MCL Sprain Diagnosis & Valgus Stress Test

A bit about me for those of you curious...
I'm currently a third medical student (26M), living life one day at a time. I'm not the smartest student but I have a passion for helping in the community. I spent the first 2 years helping out with projects and volunteering as much as I could. 2 years later I'm still enjoying life. I go to school at a 4 year program, with a emphasis on clinical reasoning "learn what you need to be clinician with character" model.
What is Med like...?
It's hard, the article "101 things you wish before starting med" is true and its gets worse the further along you go. There are busy times especially during exam season. Flip side you learn so many cool and interesting things. Anatomy is hit or miss, those that love it the course wont go into enough depth, and those that don't it can feel overwhelming. Suturing cuts is a lot harder to do with a real person than on poultry. Suturing skill takes a long time to master compared to many other skills.
Each year of pre-med, med, residency, has its own challenges that you have to get through. It's always take it a day at a time.
Pre-med = "will you become a doctor?"
Med = "What kind of doctor will you become?"
Residency = "Where will you be a doctor?"
Overall, through medicine and even into first year residency (what's called a junior resident) you face so many "IDK WTF I'm doing..." moments over and over. But it all gets better with time, reminding yourself so many others made it through. Some of the coolest specialized doctors that have awesome skills were once in your shoes. Medical Students, Residents, and Doctors are great at masking their internal feelings really well.
What kind of doctor do you want to be?
OBGYN, I usually get heads turning because I'm a guy. I had an inkling before I started med, after I held my oldest sisters set of twins (her youngest ones). I explored my interest early on in med school and fell in love with it. Even after 2 years of school, I'm still super passionate about it. The most relaxed, peaceful, intimate births I ever saw were actually midwifery births. Having a midwife as a research supervisor she offered me the opportunity to be there for a few natural home births. Their isn't a right or wrong way with birthing practices as long as its a safe experience.
This question comes up a lot especially during your third year. Its usually asked like so "what do you want to do?", "what you want to be when you grow up?", "what are you interested in?", "What you want to do with your life?". Doctors and nurses ask about it way more than most lay-people unless they know a few doctors.
What are some cool memories.?
My most found memory was delivering my first baby as a first year medical student. I have since developed a passion for obstetrics. After delivering four more I found I enjoy that special emotional moment. Mom was a ER nurse that was having her first baby. I barely remember what I was doing during it because I was so nervous. After it was all done, I can remember the mom asking "How many babies have you delivered?......". The doctor looks at me and says "go ahead". The mom continues "Tell me I'm your first!".... I nod and say "Yeah".
After working a 24-hr shift with my doctor mentor. She drove me home after a long night. I still fondly remember the care she did in helping on that wet 8am morning. I always admire her ability to focus so much on personal growth. Her clinical practice has had such a positive influence on me as a future doctor (one day)!
One busy afternoon shift on the labor floor, there was no beds open, no assessment beds, with 6 women lined up in labor (waiting to be assessed). The staff were so overloaded, including my doctor mentor I was working with. I was tasked by my mentor to transport a woman (with twins) in labor to the ultrasound department. One catch she was a ruptured placenta previa! Basically the placenta is over the cervix and bleeds like crazy when the water breaks. The whole time I thought to myself 'I hope this woman doesn't die on me!'.
During the start of the pandemic I volunteered a lot with covid-testing. Granted I was in a high risk area testing a number of people, but it was thrilling. It was a rush to do the screening tests day after. I became an infectious disease fanatic during lockdown.
Any cool/amazing experiences in the hospital/clinic/etc...?
I did an optional experience in the NICU, where I toke care of a number of sick babies over a month. Day one the doctor I worked with, hit me with loads of questions around chest x-rays in newborns. I had no clue how to answer her. She walked me through afterward. Granted a harsh way to learn, but at the end I still know all the tubing placement really well.
During my same NICU experience, I got the opportunity to help out with a neonatal resuscitation. Oh man it was a emotional experience! Seeing this sick baby that was struggling to make it. I had a hard enough time being there, I couldn't image being the mother (who luckily wasn't in the same room). How could the doctors and nurses work in this field?
Once I went to assess a man with really bad prostate cancer to determine whether he could get surgery to cure him. It was an emotional interview, poor guy was almost crying the whole time. In the end he qualified for surgery which was relief. But its one I still look back on. He only learned he had aggressive prostate cancer 2 months before I he came to the clinic, had imaging, a biopsy.
I volunteered to help a 5th year resident with seeing patients in the hospital after surgery at 7am. He came 20 minutes late, which left me to see each patient on my own. One patient (whose surgery I was present for) suddenly had extreme pain just above his bladder. I'm there trying to figure out what's going on as a rookie. Documenting in the computer as I'm fumbling. I finally called the resident to come over and look him over. He comes takes a 30 second check, which involved touching his stomach area and hips. He asks the nurse to get an x-ray, and check his hydration every 2 hours! I told him I had to leave for a meeting in 20min. He approves and lets me leave. What a morning for things to crash!
My first trauma patient was a youngish woman that had appenditicitis. I thought she need surgery, but the residents and even the doctor supported just medications. It helped highlight that context is everything with medical/surgical treatment. There's general rules but still need to think every option.
My first call shift involved 26 hrs awake no sleep. It was the first time I experienced a patient yelling at me. A middle-age man came in with a painful hernia, came to the ER. I went to see him, asked him a bunch of questions and examined the hernia. Consulted the resident and got he set for an operation. He goes upstairs and gets crabby with the nurses asking "Why am I in the hospital?! What are you guys going to be doing?!!". A nurse calls and ask if I could talk with the patient about what's the plan moving forward. I go to see him and he yells at "I'm going to be having surgery?" As calmfully as I could told him "I see your upset, we're trying our best to help you, I'll let you know what were doing, than explain what's going on...". I elaborate "We need to do a hernia operation to prevent your small Intestine from getting caught inside the bowel. We just need to book space for your surgery right now... We are behind because we have 2-4 emergency operations tonight and 3 other minor surgeries to do yet."
My first day of orthopedic surgery was a hallux valgus osteotomy. It was surprising and shocking at the start because orthopods are violent with use of chisels, hammers, saws. I felt off for the first two but I managed to cope with the 3rd/4th one. The surgeon got me to suture during every procedure to as best as I could. Gave me feedback as I went along. At the end of the day the surgeon told me "You might want to practice your suturing when you can, try to look good when you get onto OBs rotation." - tba (Feb/mar 2021)
During Ortho, I got to spend the day with a new surgeon that just finished fellowship. He was working in the sports clinic elective OR on a really big tall man with a completely torn ACL. The surgery was to replace the ACL. The surgeon let the fellow start off the surgery with measuring the patellar tendon then removing a piece of it with some bone. The surgery did not go well, as the fellow removed too much tendon. The surgeon advised him to try to limit mistakes because the can really pile up. He also didn't remove enough bone to graft into the knee. To make matters worse the fellow instead of preparing the surface of the ACL for reconstruction. He completely destroyed the PCL (the good ligament) all while the surgeon was prepping the harvested ligament and bone removed from the patellar tendon. When the surgeon came in and realized the damage he had a difficult time holding himself together "he was that frustrated'! He told the fellow to leave the room which he did. He tried to fix the damage but unfortunately the PCL was too badly damaged to repair, so he bandaged the leg and transferred him to the nearby hospital. He contacted the fellowship director for a complaint and carried on with the rest of the OR slate (this is when Covid was starting to get bad). I didn't do much to help aside from suturing the ports and incisions. I felt bad for the patient, surgeon and even the fellow. It was all around mess to try and clean up.
On my single call shift during orthopedic surgery. I followed the resident to assess a 10-year-old boy that injured himself after falling off a swing. On X-ray of his arm it appeared broken and needed urgent surgery. When we went to see him, he looked uncomfortable and mom did not look very well either. I still recall seeing this subtle bruise on the elbow on the inside. His pulse was also faint as well. The resident started in on booking the OR while I documented the encounter. I wish I got to see that surgery but unfortunately I was stuck in the ER seeing another patient.
What do you do in your Free time?
Well I like to make reddit posts, have a bunch from an older account elsewhere. I learn and make cool memes.
I visit and talk with my mom a lot. She's fascinated by the many cool things that I experience and learn day after day. I still find her life story so amazing in many ways. She's lived a life unlike anyone I've ever heard.
I recently decided to improve my health through doing Yoga daily for 15-25 minutes a day. With lockdown in effect where I live, theres not option to live the house. On top of that I'm super busy with hospital shifts what free time do I have.
Describe your ideal job and work?
Well I'd ideally like a surgical practice. I love working with my hands and I love the intensity of surgery. I feel like I could be there all day there, doing procedure after procedure. I've sat a number of times at home in my free practicing suturing to get those skills down. Outpatient clinic is nice because it breaks the monotony and you get to understand your patient more than in the OR.
Where are you at with your clinical training? (... rotation)
Before I started in the hospital I have had clinical training in OBGYN, and Neonatal/perinatal medicine, and community walk-in Family Medicine. Other areas I've spent some time in (like a day) include urology, forensic pathology, infectious disease, oncologic surgery, nephrology, cardiology, Emergency. My clinic rotation experience is described elsewhere.
My current rotation is Anesthesiology.

Would You Rather Go 30 Days Without Your Phone Or Your Entire Life Without Dessert?

Dessert, all those calories gone. I don't care about candy or dessert anyway. Its a sin in med school to order non-diet drinks. Bring a box of regular coke or Pepsi none takes it. Coke Zero, Diet Pepsi, diet ginger ale ONLY. lol
Going 30 days w/o a phone is impossible in healthcare. I would need to have a 30-day vacation for that to be possible.

Would You Rather Be The Best Player On A Horrible Team Or The Worst Player On A Great Team?

The latter = as a struggling stressed out med student, I related to the later case. One of the many medical doctor adage is "P stands for Physician". If your a real medical student you celebrate a passing score regardless of your 1st or 100th. Just don't be the one that fails it leaves you an emotional mess. Its one thing to celebrate the success of getting into med its a whole other experience celebrating graduation.

Who Or Where Would You Haunt If You Were A Ghost?

The operating room would be nice. I could still watch surgeries without hassle. No anyone asking why am there. No risk of fainting from low blood sugar or from feeling overwhelmed. No need to worry about wearing scrubs.
The catch: you wouldn't be able to help out with the surgery in any way. Which is the coolest part of the whole experience. Even holding the retractors or laparoscopic camera helped stay far more engaged.

Have You Ever Worn Clothing With The Labels/Tags Still Attached?

A few times, the most embarrassing was leaving a sticker on my ass cheek.
Scrubs have barcodes attached that

If You Got Stuck In An Elevator And Were Forced To Listen To Only One Song, What Would It Be?

Taylor swift - shake off
Please no Deaf Leppard, or Led Zeppelin. Literally every surgeon I've worked with so far listens to heavy metal all the time.

Who Would You Most Like To Sit Next To On A 10-Hour Flight And Why?

Someone who will to talk for a good portion of the trip. Flying is almost inevitable as a healthcare provider, you do it enough times a year. Best to make the trips as nice as possible. Being able to talk and share personal stories through the flight makes time fly by faster.

last edit: 11-21-2020 ... 11-08-2020 ... 10-31-2020 ...

[OC] The Correlation & Causation Between Hip Width and Knee Pain

Injury breakdown: Why the Lakers have been so conservative with Lonzo’s MCL Injury

Hey what’s up ya’ll – I filmed this vlog & wrote a blog about a week ago on Lonzo’s MCL and conservative rehab timeline. Sharing it today, hopefully in honor of Zo’s return tonight. I’ll do my best to answer questions as promptly as I can.
For reference - I’m a Doctor of Physical Therapy
Streamable:
Vlog Part 1
Vlog Part 2
Blog:
Why are the Lakers being so conservative with Lonzo’s MCL injury?
Lonzo Ball's MCL injury occurred on January 13th during the overtime win in Dallas and hasn’t played since. The team only specified the exact nature of the injury – an MCL grade I tear - after photos were released of Lonzo with a TENS unit on the medial (inner) aspect of his knee:
https://imgur.com/fMP8KsS
Don’t let the word “tear” scare you, any sprain involves tearing of fibers, it’s simply a matter of extent.
In general, a grade I tear is the mildest as grade I = 0-25% tear, grade II = 25-75% tear, and grade III = >75% tear, basically a full rupture.
The usual timeline of recovery and return to sport for an MCL grade I injury is 1-3 weeks. We’re now coming up on nearly 4.5 weeks and Lonzo's MCL still has him on the sidelines.
So what gives?
Is the team hiding something, is Lonzo too busy promoting BBB to do his rehab, or something else?
In my expert opinion, the ultra conservative timeline makes sense based on the MCL’s structure, function, how it affects basketball movement, and Lonzo’s specific style of play.
Let’s start with the structure and function of the MCL itself.
I. What is the MCL and what does it do
MCL Structure
The MCL is a flat broad ligament on the medial (inner) aspect of the knee – it originates on the femur and attaches to both the tibia and meniscus. Take a look:
https://imgur.com/Lld1DgM
MCL Function
The MCL is one of the four major knee ligaments that passively stabilizes the knee - 3 of the 4 major ligaments are pictured above (only the PCL isn’t pictured, it resides on the posterior aspect of the knee).
The MCL stabilizes the knee in five key ways:

Resists valgus force: valgus refers to a sideways force that is traveling lateral to medial. This picture illustrates it: https://imgur.com/2zTqg9Q
Provides rotational stability, particularly when the knee is extended
Prevents hyper-extension of the knee
Provides joint proprioception
1. Proprioception refers to a sensory feedback loop that gives your brain data on the angle and velocity of your joint. This allows your brain to make adjustments and if needed create an active muscle contraction to provide an active stabilizing force.
2. Ligaments, when tensioned, are key players in providing that information. Over-stretching of the ligament can result in this proprioceptive feedback loop being impaired.
Takes load off the ACL, prarticularly by helping with rotational and extension stabilization

So how does this general function of the MCL apply to basketball movements?
II. Lonzo Ball's MCL and basketball movements
If you’re thinking “the MCL is basically involved in every basketball movement” – you’re spot on.
However, there are specific things to look at, some less obvious than others.
Valgus force movements
Basketball is rife with valgus force.

