shock absorbers. On the other hand, passive stabilization refers
to anatomy like the ligaments and joint capsules which don’t actively contract but provide
added static stability to help keep joints within their normal range of motion. These passive constraints are secondary stabilizers
and generally don’t attenuate nearly as much stress as the active stabilizers. To
that point, we’re seeing more and more research showing that after an ACL rupture, extensive
rehab and muscle strengthening can be just as effective as surgical intervention and
rehab. Highly functioning muscles and tendons can actually make up for the loss of stability
from the ACL. When Demarcus loaded his left leg to jump,
his left quad, hamstrings, and calf/Achilles complex – the primary active stabilizers during
that movement which should’ve been taking the majority of that load – didn’t, leaving
the ACL to fend for itself and take on a level of stress it wasn’t built for, resulting
in the full rupture. This lack of active stabilization is an extremely
red flag and fundamentally compromises the mechanics and function of the body. There
are two primary underlying reasons I can think of for why Demarcus’ active stabilizers
were compromised: The most obvious reason is muscular strength
and endurance deficits. As I said earlier, the research shows it can take over two years
to achieve equal side to strength after an Achilles rupture with calf atrophy lasting
even longer. Further, you add his partial quad tear which
further exacerbates the side to side strength deficits. The cherry on top is that Demarcus was in
rehab for the better part of 18 months which naturally results in a loss of overall fitness
as well. This only compounds the strength deficits as well. The neuromuscular system is the connection
between the nerves and the soft tissue – muscles, tendons, ligaments, and so on. The wiring – the nerves – signal the machinery – the soft tissue – to turn on when they’re needed. If that connection is damaged or hindered, it leads to altered muscle and tendon activation
and altered proprioception, which is your body’s unconscious awareness of joint positioning,
transmitted to the brain by tiny cells called proprioceptors housed in muscles and ligaments.
In other words, the active stabilizers are impaired because the nerves aren’t telling
them what to do or when to do it, as quickly as the nerves should be. Research shows that injuries – particularly
those with excessive swelling – can hamper and inhibit the neuromuscular system, called
neuromuscular inhibition. Further, recent research is actually showing that the brain
itself is affected after certain injuries with changes to the brain’s postural and
movement control centers. This isn’t only after severe injuries, even minor ankle sprains
are potentially resulting in those brain changes. Everything in the mind and body is connected
and now the research is beginning to reinforce the practical changes. Even if we do assume that Demarcus’ muscle
and tendon strength and endurance was the level it needed to be, it wouldn’t matter
if the wiring wasn’t working. That’s the danger of neuromuscular inhibition, it fundamentally
compromises the entire system. All in all, I had a positive outlook for Cousins
when the team originally signed him – he was extremely motivated, lost significant weight
to decrease the load on his body, the partial quad tear had healed, and the research shows
it typically takes about two years for players to return to pre-injury levels after an Achilles
rupture. I was looking forward to seeing him really
ramp up closer to his old form as he hit that two year mark near the 2020 All-Star break
and into the playoffs. But that all changed when I saw how the injury happened and the
mismatch between mechanism and severity. The red flags began waving. Accordingly, I’m fairly confident that if
he didn’t get injured now, it would’ve happened at some point during the season.
These fundamental deficits now indicate to me that it’s an extreme long-shot for him
to ever get close to his previous form or perhaps even make it through a season healthy
as he faces yet another lengthy 7-9 month rehab process, even more residual deficits
that will further build on and compound his current ones, and another overall loss in
fitness. The key thing for him right now is simply
to get his mind right. Thanks for watching. My goal is to provide
you with in-depth, evidence based, narrative free analysis and you can always find me on
IG and Twitter @3CBPerformance along with my own YouTube channel where I deep dive into
player injuries of all shapes and sizes. 3CB out.

3 Responses

  1. icky micky says:

    this was a fantastic breakdown– i had never heard of many of these concepts (like moi and the different stabilizations), and while im obviously not an expert, i feel like i could explain it to someone else 🙂 great video all in all; i appreciate the boundary between on and off court situations

  2. Eddie Torres says:

    Another great video. Keep it up. U r providing very informative videos with swift editing

  3. Nate Dixon says:

    The visual aid of describing a mismatch by showing Danny Devito and Arnold Schwarzenegger together from the movie Twins was a nice touch.

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