Lateral movement
1. Things like pushing off laterally and reversing direction while defending, a jab-step, lateral explode off the dribble, crossing-over, etc. all create valgus force at the knee at the knee and tension Lonzo Ball's MCL.
Running
1. Each time your foot hits the ground during running, there’s a valgus force at your knee. This is due to the kinetic chain of your foot and hip.
2. When your foot hits the ground, it pronates (flattens) to absorb force. Your tibia is coupled to your foot (specifically the talo-crural joint) so it internally rotates. Your femur is coupled to your tibia so it also internally rotates. This chain biases your knee into an inward (valgus) position.
3. At your hip, the force from the ground (ground reaction force or GRF) travels up into your hip and tilts the pelvis up, resulting in hip adduction. This also biases your knee into a valgus position.
4. Here’s a look at the anatomy and what it looks like in real life: https://imgur.com/BnMWaF7 https://imgur.com/jNyWaiC
Landing
1. The mechanics of landing are basically the same as running once your feet hit the ground – however, the force when you hit the ground is amplified significantly.
2. Some studies have shown that dropping from a height of 60cm (roughly 24 inches) results in a vertical ground reaction force (VGRF) that’s roughly 6.5x your body-weight. The average NBA vertical jump is roughly 71cm (roughly 28 inches).
3. There are also other landing factors that affect the amount of force produced. These are landing strategy (2 feet vs 1 foot), foot placement( fore/midfoot vs heel), and knee angle (soft bent knees vs stiff straight knees). The latter - 1 foot landing, heel foot placement, and a stiffer knee angle - all increase the amount of force when landing.
Jumping
1. The loading phase of jumping results in a valgus force at the knee – this cringeworthy picture of RG3 at the NFL combines demonstrates that: https://imgur.com/1H3wu7P

Rotational Movements
Basketball is also rife with rotational force.
Pivoting, changes of direction like when navigating screens or having to quickly tag and recover defensively, turn and go on fastbreak, etc. all require rotary stabilization of the knee and put extra load on Lonzo Ball's MCL.
Hyper-extension
Decelerating puts a significant load on Lonzo Ball's MCL and knee to control extension.
Basketball is full of quick and dynamic deceleration such chasing after a long board and then stopping on a dime to avoid going out of bounds, chasing down a defender on the break and then slowing down to get into good defensive position, closing out hard and then stopping to guard against the drive, etc.
These all require extension stabilization of the knee and create added stress on Lonzo Ball's MCL.
Unanticipated movements
Basketball is a contact sport - don’t tell James Harden - that involves multi-tasking and multiple variables that you can’t control. This is inherently going to result in a risk for unanticipated and potentially awkward movements.
In these non-ideal scenarios, the Lonzo Ball's MCL needs to be strong and functioning appropriately.
III. How does Lonzo Ball's MCL affect his role and style of play?
There are unique aspects of his specific role and style of play that put more load & responsibility onto Lonzo Ball's MCL.

Lead guard role
1. As a perimeter defender who is often involved at the point of attack, it’s imperative that he can move well, stop, change direction laterally and be able to navigate PnR coverage effectively.
2. As the primary ball-handler, he’s often involved in attacking defensive PnR coverages. This requires laterally exploding around the screen, attacking the big, getting into and navigating the paint, changing directions quickly whether to re-route his drive, double-back for a second screen, or find a shooting window behind a sagging coverage. In each of these cases, Lonzo Ball's MCL is absorbing constant valgus, rotary, and extension loads.
High pace
1. Lonzo – by all accounts, for his entire life – has always played at a high pace and breakneck speed. He is running more than most players and constantly starting/stopping at high speeds – resulting in increased load on his MCL.
Rebounding rate and penchant for weak-side shot blocking
1. Lonzo's penchant for rebounding and blocking shots means he’s jumping and landing more, often in crowded spaces.
2. More jumping and landing reps means an increased load on his MCL. Additonally, landing in crowded spaces results in increased variability in his landing mechanics which increases the stress on Lonzo Ball's MCL.
Multi-tasking while rebounding
1. A really unique trait of Lonzo – and part of what makes him so dangerous when rebounding – is he will multi-task during landing by looking up-court while grabbing the board to take a mental picture and then instantly throw his hit-ahead passes.
2. This can result in increased variability of landing as Lonzo's relying more on sensory feedback to control his landing (more on that below) and, you guessed it, added stress to his MCL.
Vertical jump
1. Zo has significant vertical bounce – he’ll consistently do it when he’s going after boards but it’s most evident if you watch his dunk reels, the kid can get up.
2. That jumping height results in increased valgus force while jumping and landing, significantly increasing the amount of load through his MCL. However, Lonzo has two mitigating factors to reduce that force: he usually jumps off two-feet and he's relatively light for his size.
Lakers’ defensive switching schemes
1. The Lakers’ defense is predicated on switching which results in guards switching onto bigger players. In these cases, the guards have to play with greater leverage and absorb more force while defending and boxing out – all of which means increased valgus, rotary, and extension load for Lonzo Ball's MCL.
His Jumper
1. Before everyone gets into a tizzy and starts piling on his shooting mechanics, I only threw this one in as bio-mechanical food for thought – I went deep into the rabbit hole of bio-mechanics and came out with this.
2. His gather and shooting track being so far on the left side of his body likely equals a weight-shift and added load to his left leg and knee. You could use a force-plate to measure the weight transfer but I’d wager all my Southwest Airlines free drink coupons that it’s extremely marginal and basically irrelevant as it relates to his MCL.

IV. The Rookie & Team Factor
The reality of being a premier rookie in the NBA is that it’s a brutal transition from college to the pros.
According to sports-reference.com, Lonzo played 36 total games at UCLA (including the pac-12 tournament and the NCAA tournament), averaging 35 mins per game.
The NBA regular season alone is 82 games, and according to basketball-reference.com he’s averaged 34 minutes per game thus far.
If you extrapolate that out, that’s approximately a 220% increase in sheer minutes alone! Then you factor in other variables:

Increased intensity of the play
Differences in strength and conditioning between him and seasoned players
Very limited time to recover and strengthen
Increased off-court variables (sponsorship and marketing responsibilities, more media coverage, constant travel)

Lonzo’s body and mind are basically being over-loaded. It’s difficult for players at their physical peak to stay healthy let alone a rookie. Every time I hear “these guys are just soft”, I audibly laugh – we just know a lot better now.
The last factor to consider is that the Lakers aren’t playing for all that much. Sure, they are 6 games out of the final playoff spot, just made a trade that could possibly propel them closer to contending for it, and are trying to attract free agents by showing an improvement in play…but all that pales in comparison to their long-term goals. The current risk/reward of playing Lonzo too soon completely tilts toward risk.
V. So how do all these factors inform an ultra conservative timeline?
Due to these factors, the rehab for Lonzo Ball's MCL is multi-factorial, very involved, and biases towards being ultra conservative. It’s critical he’s at 100% physically and mentally before he gets back.
The team has to address all of the following in order to heal the current injury and reduce future injury risk:

Healing of Lonzo Ball's MCL itself
- Reducing inflammation in the surrounding tissue
Correcting bio-mechanical musculoskeletal factors (such as weakened or fatiguing muscles)
- Increased knee valgus, decreased shock absorption
Addressing the nervous system
- Neuro-Muscular: muscle firing and sequencing
- Neuro-motor control: running, jumping, and landing mechanics
- Sensorimotor control: proprioceptive system (provides unconscious feedback to your brain as to where your body parts are in space & the angle and velocity of your joints) & vestibular system (inner ear, vision, and auditory - is the dominant sensory input for movement and head position – key for balance, spatial orientation, eye control, and being secure/confident with movement.)
Mitigating neuro-cognitive pain
- The body and brain become conditioned to feel pain if they are constantly put through a painful movement
- Lonzo’s activity will start with pain free movements and then gradually, incrementally progress to movements that were painful

In general, the medical staff will incrementally clear him to do more activity based on how his MCL and body responds and recovers. We’ve had a couple updates in that incremental progression in the last handful of days.
On Saturday (2/10), Lakers sideline reporter Mike Trudell tweeted: “Lonzo Ball has progressed to doing drills at full speed and hasn’t had any set backs. Next step is to drills with some contact from asst. coach Miles Simon. After that, practice w/ rest of team.
That Monday (2/12), Coach Luke Walton when speaking to the media: “Lonzo did everything in practice except the contact stuff….there’s nothing penciled in and if he’s able to do more that’s great but we won’t know anymore until we see how he feels…you don’t just go from zero practice to full contact practice, you go to doing practice non-contact and then you do some more contact, and if that feels good, then you get back to playing again.”
And finally on Tuesday (2/13), Mike Trudell summing up Luke's post-practice update: “Luke on Lonzo: ‘We’re not gonna play him tomorrow (at New Orleans). With the back to back and a week off after that, the progress is great but just doesn’t make sense to risk it right now.’”
This reiterates that the current risk/reward calculation tilts too far toward risk.
VI. The long-term prognosis for Lonzo Ball's MCL injury
I’m not worried about Lonzo’s Ball MCL in the long-term. The MCL has a very established protocol and Marco Nunes has handled himself extremely well since taking over as medical lead once Garry Vitti retired (I’d argue significanty better but that’s a different topic).
However, there’s one crucial detail we don’t know. The team hasn’t said anything about the mechanism of Lonzo Ball's MCL injury– specifically if it was impact or a non-impact injury.
Although every injury is worrisome and needs to be addressed, an impact injury is significantly less worrisome long-term than a non-impact injury.
An impact injury is simply too much force from an external variable going through the MCL, resulting in a tear. It’s like coming down on someone’s foot and spraining your ankle – what can you really do about that? Not much.
A non-impact injury commonly speaks to an underlying problem – like a bio-mechanical and/or nervous system deficit – that is resulting in excessive load on the MCL. The sources of such problems are far more convoluted.
The good news is that Lonzo, by all accounts, is inching closer to returning. His activity level is increasing but there’s no set progression or timetable – if he responds well and doesn’t have increased inflammation or pain, then he gets bumped up to the next level of activity.
It’s a methodical, systematic, and very conservative return to play protocol for Lonzo Ball– and for good reason.
original vlog
original blog
Thanks for watching or reading. As always, I appreciate any support and feedback. I've had multiple requests about Kawhi - that's in the pipeline.

Research Project - Final Draft

When someone tears their anterior cruciate ligament (ACL) the medically provided options are to receive a ligament graft from either your patellar tendon, hamstring, from a cadaver tendon, or an artificially crafted replacement. It is widely known and commonly accepted throughout the world that a torn ligament, specifically one within the knee joint, cannot repair and heal itself effectively. This stigma, in addition to the research by John Feagin in the 1970’s, led to the medical field to ultimately deciding that the ACL cannot heal on its own, so they collectively abandoned suturing in favor of graft reconstruction. Having short-term memory for failures is great and that seems to be the case with suturing the torn ligament back in the 70’s and the belief that it is an ineffective procedure. However, our knowledge and technology has advanced drastically since then and the dogma that is paired with lacerated ACL’s has since been debunked. Additionally, there are other methods and technologies that have since been developed that can and do provide much greater outlooks for the recipients of such procedures. It is my belief that these newly discovered solutions need to be given more recognition. Instead of limiting the options for people suffering from a torn ACL, having to decide if they want to steal from another part of their body or by alternative means, they should at least be presented all the alternative options. In order to achieve such measures people must be informed and those with the capabilities and resources need to be more progressive in the cause.
It is the opinion of many, medical professionals included, that there are only a handful of options when it comes to ACL repair. Option one is of a graft from your own self, either from your hamstring or the central 1/3 of your patellar tendon. Option two is to receive what is called an allograft. Essentially the allograft route is to take the tendon or ligament from a cadaver and use it to replace the torn ACL. A synthetic graft is the other alternative that you would be given if this procedure was needed. Looking at multiple sources and sites that offer ACL repair surgery these are the options that you will find and that are made available. What is failed to be conveyed and that they neglect to tell you though is that there are other potential procedures that could offer a better and more desired result. Unfortunately, there are rules and regulations that prevent some of these from being available to everyone, despite promising results. One alternative procedure is known as the Bridge Enhanced ACL Repair (BEAR). This method eliminates the need for any type of graft and instead uses growth factors and cells to supplement a suture repair of the ACL.
Doing any sort of medical research is difficult. Especially when dealing with surgery the process and amount of time that it takes to be permitted an opportunity of trials with humans is extensive but necessary. Because of the sensitivity and necessity to tread lightly when experimenting with new methods of repairing the body much of the current research and studies are primarily limited to the results from animals or very small case studies. In one study they were only able to get 17 volunteers, another did a little better with 26, one only got 6 total knees from cadavers, and for Dr. Murray her tests thus far have been limited to porcine knees (pig knees). Any available methods are great but given that 1 in 300 people in the United States alone is affected by this specific injury, but until the research gets further along in the process of being effective and approved these small case studies and alternative materials are the best available options. Although the proposed new procedures have clouds of doubt surrounding their credibility and applicability to a normal functioning human being, should be no major cause to disregard all the current research and results. All great discoveries started somewhere and especially when it comes to medical advancements it is better to be safe and get it all right on a much lower risk stake than to gamble with a human’s future.
Why would you elect for surgery to repair your torn, ripped, or severed ACL? On many sites providing information about ACL tears they state something along the lines of not everyone needing a reparatory procedure. It is commonly known as a major sports injury and people enjoy arguing that it only pertains to and benefits those who are athletes and wanting to maintain their current lifestyle/careers. The anterior cruciate ligament is essential for normal knee function and stability. It prevents excessive anterior translation of the tibia on the femur, excessive internal rotation of the tibia, and knee hyperextension, protects the knee from excessive valgus forces (bending the knee sideways toward the body). For these reasons alone I am led to strongly believe that this type of surgery is essential for anyone who tears their ACL no matter what stage of life they may be in. All these functions are a pivotal part of daily living and on top of the mechanical value, when ruptured or torn it can cause swelling and pain in your knee joints. People are still able to walk and move around to a certain extend if this ligament is damaged, but it severely limits their abilities and eventually will cause pain in the joint if not treated properly and timely.
Just as any other surgery out there, the cost to repair a torn ACL is expensive. The reasoning for this has many facets to it. In order to even begin a study, it requires a great deal of funding and harmoniously with any successful and meaningful advancement (aside from a very select and rare few) time. Pair them together and it is easy to see that by the time you get to the end and final result you’ve racked up quite a bit of financial investment into the project.
“The cost of bringing a tissue engineered product through to the bedside is expensive and time-consuming , with little academic recognition for this type of work. However, this type of work can be instrumental in moving a product from bench to bedside and it can be done in the framework of an academic laboratory”
The cost for an ACL surgery is already at $18,975 on average in the United States of America. Included in this price are the procedure, hospital stay, medications, rehab and equipment as necessary. Surprisingly enough this surgery doesn’t even crack the top 10 on a list of most expensive. If we are being honest, any form of medical surgery is going to cost a small fortune. On the positive side, with procedural improvement over time the price will eventually decrease. Less recovery time equates to less medications and therapy and therefore the cost will decrease. And, when it’s all said and done, we only have one body and it’s worth the cost.
Beginning in 1916 with a lieutenant-colonel in the first world war, the biased dogma of a torn anterior cruciate ligament being unable to heal was born. The man’s name was Robert Jones and 60 years later his observation that “the operation of stitching the ligaments is absolutely futile as a mechanical procedure. Natural cicatricial tissue, allowed to mature without being stretched, is the only reliable means of repair.” was “confirmed” by Feagin and Curl when they “…published their…follow-up of West Point cadets who had ACL repair(s)…” This all accumulated in 1970 with the medical profession declaring that the ACL cannot heal and that they would abandon suturing the torn ligament in favor of graft reconstruction. You can buy into this all you want but it simply is not true, and Dr. Murray has evidence to prove it. While walking around campus one day she saw a friend on crutches and after a friendly conversation was informed by this friend (a medical student at the time) following a comment that she made that her torn ACL would not heal because, like so many others believe, ligaments cannot heal, especially the ACL. Dr. Murray found this preposterous and got to work studying up on the matter. Now thanks to her extensive research we know that this dogma is in fact not true. Within the knee cavity synovial fluid is constantly being flushed through the joint. This fluid prevents the blood from clotting which in turn negates the natural healing process of the body. Because of the inability to complete the natural healing process it led medical professionals to conclude that it was an impossible feat. With her BEAR method however, she was able to figure out a way to provide a barrier from the fluid and fill it with blood so that the ligament can heal itself over time. In summary, ligaments can in fact heal themselves they just need a little help sometimes. Plus, a bonus is that this method showed less post-traumatic osteoarthritis than other repair methods used.
There are so many methods out there already that could help in the ongoing search for improvements with ACL injuries. In a very brief amount of researching I was able to find multiple processes already in development. We need to do a better job of finding funding for the doctors and researchers in their endeavors to make these more practical and implement them for the benefit of those affected by this injury. Primarily I believe that a good amount of funding can and ought to come from the major athletic associations as well as universities. Athletes are the main contributors to the injury statistics, and it would only make sense for the organizations and universities that they play for to invest in research aimed to better improve the lives of their athletes. On a side note, these organizations and associations make billions, not millions, billions of dollars off of the athletes in their employ. From a business standpoint it makes perfects sense to invest in these sorts of studies. Universities have responsibility two-fold in my book. The first is to the student athletes that are a major financial resource to them. Secondly, it is an excellent opportunity from an academic standpoint. The school would be providing resources and opportunities to countless students, professors, etc. which can and would in turn result in notoriety and overall betterment for the medical field.
I acknowledge that there are some that may argue investing this amount of resources into one specific surgery is unnecessary and could even seem biased. However, by focusing on this one specific area it can open the doors to countless other improvements in multiple ways. For starters, by specifically putting attention into the ligaments of the knee Dr. Murray was able to discover that the body is in fact able to heal ligaments. By this discovery it opens potential methods of surgery that were once believed to be impossible. Another counterargument that could be made against my stance is from the major associations, committees, organizations and universities. We all know them to have the dogma of being greedy with their money and resources at times, but we know that they have plenty of it. However, in respect to the great and free country that we live in of the United States of America it would not be right to completely force them into it. Instead, they should act of their own volition and desire to improve in areas that need improvement.
I have spent hours looking over articles and researching the citations of the citations of the citations. All in an effort to better understand our current state of knowledge and aspirations for improvement when dealing with an injury that affects one in three-hundred people of this country. It started as a desire to know if there some way to speed up the recovery process associated with such a devastating knee injury. Unfortunately, the further I got the more my research took a turn towards improving the procedure itself and the outcomes, both short and long term, following such a procedure. It was not the outcome I set out to find but it was not a waste. I found that there are people currently and actively out there already working on improving the methods and developing new ones. Opening my eyes, it is apparent that before focusing too much on shortening the recovery time (which is still a major necessity) perfecting the results is equally, if not more, important. I hope that this will get individuals, organizations, associations, and universities with the means more invested in providing opportunities to advance the field.
Bibliography:

Davarinos, N., Nikolaos, O'Neill, James, B., Curtin, & William. (2014, April 17). A Brief History of Anterior Cruciate Ligament Reconstruction. Retrieved April 20, 2020, from https://www.hindawi.com/journals/aos/2014/706042/
Jones, R. (1916, August 5). VI. DISABILITIES OF THE KNEE-JOINT. Retrieved April 20, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2348969/?page=4
Foxworth, Domonique. “New ACL Surgery Could Cut Rehab and Recovery Time in Half.” The Undefeated, The Undefeated, 22 Sept. 2016, theundefeated.com/features/new-acl-surgery-could-cut-rehab-and-recovery-time-in-half/.
Kohl, Sandro, et al. “A Novel Technique, Dynamic Intraligamentary Stabilization Creates Optimal Conditions for Primary ACL Healing: A Preliminary Biomechanical Study.” The Knee, vol. 21, no. 2, Mar. 2014, pp. 477–480. EBSCOhost, doi:10.1016/j.knee.2013.11.003.
Poslusny, Catherine. “What Is the Cost of Arthroscopic Knee Surgery in the U.S.?” New Choice Health Blog, New Choice Health, 24 July 2018,
Hao, Zi‐Chen, et al. “Stem Cell Therapy: A Promising Biological Strategy for Tendon-Bone Healing after Anterior Cruciate Ligament Reconstruction.” Cell Proliferation, vol. 49, no. 2, Apr. 2016, pp. 154–162. EBSCOhost, doi:10.1111/cpr.12242.
Parker, G., Parker, G., Garrett, Parker, G., & Garrett. (2020, April 8). How Much Money Can an NFL Draft Pick Make? Retrieved April 20, 2020, from https://moneyinc.com/much-money-can-nfl-draft-pick-make/
Who We Are. Retrieved April 20, 2020, from http://www.ncaa.org/about/who-we-are
Quinn, E. (2018, October 2). 10 Tips to Speed Your Recovery From ACL Surgery. Retrieved April 20, 2020, from https://www.verywellhealth.com/recovering-from-acl-surgery-3120753
Al Muderis, Munjed. “ACL Reconstruction Treatment Options.” Munjed Al Muderis: Hip Surgeon Sydney, www.almuderis.com.au/knee-surgery/acl-reconstruction/information/acl-reconstruction-treatment-options
Cluett, Jonathan. “Which Type of ACL Graft Should You Choose?” Verywell Health, Verywell Health, 26 Oct. 2019, www.verywellhealth.com/acl-surgery-graft-options-2548474
“How Much Does ACL Reconstruction Cost? - CostHelper.com.” CostHelper, health.costhelper.com/acl-reconstruction.html.
Meister, Martin, et al. “ACL Suturing Using Dynamic Intraligamentary Stabilisation Showing Good Clinical Outcome but a High Reoperation Rate: A Retrospective Independent Study.” Knee Surgery, Sports Traumatology, Arthroscopy, vol. 26, no. 2, Feb. 2018, pp. 655–659. EBSCOhost, search.ebscohost.com/login.aspx?direct=true&db=s3h&AN=127735317&site=eds-live.
Neff, DM. “Anterior Cruciate Ligament (ACL) Surgery.” Health Library: Evidence-Based Information, Mar. 2018. EBSCOhost, search.ebscohost.com/login.aspx?direct=true&db=nup&AN=2010793816&site=eds-live.
Ochen, Yassine, et al. “Surgical Treatment of Acute and Chronic AC Joint Dislocations: Five-Year Experience with Conventional and Modified LARS Fixation by a Single Surgeon.” Journal of Orthopaedics, vol. 17, Jan. 2020, pp. 73–77. EBSCOhost, doi:10.1016/j.jor.2019.08.030.

[OC] 3 Potential Underlying Causes of the NFL's ACL Problem

Hey everyone, I’m back and on the latest edition I explore three potential underlying causes of one unfortunate reality that comes with the start of summer OTAs and camps, ACL tears.
You can find the original piece here on my sports blog TheInjuryInsight.
A running back hoping to prove his value as a starter after years of being relegated to a “situational role” takes the hand-off in a seven-on-seven drill, and accelerates toward the “B” gap. At the last second he realizes that his offensive guard hasn’t released off the defensive tackle to get to the second level and close down on the inside linebacker.
“Well, not today bro” — the running back thinks as he instinctively sticks his leg into the ground to change direction and bounce outside…and then crumples to the ground clutching his knee.
https://imgur.com/9GP5hoK
He’s carted off the field, taken for an MRI and the worst fears are confirmed: an Anterior Cruciate Ligament (ACL) rupture.
https://imgur.com/0fOSHek
All the hours he put in leading to this moment, finally on the cusp of breaking into a starting role, hitting that lifelong goal, and now he’s faced with the spectre of a nine-month (on average) rehab process with side-to-side deficits potentially lasting two-plus years and increased risk for osteoarthritis in the knee.
To pour salt on the wound, the team could even drop him with limited ramifications (the NFL is built on non-guaranteed contracts) and move on to business as usual.
This scenario isn’t the latest script for a Lifetime movie—rather it’s what happened to Jerick McKinnon of the San Francisco 49ers, and unfortunately, many more just like him. ACL tears have become a common reality for NFL players and hopefuls as they get back to OTAs and minicamps, known as “phase 3” of the NFL offseason.
Over the past five years, there have been an average of 23 ACL tears prior to Week 1 of the NFL regular season. In 2018, that number stands at 22.
The majority of these ACL tears — nearly 73 percent according to a recent study — are non-contact injuries. Unlike a contact ACL injury where blunt force trauma to the knee or surrounding area stresses the ACL beyond its capacity, a non-contact ACL tear points to to some underlying cause(s).
After rummaging through numerous possibilities, three were bouncing around in their seats yelling, “Ooooo, pick me! Pick me!”

1 — Off-Season Training Quantity and Intensity

2 — Off-Season Training type

3 —Playing surface

Lets go through each in a little more detail:

1 — Training Quantity and Intensity

In the off-season, NFL players and hopeful NFL players aren’t allowed to work out under team supervision. Rather, they’re working with trainers or on their own to get ready for OTAs and minicamp.
This opens up a whole can of possibilities as you have players who have grown accustomed to a set and segmented scheduled that are now left to their own devices.
As one retired NFL player put it:

“You wake up with nothing to do. You’ve spent months having a schedule, and now you have none.”

Naturally, this can lead to a lot of variability in training — from taking it easy and not training most of the summer to training and working hard every single day. Extensive researchshows that a specific ratio of training quantity and intensity optimally prepares the body for current and future activity.
This ratio is known as the “Acute-to-Chronic Workload Ratio.” The terms acute and chronic, in this formula, are defined as days of activity. Acute refers to activity over the past three days and chronic refers to activity over the past 21 days. The original ratio was seven days to the past 28 days, but further research showed the 3:21 ratio as being more reliable.
This ratio dissects whether the activity level in those past 21 days was appropriate in preparing for the current three days of training. Every activity on each of those days is given an arbitrary unit (AU) based on the rate of perceived exertion, aka RPE. This is a scale of 1–10 with 1 being “watching Netflix on a waterbed” and 10 being “I might die” multiplied by the number of minutes. Those units are then totaled up for that day.
So if you had a lifting session this morning for 90 minutes at an RPE of 6 and then cardiovascular training in the afternoon for 45 minutes at a RPE of 8, that would equal (90 x 6) + (45 x 8) or 900 AU for that day. These units are averaged for the acute (last three days) period and chronic (last 21 days) periods and then divided.
Taking that one step step further, lets say player “X” got a new contract last season and goes into the summer thinking “I’m set, I’m just gonna take it easy with my own workouts and then get into shape during OTAs and minicamp.” His workload ratio could look something like this:
https://imgur.com/8EYoaf6
Ideally, that number on the bottom corner (the acute to chronic workload ratio) should be between .8 and 1.3. If that ratio is lower than .8 or higher than 1.5, studies have found the risk of soft tissue injury goes up by over five times.
https://imgur.com/eYbyzkM
In this case, player “X” is woefully unprepared for OTAs and that creates a lot of risk.
I think most people understand that “doing too much too soon” and overloading/fatiguing the body may lead to injury. Whether they follow that advice is a different story, but not doing enough and under-preparing the body is potentially just as damaging.
That’s why if you’re injured and want to get back to your activity of choice, rest alone won’t cut it. You have to gradually increase your activity intensity and/or quantity or your body will be under prepared.
To further that point, harken back to Jerick McKinnon. He tore his ACL in a non-contact manner during the last play of his first practice after returning from a calf strain that kept him out most of the Niners preseason. Mere coincidence? I highly doubt it.
I’d wager that if we tracked his AU’s and acute to chronic workload ratio, he was in that “under-prepared” zone due to being limited by his calf strain.
The body needs to be prepared and loaded appropriately to be able to handle the rigors of that activity. In the same vein, it can’t be overloaded and fatigued. It needs to be just right — the Goldilocks effect.
https://imgur.com/Hl5qAmY
If the workload ratio of Los Angeles Chargers’ Hunter Henry, who tore his ACL on the first day of OTAs, was out of whack as he transitioned from his summer programming to Chargers OTAs, that would increase his risk for increased soft tissue injury, which includes ligament injuries, five times.
Additionally, these acute to chronic ratios and risks may be compounded by the shortened amount of time NFL teams are allowed to spend with players. This may seem counterintuitive at first. NFL players having longer offseasons and less practice may mean more injury risk, and there’s a perfectly valid reason why.
By numerous accounts, the shorter amount of time for OTAs and minicamps has led to teams jumping in feet first with their players on day one rather than allowing for a gradual progression of activities.
Here’s how Dr. David Chao, aka ProFootballDoc, put it:

“Because of fewer practices, there are actually no walk-throughs. Everything is full speed, so everything puts the ACL at risk.”

I can understand the rationale from NFL coaches and staffs. They’re trying to install the same amount of information and habits in less time. That lends itself to cramming things in and jumping straight into high intensity practices.
You try telling this guy to ramp down practice intensity a little bit: https://imgur.com/ZJcO56J
(Khalil Mack probably brought up acute to chronic workload ratios and that was the final straw)
For a player who isn’t prepared for that intensity or a player who is already fatigued, they’re at a higher risk for ACL rupture, so too little or too much training quantity and intensity is potential reason number one for the NFL’s barrage of non-contact ACL tears. Moving onto number two…

2 — Training Type

There are a multitude of ways for NFL players to train during the offseason: weightlifting, which itself can be divided into different categories such as strength or muscle growth, interval training, like sprints or circuit training, endurance, plyometric, ballistic, etc., etc.
However, one type of training program has repeatedly been shown in large-scale studies (click here, here, here, here, here, or here for more info) to reduce ACL injury risk: neuromuscular training (NMT). The neuromuscular system is an unconscious feedback system through which muscles are timed and activated to optimize joint stability and promote efficient and effective movement.
https://imgur.com/2LOYhNt
If we think of the physical components of the body as the “hardware”, then the neuromuscular system is part of the “software”.
The foundation of optimizing this NMT software is exercises that involve unanticipated reactions and movement perturbations. This forces the neuromuscular system to react quickly and maintain joint stability.
Here’s a video with multiple examples: https://youtu.be/XCvfIhequOc
This maintenance of joint stability by the neuromuscular system is critical for preventing ACL injuries because most non-contact ACL injuries happen during spontaneous cutting and changes in direction in which the knee drops into a valgus (inward) and internally rotated (rotated towards midline) position.
https://imgur.com/sSBuuec
If the knee continues to dive inward and rotate, there comes a point of no return where the ACL is placed under huge stress and ruptures:
https://imgur.com/rMuQo9n
Through NMT, the neuromuscular system can recognize that unstable joint position quicker (“Ah, $%&! Red alert!”) and then activate the necessary muscles to bring that joint back into a better position.
For example, let’s say Titans’ safety Jonathan Cyprien, who tore his ACL during practice in early August, had focused more on NMT during his off-season programming. I have no idea whether he did or didn’t nor to what extent, but as he made a reactive cut during practice, and his knee dropped into an inward, high-risk position, his highly trained neuromuscular system would have recognized it quicker, got the knee joint out of danger and not allowed it to reach the point of “no return.”
In other words, NMT increases the margins for error during movement.
Based on some personal knowledge of NFL players’ offseason programs and what is available to the public (I’m the first to admit this is completely anecdotal evidence), NMT doesn’t seem to be that common.
There’s plenty of:
https://twitter.com/twittestatuses/1014435104997994498
and: https://twitter.com/twittestatuses/1015780900892823552
or: https://www.instagram.com/p/BHiQiZlDETN/?utm_source=ig_embed
But I have a much harder time finding things like this: https://youtu.be/D_8ESddi3rI
From what I’ve seen and heard, Odell Beckham Jr. is a shining beacon on the hill when it comes to training variation and challenging multiple systems.
If players are in a program that utilizes NMT (neuromuscular training), the evidence shows that it needs to be done at least two times per week with appropriate progressions throughout the regiment to be be effective.
It’s a highly skilled level of training, and I’d wager a large number of NFL athletes aren’t aware of its benefits in their offseason training. As these players get back to spontaneous changes of direction during OTAs and minicamp, they’re at a comparatively higher risk for ACL injuries.
These first two underlying causes have focused on training, but the third and final possible reason for the NFL’s ACL problem takes a sudden, sharp left turn. Don’t worry, though. This piece did NMT training. ACLs are safe.

3 — Playing Surface

The more traction a playing surface has, the more likely a player is to suffer an ACL injury (click here, here, here, here, here, here, and here for more info).
Each time Los Angeles Rams’ defensive end Morgan Fox, who tore his ACL during the first week of OTAs, stuck his foot in the ground to make a cut or change direction on the drought-stricken, high-traction grass fields, that foot had a higher chance of getting caught in the ground and torque-ing the knee.
To that point, research has found that less than five percent of ACL injuries in football occurred on a wet (low-traction) surface, whereas dry, hot weather (high-traction) was linked with a higher rate of ACL injuries. Generally, cold weather has been associated with lower rates of ankle and knee injuries, including ACL tears.
Think of this high versus low-traction situation like ski bindings going to work when a skier loses control.
https://imgur.com/GEpZeGe
High-traction conditions are akin to crashing and the bindings not freeing your foot (the foot getting stuck in the grass), whereas low-traction conditions are the same situation but with the bindings releasing your foot (the foot skids along the grass), like in the video you just saw. In the latter case, your foot and knee are clear from getting twisted.
NFL OTAs and minicamps take place in high-traction conditions — the dead heat of the summer with hot, dry conditions. Players are cutting and changing directions on high-traction surfaces, which opens them up to the risk of crashing with skis still attached to their feet.
So the next time you see a player slip on a cold, chilly surface or see a rainy-weather forecast as you make your last second fantasy changes— try thanking it instead of screaming expletives.

All in All

When you combine all three factors — an inappropriate training quantity and intensity plus lack of neuromuscular reaction training plus a higher-traction surface, it might explain this trend of non-contact ACL ruptures.
A few of you may be wondering, “Well, what about knee braces? I’ve heard those can help.” There’s no evidence that knee bracing prevents ACL tears (click here, here, and here for more info). In fact, one two-year study found that ACL injury rates were actually _higher_amongst players who wore a knee brace compared to those who didn’t.
We’ve come a long way in treating ACL injuries, and they aren’t a death knell by any means, but they still place a significant and possibly preventable physical and mental burden on the player. For those players just trying to make the team, preventing an ACL injury could mean the difference between a livelihood and foundation for their family (the minimum NFL salary is $450,000).
Although we’ll likely never know the definite root cause(s) of these non-contact ACL injuries during NFL OTAs, minicamps and training camps, I hope this piece shed some light on possible causes and ways to reduce ACL rupture rates. After all, the best injury is the one that never happens.
Thanks for reading and if you liked the piece, subscribe to the email list and follow us @3cbperformance to never miss an update. Until next time.
Feel free to ask any questions or comments as always and I’ll answer asap. You can find the original piece here

[OC]Kyrie Irving's knee: The troublesome past, recent surgeries, and onwards

Hey what’s up ya’ll – this is the latest piece from my sports injury blog & resource, theinjuryinsight.
Feel free to ask questions and comments as always, will get back to you as soon as I can. Credentials - DPT.
Hope you enjoy and the original link is at the bottom.
Kyrie Irving’s knee: The troublesome past, recent surgeries, and onwards
Recent surgery to remove 2 screws and clear up an infection in Kyrie Irving's knee has ruled him out for the rest of this season. According to the Celtics medical staff, he will likely miss 4 to 5 months.
He had originally been ruled out for only 3 to 6 weeks after a minimally invasive surgery on March 24 to remove tension wires from his patella (the kneecap). However, signs of bacterial infection were found and therefore a follow-up surgery on Kyrie Irving’s knee was performed to remove two screws from his patella.
In this piece, I’ll answer the following questions:

What is the anatomy and function of the patella?
What is the full injury history on Kyrie Irving's knee?
What did the recent surgeries on Kyrie Irving's knee entail?
What factors contribute to Kyrie's return to play timeline?
Are there any long-term implications for Kyrie Irving’s knee?

I. The anatomy and function of the patella

A. The anatomy

The patella (aka the kneecap) is a flat, inverted triangular bone that sits on the anterior (front) part of your knee joint. It articulates with the femur (thigh bone) to form the patellofemoral joint and the underside of the patella is covered with a smooth substance called articular cartilage.
Here’s what the patella bone looks like:
https://imgur.com/cjzoEL0
Additionally, the patella is a sesamoid bone – a bone embedded within a tendon or muscle. The patella is connected to two important tendons – the quadriceps tendon from above and the patella tendon from below.
This picture shows that dual connection:
https://imgur.com/9iYzzaR

B. The function

The patella has multiple functions.
It physically protects the knee joint, acts as a “spacer” to reduce friction, helps evenly distribute stress to the underlying bone, and the smooth undersurface (articular cartilage) helps the bones glide easily when you move the knee.
However, the primary function of the patella is to increase the lever arm (leverage) of your quadriceps muscle. The patella increases quadriceps strength by up to 50%!
The quads take on heavy load during any movement – they are responsible for extending (straightening) your knee and help eccentrically control (“brake”) the bending of your knee
The patella does this by actually sliding down when you flex (bend) your knee and up when you extend (straighten) your knee.
Take a look:
https://imgur.com/9iu6G8a
This change in position gives the quadriceps muscle different leverage depending on how straight or bent the knee is. Think of the patella like a balance beam – it adjusts the length, direction and force of each of its arm – the quadriceps and patella tendon – at different degrees of knee bend or straightening.
In doing so, the patella has to withstand very high forces. For example, when resisting knee flexion, the force on the patella has been shown to equal four or five times your body weight.
The strength and effectiveness of the patella is key to general movement, let alone high-level sports performance like in Kyrie’s case.
Before we get into the most recent surgeries, lets go through Kyrie Irving’s knee injury history get the full context.

II. Kyrie Irving’s knee injury history

2015 playoffs

Kyrie Irving's knee tendonitis

Kyrie’s left knee trouble began in the 2015 playoffs. According to Kyrie, it began to bother him as he overcompensated for a sore right foot – which he aggravated nearly 3 weeks prior in game 2 of the Cavs first round sweep of the Celtics.
He was diagnosed as having patellar tendonitis. As an aside, the suffix –itis meaning inflammation is actually a misnomer. Tendon injuries are rarely characterized by inflammation, but rather disorganized tissue from excess wear and tear.
Kyrie’s explanation of overcompensation could certainly have played a part as pain in the foot can alter mechanics and thus change loading patterns throughout the lower body.
Additionally, the amount of activity he had in the 2014 summefall into the NBA season likely played a key role in his tendonitis. Here's a look at his brutal schedule:

2014 Summer and into early Fall
- Kyrie was practicing with USA basketball and then playing in the FIBA World Cup (won MVP honors)
2014 Fall
- Cavaliers training camp into pre-seasoon
2014-15 NBA Season
- Kyrie played 75 out of 82 games
2015 Playoffs
- Kyrie’s first playoffs

My guess is that all this activity with little rest was the root cause of his knee tendonitis - too much activity without appropriate rest is a very common reason for tendonitis, or injury generally.
The wear and tear on Kyrie Irving's knee patellar tendon kept building over time and then the foot injury and subsequent compensation were the straws that broke the camel’s back.
The patellar tendonitis got to the point where Kyrie said he was at “30 to 40” percent, and it showed during their series with the Bulls. At one point, he went 5-23 with 2 assists over the course of 2 games – even though he still played 79 minutes (that’s a whole other issue - lets just say Kyrie's knee is very happy that he wasn't traded to Minnesota and the Thibs "40+ mins a game for starters" mentality).

2015 Finals

Kyrie Irving's knee patellar fracture

In game 1 of the Finals, Kyrie Irving’s knee seemingly gave out as he was driving to the basket with 2 minutes left in OT. He collapsed to the ground holding that left knee. Here’s a video:
https://www.youtube.com/watch?v=ImUg7xG6ibw
Upon further inspection, and Kyrie echoed this in his comments in the post-game, Klay’s knee made contact with Kyrie’s as he was trying to change direction. You can see that here:
https://imgur.com/zl58VyZ
Remember what I said above about the patella being under huge stress (4 to 5 times your bodyweight) when it’s controlling knee flexion (bending)?
Look at how much bend Kyrie’s left knee has here, placing the patella under a massive load. Klay’s contact adds an extra torque - a torque that the already stressed patella cannot handle – and it fractures. An MRI confirmed the fracture.

So what is a patella fracture?

Quite simply, it’s a break in your kneecap.
It most commonly occurs due to a direct trauma (like hitting it against the dashboard during a car accident) or indirect trauma (as in Kyrie’s cause – his quadriceps is trying to decelerate his left knee bend and the added force of Klay’s contact overloads the patella). In the latter case, the velocity of the force will determine whether the actual quadriceps tendon tears or if the patella bone fractures.
Generally, the patella can fracture in a multitude of ways. This picture is a good visual summary:
https://imgur.com/ps1G99e
For our intents and purposes, we can categorize these patellar fractures into 4 types:

Stable fracture
1. This is a non-displaced fracture where the pieces of the patella may still be in contact with each other or separated by less than 3mm.
2. Surgery usually isn’t required
Displaced fracture
1. The pieces of the patella are separated and do not line up with each other. The typically smooth joint surface may also be disrupted.
2. Surgery is usually required
3. Most commonly due to indirect trauma
Comminuted fracture
1. The patella fractures into three or more pieces
2. Most commonly due to direct trauma
Open fracture
1. The patella breaks in such a way that either part of the bone sticks out through the skin or a wound penetrates all the way down to the bone.
2. Often involves significant other damage, particularly to the soft tissues
3. Extremely serious injury with a higher risk of infection in the wound or bone due to the break in the skin. Immediate treatment is needed to prevent possible infection.

Kyrie likely had a displaced fracture – specifically a transverse displaced fracture. Although the Cavs medical staff never gave full details, I can deduce that by his mechanism of injury (indirect trauma typically leads to transverse fractures) and type of surgery…which brings me to:

Patellar surgery for Kyrie Irving’s knee

The patellar surgery for Kyrie Irving’s knee is termed tension band wiring with cannulated screw fixation. It’s very commonly used in 2-piece non-displaced transverse fractures.
2 screws are drilled into the patella and then a wire is bound in a figure-8 shape to hold the bones together. Here’s what it looks like (work safe!):
https://imgur.com/tUeLs0U
It’s like lassoing the two patella bone pieces together to keep them connected while healing. Once the fracture has healed, the wires and screws no longer serve a purpose. Usually the hardware is left in unless it causes irritation.
Generally, the outcomes for patellar fracture surgery vary depending on the severity of the injury. However, some studies have shown that up to 80% of individuals who had surgery continued to report anterior knee pain (pain on the front of the knee).
Additionally, a longitudinal (long-term) study reported that individuals who had patellar surgery reported physical issues for an average of 6.5 years after the surgery. This study also noted that there was a trend towards better outcomes for the type of surgery Kyrie had (tension band wiring in combination with screw fixation).
The moral of the story is: you don’t want to break your patella…and if you do, hopefully you don’t need surgery.

2015-2016 Season

Kyrie returned from his patellar fracture surgery on December 20th. I couldn’t find any reported issues during that season.
He went onto play out the rest of the season and playoffs, culminating with his dagger 3 in Steph Curry’s eye during the final minute of the Cavs game 7 win over the Warriors (sorry for bringing that up again, Warriors fans).

2016-2017 Season

Kyrie Irving’s knee began to flare up towards the end of the season.
On March 16 Kyrie took himself out of the game due to “left knee tightness”. On March 18, he sat out the game against the Clippers. On April 7, during a game against the Hawks, Kyrie limped to the locker room during the third quarter but returned later in the fourth.
His quotes after the game were telling, perhaps some foreshadowing:

“A terrible day for me and my knee”
“I mean it’s never easy, even the year after, just to realize that you have plates and screws in your knee and stuff like that…I don’t want it to feel sore anymore”. He added that he has “to be able to deal with it”

2017 Summer

S*** hit the fan obviously. Kyrie asked to be traded and allegedly threatened to have surgery.
It was reported Irving “needs minor knee surgery as a follow up to the procedure he underwent during the 2015 Finals to repair his broken kneecap”. Although the surgery wasn’t immediately pressing, it would “ease some of the swelling and day to day pain”.
That minor knee surgery was referring to the removal of tension wire from his patella.

2017-2018 Season

Again, Kyrie Irving’s knee flared up towards the end of the season.
On March 5
th, Coach Stevens announced that Kyrie would miss their next game, vs the Bulls, due to soreness in his left knee. Additionally, Coach Stevens reported that the discomfort began during their March 3
rd game against Houston but Kyrie chose to play through the pain.
Here’s what Kyrie said at the time:

“It’s been about two years coming off knee surgery, so you have to do things like that, stay on top of it and make sure you’re doing the right things….sometimes it may be a little bit extra just from the demand you put on your body and then also the realization of how much basketball you’ve actually been playing for the last few years.”

On March 11 against Indy, Kyrie played in the first half but did not return in the 2nd half. He reportedly mentioned having discomfort in the left knee at halftime, and after the game told reporters that his knee was aching more and the soreness was taking longer to subside. Generally, severity of pain and length of residual effects are two key signs of injury progression.
Kyrie then sat out the March 14 th game against the Wizards. Coach Stevens again confirmed that it was due to the ongoing left knee soreness.
Kyrie traveled with the team for their 2-game road trip but didn't play. Shams reported that Kyrie intended to seek another medical opinion later in the week. The Celtics left for a 4-game west coast roadie but Kyrie didn't travel with the team.
On March 24, Kyrie underwent a minimally invasive surgery (the surgeon uses the original incisions to go back into the knee rather than create new incisions) to remove the tension wires from his knee. It was reported that his patella was fully healed and knee was structurally sound. His timetable for return was set as 3-6 weeks.

Why did he need the tension wire removed?

In the majority of cases, the tension wire placed during patellar surgery doesn’t need to be replaced. It’s only removed if it is interfering with joint motion or causing irritation.
The latter was the case with Kyrie and he reportedly experienced “immediate relief” after the tension wire was removed.
However, a week later, Kyrie was ruled out for the season after needing another surgery.

What the heck happened?

During the removal of hardware, it’s considered good practice to check for infection as well. The surgeons likely removed some of the fluid from around Kyrie’s tension wire and screws and tested it in a lab for infection.
The tests came back as indicating a bacterial infection and thus Kyrie went back in for a second surgery to remove the two screws. Generally, reported hardware infection rates range from 3% to 10%.
Thankfully, the infection was not caused by MRSA. MRSA can be very difficult to deal with because it can be resistant to multiple antibiotics.
Due to the possibility of infection with metallic hardware, there’s ongoing research and investigation of non-metallic options for surgery. However, this research is still in the fledgling stages but early results have been promising.

III. Kyrie’s Irving knee rehab and return to play consideration

The Celtics medical staff has set a 4-5 month timetable for Kyrie’s return. I’ve organized his rehabilitation and return to play considerations into micro (tissue and bone), mezzo (systemic), and macro (contextual) factors.

Micro (the tissue and bone)

Clear out the infection.
- Kyrie will be given a course of antibiotics to deal with the specific bacteria and the medical work-up will continue to make sure that all tissue and bone in his patella are cleared of infection. Depending on the specific type of bacteria, this can take from 2 to 6 weeks.
Bone healing
- The reason why the timetable on the second procedure is so much longer is because the screw removal leaves two holes in Kyrie’s patella. This bone has to heal and re-fill. Studies show that it can take up to 18 weeks for bone mass to return to near normal after screw removal.
Pain, mobility, strength
- Kyrie’s physical rehab will consist of mitigating pain, maintaining full knee joint mobility, and then a progressive step-wise strengthening progression.
- The key with strengthening is that you want to sufficiently challenge the musculature so it remains active and doesn’t atrophy but not the point that it overloads the patella and causes pain.
- The strengthening will begin with isometric holds (contraction without movement, progressing to contraction against resistance), move onto active movements that progressively add load, and finally progress to dynamic movement and sport-specific movements.

Mezzo (systemic factors)

Bio-Mechanics
- With any injury, especially the lower body, it’s important to evaluate the bio-mechanical chain (no body part lives in isolation). Think of this chain as a railroad track – affecting it one place, whether that’s downstream or upstream, is going to have ramifications on the entire track.
- For Kyrie’s left knee, there are two key things to evaluate – the hip abductors and ankle dorsiflexion
  1. Weak/fatigued hip abductors or poor neuro-muscular hip control can lead to the knee dropping inwards (knee valgus)
  2. Limited ankle dorsiflexion can also lead to the knee dropping inwards (knee valgus)
  3. Here's a picture of knee valgus occurring during both jumping and landing: https://imgur.com/DZJ07rC
- In both these cases, the railroad track of the lower body is affected and it throws off the mechanics at the knee.
- Dynamic and sport-specific movements
- Basketball involves a lot of high intensity, high load movements in multiple directions. Jumping, in particular, puts a large stress on the patella so it’s important to review Kyrie’s jumping mechanics.
- There’s possibility for compensatory movements due to pain or poor confidence in movement. Kyrie already mentioned this as the cause for his original left knee tendonitis (that seems like ages ago, doesn’t it?)
Proprioceptive and vestibular systems (feedback systems that inform the body’s awareness of itself in space)
- These two systems are key in providing information to the brain and making small movement adjustments and adaptations.
- The proprioceptive system can directly be affected by injury as it uses receptors near the muscles for feedback. In Kyrie’s case, residual swelling from his surgery can interfere with these receptors.
- Due to the above, it’s important for the vestibular system (your body’s primary balance system – it involves your vision and inner-ears) to be operating at its peak and mitigate potential proprioceptive deficits.
Arthrogenic muscle inhibition (AMI)
- AMI occurs due to swelling in the joint. It inhibits the contraction of the muscle. With knee joint swelling, there’s evidence of weakness in the quads because they won’t fire as effectively.
- It’s possible Kyrie has been dealing with AMI throughout his knee injury saga.
  - He’s constantly been battling irritation and soreness (which is commonly caused by inflammation) in the left knee
  - Surgery is increases swelling in the left knee
  - He may have chronic swelling in the knee due to repetitive micro-trauma of the soft tissues surrounding his knee
- It’s crucial to reduce knee joint swelling to restore normal quadriceps activity
The central nervous system (CNS) and pain science
- Kyrie Irving’s knee pain is long-standing and chronic at this point. This can have huge ramifications on his pain perception and sensitivity to it.
- The brain has one goal – protect its vessel (the body) and it’s constantly assessing how dangerous something is. If it perceives a threat, it sends a pain signal to alert the body to danger. Here's an overview: https://imgur.com/KPKFfV4
- This response can be very beneficial (adaptive) in the short-term but with chronic lingering injuries, it can become detrimental (maladaptive) and continue to send pain signals even after the tissue or bone itself has healed. This is why tissue and bone healing alone aren’t indicators that a player is ready to return to play.
- Chronic pain responses can lead to increased sensitivity of pain. There’s a saying “neurons that fire together, wire together”. Essentially, when groups of neurons fire together (like during a specific movement), they become more efficient and the threshold to activate them decreases.
- This is great for certain things like increasing the efficiency of a movement or recognizing patterns. However, when applied to pain, constant activation of the same pain circuit (like pain with certain movements or pain in certain body regions) leads to decreased stimulus required and more efficient firing of pain circuits. This means increased sensitivity to pain & increased pain response
- Another aspect of pain sensitivity is termed “neuro-tagging”. The brain creates memories of experiences (called neurotags or neurosignatures) to organize them efficiently. Each memory creates a certain output. For example, when you hear a certain song or smell a certain scent, it may instantly harken you back to a memory or experience. That’s due to a neurotag.
- The same exact thing applies to pain. A certain movement or context elicits a pain response and over time, that movement is neuro-tagged as being painful – in other words, you’re conditioned to feel pain with that movement.
- Lastly, there's an aspect of pain science that I call "fixation". When you have chronic pain, you tend to focus more and more on the body part and become increasingly aware of it. Studies have shown that the area in the brain responsible for that body part actually grows in size (this is called cortical re-organization). This creates increased awareness and feedback of that area (like “shining a spotlight on it") which leads to more pain

Macro (contextual factors)

Kyrie’s mental and emotional state
- Your mental and emotional state affects your perception of injury, your mood (angefrustration/depression/etc.), stress response, and therefore your recovery.
- Kyrie has been through a lot with that left knee.
  - We know he’s been dealing with it for years so that alone is frustrating and he’s even expressed that publically.
  - Additionally, Coach Stevens mentioned how down and frustrated Kyrie was with the most recent surgery and not being able to play in the playoffs
- However, there are also some key positive indicators.
  - Kyrie’s IG post after the Celtics announced he would be out was characterized by resilience and forward thinking.
  - Additionally, it’s been reported that he was feeling very good after the tension wire removal and Coach Stevens said it looked like he was on pace to be back closer to 3 weeks before the infection was found. That’s huge for Kyrie’s peace of mind.
The Celtics current context
- The organization itself understands the risk/reward with Kyrie and allowing his recovery to play out, extended or not. For example, here’s what Boston GM Danny Ainge said:
  - “We knew there would be maintenance issues…we’re just extra cautious. We have the good fortune of being extra cautious right now.”
- As Ainge alluded to, the team is in a really good spot. It pains me to say it as a Laker fan but it’s the obvious truth (thank you Billy King and Colangelo). They have key veteran pieces mixed in with superstars, a bevy of young talent, and multiple draft picks.
- There’s no reason to bring Kyrie back too soon, especially since they get Hayward back next year AND Kyrie goes into the last year of his contract. There’s a very salient cautionary tale this season, IT, of what can happen when you try to play your way back into NBA shape after a major injury.
- On a side-note, the Celtics may now place greater priority on re-signing Rozier who has played well in Kyrie’s absence and is a nice insurance policy in the short-term.

The under-lying takeaway of all these points is this: Patience is VITAL with his rehab and return to play timeline. There are many factors at play here other than just the tissue and bone healing, and the Celtics seem to understand that risk/reward calcuation well.

IV. Are there any long-term ramifications for Kyrie Irving’s knee

Even with successful treatment, a patellar fracture does come with some long-term risk factors.

A. Arthritis

Even with the patella being healed, the articular cartilage (the smooth substance on the undersurface of the patella) can be disrupted and damaged, leading to pain and stiffness over time.
Here's what it can look like:
https://imgur.com/0KUPOCk
Normally, the patella is fully covered in that white substance (the articular cartilage). Here you can see how it's eroded and has exposed the bone. This results in decreased gliding of the patella, changed loading patterns at the knee, and increases the risk of "bone on bone" action.
However, severe arthritis occurs in a small percent of individuals with patellar fractures. Mild to moderate arthritis is far more common.
Considering Kyrie Irving’s knee injury history, the amount of wear and tear that comes with being an NBA player, and the amount of load his quick burst, start/stop style puts on his knees – I’d say it’s more likely than not that Kyrie has to manage some pain and stiffness in that left knee - possibly stemming from mild to moderate arthritis as he gets into the later arch of his career.
Now that doesn’t mean he will have another major injury – a lot of players effectively deal with the pain and stiffness that comes along with wear and tear to their joints.

B. Muscle weakness

As I touched upon above with AMI, there can be weakness in the quadriceps muscle following patellar surgery. For some individuals, this is a permanent and often coincides with some loss of overall motion in the knee.
For Kyrie, with the medical staff and tools he has around him, I don’t consider this to be likely at all. Swelling will be managed proactively and there will be a committed focus on getting his quad strength and activation back to normal.

C. Pain

Long-term pain has been found to be common in individuals with patellar fractures. This could be due to the chronic pain science I touched on earlier in conjunction with the arthritis and muscle weakness that can develop.
As I said before, I’d expect Kyrie Irving's knee to have some stiffness and pain that has to be managed going forward. He may feel more comfortable wearing a knee brace or some support to give an added sense of stability and feedback.

V. The overall takeaway for Kyrie Irving’s knee

There’s no doubt that Kyrie Irving’s knee injury history, recent infection, and long-term risk factors are troublesome and obviously not ideal.
However, there are also some huge positives here. He felt instant relief after removal of the tension wire, the infection is very treatable, and he’s in a situation where the Celtics team is setup for the future and can be very patient with his recovery.
Lastly, I think the biggest takeaway for Kyrie from his ongoing knee saga is this:
Trying to “suck it up” and play through nagging irritation and pain rather than being proactive and treating it early often leads to much bigger issues down the line.
Here’s the original piece
Thanks for reading and until next time.
Sources: https://www.si.com/nba/2018/04/05/kyrie-irving-out-season-playoffs-knee-surgery-boston-celtics; https://www.ncbi.nlm.nih.gov/pubmed/12817660; https://www.ncbi.nlm.nih.gov/pubmed/25887644; https://www.physio-pedia.com/Patella; http://www.espn.com/nba/playoffs/2015/story/_/id/12867284/kyrie-irving-cleveland-cavaliers-left-knee-tendinitis; http://www.espn.com/nba/playoffs/2015/story/_/id/13020515/kyrie-irving-cleveland-cavaliers-fractures-kneecap-season-ending-surgery; http://www.sportingnews.com/nba/news/kyrie-irving-injury-update-knee-boston-celtics-news-nba-playoffs-finals-2015-cavs/n07pxqmg0dv31h63v6gq3clmb; https://www.ncbi.nlm.nih.gov/pubmed/27319392; http://www.vindy.com/news/2015/jun/10/cavaliers-put-players-well-being-in-good/; https://www.ncbi.nlm.nih.gov/pubmed/22902732/; https://www.ncbi.nlm.nih.gov/pubmed/26614923; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3048243/; https://cdn.bodyinmind.org/wp-content/uploads/Cortical-changes-in-chronic-low-back-pain-Current-state-of-the-art-and-implications-for-clinical-practice.pdf; https://www.boston.com/sports/boston-celtics/2018/03/26/kyrie-irving-knee-injury-surgery-update; https://orthoinfo.aaos.org/en/diseases--conditions/patellar-kneecap-fractures/; https://mikereinold.com/10-principles-of-patellofemoral/; https://www.healthline.com/health/bacterial-joint-inflammation#risk-factors; http://rebalancemd.com/wp-content/uploads/2017/08/Hardware_removal_Recovery_Guide.pdf; https://www.healio.com/orthopedics/pediatrics/news/print/orthopedics-today/%7Ba895698b-8f8d-4866-8068-6c3970fe68fd%7D/hardware-removal-is-always-more-difficult-than-expected-especially-in-children; https://www.ncbi.nlm.nih.gov/pubmed/1806500; http://www.drjoetatta.com/pain-neurotag/; https://painsciencecenter.com/the-memory-of-pain/; https://physioworks.com.au/injuries-conditions-1/patella-tendonitis-tendinopathy; http://www.espn.com/nba/story/_/id/23040436/kyrie-irving-boston-celtics-season-playoffs; https://celticswire.usatoday.com/2018/04/06/brad-stevens-explains-kyrie-irving-bacterial-infection-knee-surgery/

Transitional Species Handbook: Humans are Definitively the Descendants of A Lineage of Ape-Like Ancestors and Thus We are Still Apes (Hominids)

It is difficult to find a more scrutinized facet of Evolutionary Biology than that of our own evolutionary history. This is due to our inherent desire to feel apart from nature as it's master, rather than acknowledge our original spot seated firmly in the middle of the Serengeti food chain. There is a humbling that must occur to see oneself in the ancient apes of yesterday, scraping about in the dust of the East African Rift Valley, and yet this past of ours it written in our very bones: from how we walk to how we talk.
The following post will explore this journey from the first true hominid to ourselves, and examine why our evolution is irrefutable morphologically, paleontologically, genetically and archeologically. I will try my best not to romanticize, but this is a topic I am very passionate about so forgive me if I get a bit flowery.
First, let's quote our friends at Answers in Genesis to set the scene of Human Evolution denial before we attempt to prove it as a fact:
“Clearly, there is nothing suggesting a transition between apes and humans. All we can see from the fossil record is either apes, or humans. Saying something is a human ancestor just because its an extinct “kind” of ape, doesn’t make something a human ancestor.”
The path to humanity from the first mammal begins with the plesiadapiforms, specifically, a former resident of Montana named Purgatorius. The development of the Old world monkeys (Cercopothecoids) which led to apes will not be discussed as the topic of discourse is strictly from apes to humans, not old world monkeys.
The first relative, and the original perpetrator of habitual (occasional) bipedalism is found in the East African Rift, in what is today Kenya, Tanzania and Ethiopia. The East African Rift is the boundary between two tectonic plates that sprawl across Africa and India, which now separate the lush tropical rainforests of West Tanzania and the Congo from the flat Serengeti that dominates where our ancestors first climbed down from the trees out of necessity. So who were these ancestors? There are some 17 species of well documented Hominids. 20, if you count some of the less supported fossils.
Let's Dive in!
Part 1: The Recipes for Genus Sahelanthropus (oldest ape -like ancestor) and Homo sapiens
Sahelanthropus tchadensis

Low encephalization (Brain case size: 300-350 cm SQ)
Habitual Bipedality (No valgus knee, opposable toes, Foremen Magnum more behind the skull, Shorter Hindlimbs)
Dentition (2:1:2:3 but no parabolic palate and large canines)
Face morphology (High Prognathism, reduced zygomatics, saggital crest, no forehead, heavy browridge)
Reduced Sexual Dimorphism (This will rise with the Australopiths and reduce again in Homo)
No tool use
No culture

Homo sapiens

High encephalization (Brain case size: 1200-1300 cm SQ)
Obligate Bipedality (Valgus knee, Bowl shaped Pelvis, Inline Big toe, Ventral Foremen Magnum, Longer Hind Limbs)
Dentition (2:1:2:3, Parabolic Palate, Reduced Canines)
Face Morphology (Reduced Prognathism, Sharper Zygomatics, Loss of Saggital Crest, Elongated Forehead, Brow Ridge Reduction)
Reduced Sexual Dimorphism
Tool use (Fire, Stone Tools, etc)
Culture (Cave Art, Jewelry Etc)

Part 2: The Players in the Game (Brain Cases in cm SQ)
The Early Hominids
3 Genera
Sahelanthropus
Orrorin
Ardipithicus (Kadabba and Ramidus)
Highly variable
Bipedal at least habitually (more than chimpanzees and bonobos)
Dentation microwear indicates frugivory and some omnivory
Mostly ape-like
Sahelanthropus tchadensis (7 MYA):
Brain case: 300-400
Sahelanthropus tchadensis is one of the oldest known species in the human family tree. Walking upright may have helped this species survive in diverse habitats, including forests and grasslands, although it definitely spent time in the trees.
This species had a combination of ape-like and human-like features:
Ape-like features included a small brain (even slightly smaller than a chimpanzee’s), sloping face, very prominent browridges, and elongated skull.
Human-like features included small canine teeth, a short middle part of the face, and a spinal cord opening underneath the skull instead of towards the back as seen in non-bipedal apes. The spinal cord opening (foremen magnum) is what tells us this animal was at least partially bipedal, although it was likely cumbersome at times due to no in-line big toe!
Found in Chad
Orrorin tugenensis (6 MYA)
Brain Case: 300-400
Living around 6 million years ago, Orrorin tugenensis is the one of the oldest early humans on our family tree.
Individuals of this species were approximately the size of a chimpanzee and had small teeth with thick enamel, similar to modern humans.
he most important fossil of this species is an upper femur, showing evidence of bone buildup typical of a biped - so Orrorin tugenensis individuals climbed trees but also probably walked upright with two legs on the ground similar to Sahelanthropus.
Orrorin is at the base of the human family tree, and has more ape-like features than human-like ones -- except that it walked upright on two legs when on the ground.
Found in Tugen Hills, Kenya
Ardipithicus kadabba (5.8-5.2 MYA)
Brain Case: 300-400
Ardipithecus kadabba was bipedal (walked upright), probably similar in body and brain size to a modern chimpanzee, and had canines that resemble those in later hominins but that still project beyond the tooth row.
One bone from the large toe has a broad, robust appearance, suggesting its use in bipedal push-off.
Yohannes Haile-Selassie discovered 11 specimens from at least 5 individuals
Found in Middle Awash in Eithiopia
Ardipithicus ramidus (4.4 MYA)
Brain Case: 350-400
The foot bones in this skeleton indicate a divergent large toe combined with a rigid foot – it's still unclear what this means concerning bipedal behavior. The pelvis, reconstructed from a crushed specimen, is said to show adaptations that combine tree-climbing and bipedal activity.
The discoverers argue that the initial ‘Ardi’ skeleton reflects a human rather than a Pan ancestor as Ardi was not chimpanzee-like (bipedality, low sexual dimorphism and higher encephelization).
A good sample of canine teeth of this species indicates very little difference in size between males and females in this species. Ardi’s fossils were found alongside faunal remains indicating she lived in a wooded environment.
Discovered in Middle Awash Eithiopia
The Australopiths (Savannah Bipeds)
Likely gracile with larger overall size than chimpanzees.
Larger brain size (even accounting for overall size) than chimpanzees
Dentation is megadont and the palate is midway between human and chimpanzee in regard to parabolic shape. Molars getting larger.
Arms still longer than legs, foremen magnum continuing to move ventrally.
More bipedal than the ardipiths, but still some time in trees.
Thick tooth enamel (a human trait)
Still apelike development (rapid infant growth)
Australopithicus anamensis (4.2-3.9 MYA)
Complete enough brain case not found, brain cc unknown
Australopithecus anamensis has a combination of traits found in both apes and humans.
The upper end of the tibia (shin bone) shows an expanded area of bone and a human-like orientation of the ankle joint, indicative of regular bipedal walking (support of body weight on one leg at the time). Long forearms and features of the wrist bones suggest these individuals probably climbed trees as well.
Found in Kanapoi, Kenya
Australopithicus afarensis (3.8-2.9 MYA)
450-500 cc brain
Au. afarensis had both ape and human characteristics: members of this species had apelike face proportions (a flat nose, a strongly projecting lower jaw), and long, strong arms with curved fingers adapted for climbing trees. Despite climbing, big toe is almost completely in line, indicating frequent time on the ground as well.
They also had small canine teeth like all other early humans, and a body that stood on two legs and regularly walked upright with a valgus knee similar to modern man.
Their adaptations for living both in the trees and on the ground helped them survive for almost a million years as climate and environments changed.
Remains from over 300 individuals have been found, and indicate heavy Sexual Dimorphism (perhaps in line with modern chimpanzees)
First found in Hadar, Eithiopia (Lucy)
Australopithicus africanus (3.3-2.1 MYA)
480-500 cc brain
Au. africanus was anatomically similar to Au. afarensis, with a combination of human-like and ape-like features.
Compared to Au. afarensis, Au. africanus had a rounder cranium housing a larger brain and smaller teeth, but it also had some ape-like features including relatively long arms and a strongly sloping face that juts out from underneath the braincase with a pronounced jaw.
Like Au. afarensis, the pelvis, femur (upper leg), and foot bones of Au. africanus indicate that it walked bipedally (valgus knee and inline big toe), but its shoulder and hand bones indicate they were also still well adapted for climbing.
Found in Southern Africa (potentially a migratory branch of A. Afarensis)
Our Paranthropine Cousins (The "Robust" Australopiths)
Known as the “robust” Australopiths
Brain size slightly larger than their Australopith cousins
Huge megadont teeth (primarily molars)
Massive zygomatics and sagittal crests in males
Despite being a cousin (and not direct relative) to us, the hominid trends continue: Bipedal (ventral FM), reduced canines, ^ brain, ^ size, almost inline big toe, valgus knee and bowl-trending pelvis.
Differences that make them likely cousins rather than relatives: HIGH sexual dimorphism (males were much larger), Huge zygomatics and sagittal crest, massive molars suggesting a heavily plant based diet.
Due to character restraints, the Paranthropines will not be covered in depth. There are three well known species, P. aeithiopicus, P. robustus and P. Boisei (2.7-1.2 MYA)
They are fascinating though! Check them out and perhaps we can cover them in another post.
Homo habilis (2.4-1.6 MYA)
Brain case: 550-700
The first animal classified as genus Homo, rather than an australopithicine. It has reduced prognathism, smaller canines and a smaller brow ridge. It's small, like it's predecessors, but it's body ratio is trending towards human, although the arms are still "too long". It was certainly obligately bipedal, due to it's knees and ventral foremen magnum. H. habilis is found frequently with stone tools. Sexual dimorphism is shrinking again, and long species reign shows a broad range of encephilization. Ape like traits include brain case, face morphology (brow ridge and small s. crest still present, prognathism reduced but still accounted for).
Homo rudolfensis (1.9-1.8 MYA)
Brain Case: 775
Considered unique from H. habilis, but only recently so. It has unique features not within species variety in the constraints of natural selection: "larger braincase, longer face, and larger molar and premolar teeth. Due to the last two features, though, some scientists still wonder whether this species might better be considered an Australopithecus, although one with a large brain!" If H. rudolfensis is a transitioning form of H habilis, it likely used tools as well although to my knowledge no direct tools have been found with it.
Homo georgicus (1.7 MYA)
Brain Case: 600
is somewhat controversial in it's ranking. It has a small braincase size for Homo and more "old traits": showing a species primitive in its skull and upper body but with relatively advanced spines and lower limbs, providing greater mobility. They are now thought to represent a stage soon after the transition between Australopithecus and Homo erectus, and have been dated at 1.8 million years before the present. Tool use is observed both in finding tools with the specimens and cuts in animals bones found alongside specimens.
Homo ergaster (1.9-1.5 MYA)
Brain Case: 600-910
Also is controversial in it's ranking. It's high cranial diversity and occipital traits make it likely that H. eragaster is either a late transition of Homo erectus or is actually early representations of H. erectus itself. However,H. ergaster may be distinguished from H. erectus by its thinner skull-bones and lack of an obvious supraorbital foremen, and from H. heidelbergensis by its thinner bones, more protrusive face, and lower forehead. Tool use, just as the previous.
Homo erectus (1.8 MYA- 145,000)
Braincase: 900-1000
One of the best represented fossils in many regards. It can be difficult to pinpoint exactly how many due to it's many subspecies and reputation as a highly variable species. It sports unique teeth from modern humans, as well as many cranial features (such as zygomatics). It's brain case is far smaller than even our smallest range for a normal phenotype, and yet, H. erectus settlements show fire use and more sophisticated tools than it's predecessors. This animal is found nearly all over, from Africa to Europe to Asia. It is likely it proliferated into the H. neanderthalensis (we have genetic hybrid bones) Denisovans and H. floresiensis.
And of course for reference, Us!
Homo sapiens: 300,000-present
Brain case: 1200-1350 cm SQ, 4-6 ft
Homo sapiens is known to have several traits which place it in genus homo, and a few which make it unique from the others also in it. Tall, lanky posture with enormous brains (focused on the frontal lobe) and advanced tool use. Anatomically modern humans can be classified by lighter build skeletons than their predecessors. Skull is thin-walled and high-vaulted with flat, near vertical foreheads. Reduced prognathism and brow ridges as well, small mandibles and teeth comparatively. Narrow hips support the most efficient biped hominid of all time.
The trend over all can be seen as so:
Sahenanthropus, Orroren, Ardipiths
-bipedality develops
-face morphology begins to change
-bipedality becomes more efficient
Australopiths
-encephilization begins to increase at a faster rate
-face morphology changes to accommodate brain case
-Pelvis morphology changes to accommodate brain case size during birth
Homo
-Growth rates slow, and longer adolescence is seen
-Brain case allows for development of frontal lobe
-Frontal Lobe development instigates tool use
-Tool use eases life, allowing for culture
Below is a slightly more in depth look at the trends:
- Bipedalism
a) How? Reshaping of the pelvis, knee, ankle, foot and location of the foremen magnum.
b) Why? The reason for the journey out of the trees and onto the ground has been subject of dispute for decades. The current theory suggests that the East African Rift split separated a population of the Common Ancestor of Humans and Chimpanzees/Bonobos, leaving the latter in a flatter, less-forested Savanah and the former in the lush jungles. This forced the ancient hominids from the dwindling trees and onto the ground, where the grass was tall and seeing over it (to locate predators) was invaluable. We know they already could stand and walk bipedally (all great apes today can for periods of time) it became a matter of doing it often. Those who could, survived to reproduce and we see a trend of Bipedality. Additionally, this freed the hands for carrying young, bringing food back to a “home base” and later, tool use.
- Brain size
a) How? Reducing prognathism and the size of teeth and expanding the brain case.
b) Why? Intelligence increases fitness! But then, why do we not see this in other species? We do see a trend for increasing “smarts” in some, such as cetaceans or the great apes, but upping intelligence takes mutation and an environment that selects for it heavily. It is difficult to see it evolve in a lifetime.
- Culture
a) How? Increasing intelligence and social relationship dependency.
b) Why? With intelligence comes empathy and existential questions. These three factors lead to the development of new innovations for survival (smarts), Helping the downtrodden members of the group (empathy) and the advent of burial and symbolism (existential questioning).
Other factors such as
- Loss of hair: Humans are one of the most efficient animals in the world at avoiding overheating by dissipating it through sweat.
- Speech: We sacrificed the ability to eat and breath at the same time for advanced vocal cords. Human babies’ larynx match adult chimpanzees until juvenile development.
- Loss of Sexual Dimorphism: Human partition work more equally due to a more minute difference in the genders (5-11% dimorphic)
- Dental adaption: Loss of canines and increased molars came with brain size increase, and the smaller teeth came to no detriment as we began to use tools.
Part 3: We're All Damn Dirty Apes (Closing)
“Clearly, there is nothing suggesting a transition between apes and humans. All we can see from the fossil record is either apes, or humans. Saying something is a human ancestor just because its an extinct “kind” of ape, doesn’t make something a human ancestor.”
Sorry Answers in Genesis. This is abjectly false.
Human beings are bipedal, intelligent hominids that reign supreme on this Earth in regards to dominion over every other species. We are all encompassing on this planet and using our powerful brains and ability to hunt persistently we managed to rise from the grasslands of East Africa and become the formidable species the world sees today. We are not just a part of nature, we are the very essence of it. A perfect story of evolution yielding an unstoppable (not necessarily a good thing) force.
Humans are animals. But what separates us from other organisms is our intelligence and our incredible empathy. Neither are totally unique to us, but no other animal sees it in the spades we do. Humans represent a beacon of emotion and passion and artistry. We create endless symphonies, sculpt mighty megaliths and write epic tales that wind through time and generations. We learned to navigate using the stars and reached every continent, and when the sea was sated we created planes to explore the sky. The gravity of our planet couldn’t even hold us back as humans journeyed into the stars and set foot on the moon above. We craft medicines and cure diseases, suck oil from the ground to power our cars, build towers that scrape the belly of the sky. Humans care deeply for one another, and for other species as well, domesticating animals that once hunted us for the sake of companionship. We stand apart in the Animal Kingdom as creatures forged in the dust of the Savanah and gifted with the spark of curiosity. We don’t learn so that we may survive, we survive so that we may learn more about this grand, extravagant world we roam.
TL;DR Through the 17 + Hominids of the fossil record, we see morphologic trends that connect humans and our ancestors. These trends bind us to the animal kingdom and allow us to peer into our rich ancestry as we try to learn more about ourselves.
*I will add the numbers of fossils we know each species from later when I have access to my text.

Transitional Species Handbook: Humans are Definitively the Descendants of A Lineage of Ape-Like Ancestors and Thus We are Still Apes (Hominids)

It is difficult to find a more scrutinized facet of Evolutionary Biology than that of our own evolutionary history. This is due to our inherent desire to feel apart from nature as it's master, rather than acknowledge our original spot seated firmly in the middle of the Serengeti food chain. There is a humbling that must occur to see oneself in the ancient apes of yesterday, scraping about in the dust of the East African Rift Valley, and yet this past of ours it written in our very bones: from how we walk to how we talk.

The following post will explore this journey from the first true hominid to ourselves, and examine why our evolution is irrefutable morphologically, paleontologically, genetically and archeologically. I will try my best not to romanticize, but this is a topic I am very passionate about so forgive me if I get a bit flowery.

First, let's quote our friends at Answers in Genesis to set the scene of Human Evolution denial before we attempt to prove it as a fact:

“Clearly, there is nothing suggesting a transition between apes and humans. All we can see from the fossil record is either apes, or humans. Saying something is a human ancestor just because its an extinct “kind” of ape, doesn’t make something a human ancestor.”
You can explore some of their ideas here.

The path to humanity from the first mammal begins with the plesiadapiforms, specifically, a former resident of Montana named Purgatorius. The development of the Old world monkeys (Cercopothecoids) which led to apes will not be discussed as the topic of discourse is strictly from apes to humans, not old world monkeys.
The first relative, and the original perpetrator of habitual (occasional) bipedalism is found in the East African Rift, in what is today Kenya, Tanzania and Ethiopia. The East African Rift is the boundary between two tectonic plates that sprawl across Africa and India, which now separate the lush tropical rainforests of West Tanzania and the Congo from the flat Serengeti that dominates where our ancestors first climbed down from the trees out of necessity. So who were these ancestors? There are some 17 species of well documented Hominids. 20, if you count some of the less supported fossils.
Let's Dive in!
Part 1: The Recipes for Genus Sahelanthropus (oldest ape -like ancestor) and Homo sapiens

Sahelanthropus tchadensis

Low encephalization (Brain case size: 300-350 cm SQ)
Habitual Bipedality (No valgus knee, opposable toes, Foremen Magnum more behind the skull, Shorter Hindlimbs)
Dentition (2:1:2:3 but no parabolic palate and large canines)
Face morphology (High Prognathism, reduced zygomatics, saggital crest, no forehead, heavy browridge)
Reduced Sexual Dimorphism (This will rise with the Australopiths and reduce again in Homo)
No tool use
No culture

Homo sapiens

High encephalization (Brain case size: 1200-1300 cm SQ)
Obligate Bipedality (Valgus knee, Bowl shaped Pelvis, Inline Big toe, Ventral Foremen Magnum, Longer Hind Limbs)
Dentition (2:1:2:3, Parabolic Palate, Reduced Canines)
Face Morphology (Reduced Prognathism, Sharper Zygomatics, Loss of Saggital Crest, Elongated Forehead, Brow Ridge Reduction)
Reduced Sexual Dimorphism
Tool use (Fire, Stone Tools, etc)
Culture (Cave Art, Jewelry Etc)

Part 2: The Players in the Game (Brain Cases in cm SQ)

The Early Hominids
3 Genera
Sahelanthropus
Orrorin
Ardipithicus (Kadabba and Ramidus)
Highly variable
Bipedal at least habitually (more than chimpanzees and bonobos)
Dentation microwear indicates frugivory and some omnivory
Mostly ape-like

Sahelanthropus tchadensis (7 MYA):
Brain case: 300-400
Sahelanthropus tchadensis is one of the oldest known species in the human family tree. Walking upright may have helped this species survive in diverse habitats, including forests and grasslands, although it definitely spent time in the trees.
This species had a combination of ape-like and human-like features:
Ape-like features included a small brain (even slightly smaller than a chimpanzee’s), sloping face, very prominent browridges, and elongated skull.
Human-like features included small canine teeth, a short middle part of the face, and a spinal cord opening underneath the skull instead of towards the back as seen in non-bipedal apes. The spinal cord opening (foremen magnum) is what tells us this animal was at least partially bipedal, although it was likely cumbersome at times due to no in-line big toe!
Found in Chad
Orrorin tugenensis (6 MYA)
Brain Case: 300-400
Living around 6 million years ago, Orrorin tugenensis is the one of the oldest early humans on our family tree.
Individuals of this species were approximately the size of a chimpanzee and had small teeth with thick enamel, similar to modern humans.
he most important fossil of this species is an upper femur, showing evidence of bone buildup typical of a biped - so Orrorin tugenensis individuals climbed trees but also probably walked upright with two legs on the ground similar to Sahelanthropus.
Orrorin is at the base of the human family tree, and has more ape-like features than human-like ones -- except that it walked upright on two legs when on the ground.
Found in Tugen Hills, Kenya
Ardipithicus kadabba (5.8-5.2 MYA)
Brain Case: 300-400
Ardipithecus kadabba was bipedal (walked upright), probably similar in body and brain size to a modern chimpanzee, and had canines that resemble those in later hominins but that still project beyond the tooth row.
One bone from the large toe has a broad, robust appearance, suggesting its use in bipedal push-off.
Yohannes Haile-Selassie discovered 11 specimens from at least 5 individuals
Found in Middle Awash in Eithiopia
Ardipithicus ramidus (4.4 MYA)
Brain Case: 350-400
The foot bones in this skeleton indicate a divergent large toe combined with a rigid foot – it's still unclear what this means concerning bipedal behavior. The pelvis, reconstructed from a crushed specimen, is said to show adaptations that combine tree-climbing and bipedal activity.
The discoverers argue that the initial ‘Ardi’ skeleton reflects a human rather than a Pan ancestor as Ardi was not chimpanzee-like (bipedality, low sexual dimorphism and higher encephelization).
A good sample of canine teeth of this species indicates very little difference in size between males and females in this species. Ardi’s fossils were found alongside faunal remains indicating she lived in a wooded environment.
Discovered in Middle Awash Eithiopia
The Australopiths (Savannah Bipeds)
Likely gracile with larger overall size than chimpanzees.
Larger brain size (even accounting for overall size) than chimpanzees
Dentation is megadont and the palate is midway between human and chimpanzee in regard to parabolic shape. Molars getting larger.
Arms still longer than legs, foremen magnum continuing to move ventrally.
More bipedal than the ardipiths, but still some time in trees.
Thick tooth enamel (a human trait)
Still apelike development (rapid infant growth)
Australopithicus anamensis (4.2-3.9 MYA)
Complete enough brain case not found, brain cc unknown
Australopithecus anamensis has a combination of traits found in both apes and humans.
The upper end of the tibia (shin bone) shows an expanded area of bone and a human-like orientation of the ankle joint, indicative of regular bipedal walking (support of body weight on one leg at the time). Long forearms and features of the wrist bones suggest these individuals probably climbed trees as well.
Found in Kanapoi, Kenya
Australopithicus afarensis (3.8-2.9 MYA)
450-500 cc brain
Au. afarensis had both ape and human characteristics: members of this species had apelike face proportions (a flat nose, a strongly projecting lower jaw), and long, strong arms with curved fingers adapted for climbing trees. Despite climbing, big toe is almost completely in line, indicating frequent time on the ground as well.
They also had small canine teeth like all other early humans, and a body that stood on two legs and regularly walked upright with a valgus knee similar to modern man.
Their adaptations for living both in the trees and on the ground helped them survive for almost a million years as climate and environments changed.
Remains from over 300 individuals have been found, and indicate heavy Sexual Dimorphism (perhaps in line with modern chimpanzees)
First found in Hadar, Eithiopia (Lucy)
Australopithicus africanus (3.3-2.1 MYA)
480-500 cc brain
Au. africanus was anatomically similar to Au. afarensis, with a combination of human-like and ape-like features.
Compared to Au. afarensis, Au. africanus had a rounder cranium housing a larger brain and smaller teeth, but it also had some ape-like features including relatively long arms and a strongly sloping face that juts out from underneath the braincase with a pronounced jaw.
Like Au. afarensis, the pelvis, femur (upper leg), and foot bones of Au. africanus indicate that it walked bipedally (valgus knee and inline big toe), but its shoulder and hand bones indicate they were also still well adapted for climbing.
Found in Southern Africa (potentially a migratory branch of A. Afarensis)

Our Paranthropine Cousins (The "Robust" Australopiths)
Known as the “robust” Australopiths
Brain size slightly larger than their Australopith cousins
Huge megadont teeth (primarily molars)
Massive zygomatics and sagittal crests in males
Despite being a cousin (and not direct relative) to us, the hominid trends continue: Bipedal (ventral FM), reduced canines, ^ brain, ^ size, almost inline big toe, valgus knee and bowl-trending pelvis.
Differences that make them likely cousins rather than relatives: HIGH sexual dimorphism (males were much larger), Huge zygomatics and sagittal crest, massive molars suggesting a heavily plant based diet.
Due to character restraints, the Paranthropines will not be covered in depth. There are three well known species, P. aeithiopicus, P. robustus and P. Boisei (2.7-1.2 MYA)
They are fascinating though! Check them out and perhaps we can cover them in another post.

Homo habilis (2.4-1.6 MYA)
Brain case: 550-700
The first animal classified as genus Homo, rather than an australopithicine. It has reduced prognathism, smaller canines and a smaller brow ridge. It's small, like it's predecessors, but it's body ratio is trending towards human, although the arms are still "too long". It was certainly obligately bipedal, due to it's knees and ventral foremen magnum. H. habilis is found frequently with stone tools. Sexual dimorphism is shrinking again, and long species reign shows a broad range of encephilization. Ape like traits include brain case, face morphology (brow ridge and small s. crest still present, prognathism reduced but still accounted for).
Homo rudolfensis (1.9-1.8 MYA)
Brain Case: 775
Considered unique from H. habilis, but only recently so. It has unique features not within species variety in the constraints of natural selection: "larger braincase, longer face, and larger molar and premolar teeth. Due to the last two features, though, some scientists still wonder whether this species might better be considered an Australopithecus, although one with a large brain!" If H. rudolfensis is a transitioning form of H habilis, it likely used tools as well although to my knowledge no direct tools have been found with it.
Homo georgicus (1.7 MYA)
Brain Case: 600
is somewhat controversial in it's ranking. It has a small braincase size for Homo and more "old traits": showing a species primitive in its skull and upper body but with relatively advanced spines and lower limbs, providing greater mobility. They are now thought to represent a stage soon after the transition between Australopithecus and Homo erectus, and have been dated at 1.8 million years before the present. Tool use is observed both in finding tools with the specimens and cuts in animals bones found alongside specimens.
Homo ergaster (1.9-1.5 MYA)
Brain Case: 600-910
Also is controversial in it's ranking. It's high cranial diversity and occipital traits make it likely that H. eragaster is either a late transition of Homo erectus or is actually early representations of H. erectus itself. However,H. ergaster may be distinguished from H. erectus by its thinner skull-bones and lack of an obvious supraorbital foremen, and from H. heidelbergensis by its thinner bones, more protrusive face, and lower forehead. Tool use, just as the previous.
Homo erectus (1.8 MYA- 145,000)
Braincase: 900-1000
One of the best represented fossils in many regards. It can be difficult to pinpoint exactly how many due to it's many subspecies and reputation as a highly variable species. It sports unique teeth from modern humans, as well as many cranial features (such as zygomatics). It's brain case is far smaller than even our smallest range for a normal phenotype, and yet, H. erectus settlements show fire use and more sophisticated tools than it's predecessors. This animal is found nearly all over, from Africa to Europe to Asia. It is likely it proliferated into the H. neanderthalensis (we have genetic hybrid bones) Denisovans and H. floresiensis.
And of course for reference, Us!
Homo sapiens: 300,000-present
Brain case: 1200-1350 cm SQ, 4-6 ft
Homo sapiens is known to have several traits which place it in genus homo, and a few which make it unique from the others also in it. Tall, lanky posture with enormous brains (focused on the frontal lobe) and advanced tool use. Anatomically modern humans can be classified by lighter build skeletons than their predecessors. Skull is thin-walled and high-vaulted with flat, near vertical foreheads. Reduced prognathism and brow ridges as well, small mandibles and teeth comparatively. Narrow hips support the most efficient biped hominid of all time.

The trend over all can be seen as so:
Sahenanthropus, Orroren, Ardipiths
-bipedality develops
-face morphology begins to change
-bipedality becomes more efficient
Australopiths
-encephilization begins to increase at a faster rate
-face morphology changes to accommodate brain case
-Pelvis morphology changes to accommodate brain case size during birth
Homo
-Growth rates slow, and longer adolescence is seen
-Brain case allows for development of frontal lobe
-Frontal Lobe development instigates tool use
-Tool use eases life, allowing for culture

Below is a slightly more in depth look at the trends:
- Bipedalism
a) How? Reshaping of the pelvis, knee, ankle, foot and location of the foremen magnum.
b) Why? The reason for the journey out of the trees and onto the ground has been subject of dispute for decades. The current theory suggests that the East African Rift split separated a population of the Common Ancestor of Humans and Chimpanzees/Bonobos, leaving the latter in a flatter, less-forested Savanah and the former in the lush jungles. This forced the ancient hominids from the dwindling trees and onto the ground, where the grass was tall and seeing over it (to locate predators) was invaluable. We know they already could stand and walk bipedally (all great apes today can for periods of time) it became a matter of doing it often. Those who could, survived to reproduce and we see a trend of Bipedality. Additionally, this freed the hands for carrying young, bringing food back to a “home base” and later, tool use.
- Brain size
a) How? Reducing prognathism and the size of teeth and expanding the brain case.
b) Why? Intelligence increases fitness! But then, why do we not see this in other species? We do see a trend for increasing “smarts” in some, such as cetaceans or the great apes, but upping intelligence takes mutation and an environment that selects for it heavily. It is difficult to see it evolve in a lifetime.
- Culture
a) How? Increasing intelligence and social relationship dependency.
b) Why? With intelligence comes empathy and existential questions. These three factors lead to the development of new innovations for survival (smarts), Helping the downtrodden members of the group (empathy) and the advent of burial and symbolism (existential questioning).
Other factors such as
- Loss of hair: Humans are one of the most efficient animals in the world at avoiding overheating by dissipating it through sweat.
- Speech: We sacrificed the ability to eat and breath at the same time for advanced vocal cords. Human babies’ larynx match adult chimpanzees until juvenile development.
- Loss of Sexual Dimorphism: Human partition work more equally due to a more minute difference in the genders (5-11% dimorphic)
- Dental adaption: Loss of canines and increased molars came with brain size increase, and the smaller teeth came to no detriment as we began to use tools.

Part 3: We're All Damn Dirty Apes (Closing)
“Clearly, there is nothing suggesting a transition between apes and humans. All we can see from the fossil record is either apes, or humans. Saying something is a human ancestor just because its an extinct “kind” of ape, doesn’t make something a human ancestor.”
Sorry Answers in Genesis. This is abjectly false.
Human beings are bipedal, intelligent hominids that reign supreme on this Earth in regards to dominion over every other species. We are all encompassing on this planet and using our powerful brains and ability to hunt persistently we managed to rise from the grasslands of East Africa and become the formidable species the world sees today. We are not just a part of nature, we are the very essence of it. A perfect story of evolution yielding an unstoppable (not necessarily a good thing) force.
Humans are animals. But what separates us from other organisms is our intelligence and our incredible empathy. Neither are totally unique to us, but no other animal sees it in the spades we do. Humans represent a beacon of emotion and passion and artistry. We create endless symphonies, sculpt mighty megaliths and write epic tales that wind through time and generations. We learned to navigate using the stars and reached every continent, and when the sea was sated we created planes to explore the sky. The gravity of our planet couldn’t even hold us back as humans journeyed into the stars and set foot on the moon above. We craft medicines and cure diseases, suck oil from the ground to power our cars, build towers that scrape the belly of the sky. Humans care deeply for one another, and for other species as well, domesticating animals that once hunted us for the sake of companionship. We stand apart in the Animal Kingdom as creatures forged in the dust of the Savanah and gifted with the spark of curiosity. We don’t learn so that we may survive, we survive so that we may learn more about this grand, extravagant world we roam.
TL;DR Through the 17 + Hominids of the fossil record, we see morphologic trends that connect humans and our ancestors. These trends bind us to the animal kingdom and allow us to peer into our rich ancestry as we try to learn more about ourselves.
*I will add the numbers of fossils we know each species from later when I have access to my text.

how to tell if you have knee valgus video

What causes Knee Valgus? a) Functional cause. If any part of your body is not in the “ideal” position, it can eventually lead to Knee Valgus. … We can fix this! I have listed all of the areas that you will need to address in the exercise section below. b) Structural cause. Physical changes to the bone and/or joints can result in Knee Valgus. Knee valgus is when the knees fall inside the line made by the hip and foot. How do you know it’s a problem? For force to be transferred through bone and muscle, the joints should be stacked on one another. When the knee is inside the hip and foot, there’s excessive stress on the lateral knee, ACL, MCL, and meniscus. Sometimes your knee joint can become infected, leading to swelling, pain and redness. Septic arthritis often occurs with a fever, and there's usually no trauma before the onset of pain. Septic arthritis can quickly cause extensive damage to the knee cartilage. If you have knee pain with any of these symptoms, see your doctor right away. Other Genu valgum is more commonly referred to as knock-knees. When someone with genu valgum stands with their knees together, there is a sizeable gap between the ankles of about 2 to 3 inches. The knees... You will have significant swelling and may feel that you have a very wobbly or unstable knee. Assessment tests, such as the valgus stress test will show significant movement in the joint (laxity.) The test will probably not have a definite endpoint when the medial ligament is stressed as there is no ligament stopping the movement. Severe valgus knee deformity can be challenging to manage in patients undergoing total knee arthroplasty, but it can be addressed through gap balancing and other techniques, according to a knee Knee valgus occurs when the femur rotates inward, whether due to structural deformity or weakness in the muscles and ligaments that support the knee. When it occurs both knees point towards one another in a standing position, rather than being pointed forward. Remember that your knee will have a large incision and your knee joint has been traumatized (to say the least). Recovery will take time! You will experience gradual improvement with physical therapy and exercise that can take up to a year or more. I was able to enjoy all of my old activities without pain 4 months after surgery. In addition, once knee osteoarthritis develops, it's more likely to progress (get worse) if you have a varus alignment. This is because a varus alignment causes the load-bearing axis of the leg to shift to the inside, causing more stress and force on the medial (inner) compartment of the knee. The excess pressure on one compartment of the knee increases the risk of developing osteoarthritis for patients suffering from both Valgus and Varus deformities. Chances are, the longer you have been living with these deformities, the more pain you are likely to experience, especially in severe cases.

how to tell if you have knee valgus top

Top 5 Ways to Correct Knock Knees with Exercise Etc ...

Learn how to identify the root causes of ankle overpronation and what you can do to fix this issue.Functional Ankle Mobility Drill video: https://www.youtube... Dr. Tsourmas shows the proper way to diagnose a medial collateral ligament injury, more commonly referred to as an mcl tear.Workplace Diagnosis is the first ... Valgus Knee is a condition where your knees cave inward and you have little to no "thigh gap". Stand straight and have your knees touch, is there a wide gap ... Dr. Ebraheim’s educational animated video describes the condition know as Valgus knee deformity. When the knee is not perfectly aligned from side to side, either a valgus or varus malalignment may... Top 5 Ways to Correct Knock Knees with Exercise Etc. Bob and Brad demonstrate the top ways to correct knock knees with exercise and strengthening. Check out ... Knee Strengthening exercises that will help your knees become strong and healthy. This routine will help strengthen your ankles, knees, and hips and may hel... Alternative method for stressing the medial lateral collateral ligaments:1. Extend the patient's knee and cradle the heel between your arm and body. The knee... Dr. Ebraheim’s educational animated video describing the anatomy and associated injuries of the knee joint. Disrupted quadriceps•Patient is unable to active...

how to tell if you have knee valgus

how to tell if you have knee valgus - win

Improving Pistols for Athletes with Long Legs

(1) Ankle Dorsiflexion

(2) Hip Flexion & Core Compression

(3) Hip Adduction & Internal Rotation

BG's Bio-mechanics

Q&A

[OC] The Correlation & Causation Between Hip Width and Knee Pain

Injury breakdown: Why the Lakers have been so conservative with Lonzo’s MCL Injury

Research Project - Final Draft

[OC] 3 Potential Underlying Causes of the NFL's ACL Problem

1 — Off-Season Training Quantity and Intensity

2 — Off-Season Training type

3 —Playing surface

1 — Training Quantity and Intensity

2 — Training Type

3 — Playing Surface

All in All

[OC]Kyrie Irving's knee: The troublesome past, recent surgeries, and onwards

I. The anatomy and function of the patella

A. The anatomy

B. The function

II. Kyrie Irving’s knee injury history

2015 playoffs

Kyrie Irving's knee tendonitis

2015 Finals

Kyrie Irving's knee patellar fracture

So what is a patella fracture?

Patellar surgery for Kyrie Irving’s knee

2015-2016 Season

2016-2017 Season

2017 Summer

2017-2018 Season

Why did he need the tension wire removed?

What the heck happened?

III. Kyrie’s Irving knee rehab and return to play consideration

Micro (the tissue and bone)

Mezzo (systemic factors)

Macro (contextual factors)

IV. Are there any long-term ramifications for Kyrie Irving’s knee

A. Arthritis

B. Muscle weakness

C. Pain

V. The overall takeaway for Kyrie Irving’s knee

Transitional Species Handbook: Humans are Definitively the Descendants of A Lineage of Ape-Like Ancestors and Thus We are Still Apes (Hominids)

Transitional Species Handbook: Humans are Definitively the Descendants of A Lineage of Ape-Like Ancestors and Thus We are Still Apes (Hominids)

how to tell if you have knee valgus video

how to tell if you have knee valgus top

Top 5 Ways to Correct Knock Knees with Exercise Etc ...