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The knee of an athlete is often a diagnostic dilemma. The knee obtains important biomechanical function and is supported by an array of ligaments and muscles. For these reasons it can be difficult to pinpoint the specific structure which is injured. Such a concept is to be blamed for the creation of Patellofemoral Pain Syndrome (PFPS),
What exactly is PFPS?
When you think about it what exactly does this diagnosis tell you? Essentially all that this means is we know there is pain and we know it has something to do with the Patella-Femoral Joint. In my opinion this is not a real diagnosis. What if we made clinical conclusions like this for everything? Chronic Neck Pain Syndrome or Sore Elbow Disease?
In reality, PFPS is an umbrella term to describe any possible causes of pain which can be attributed to the Patella-Femoral Joint. Such as:
-Chondromalacia Patella - Softening of the cartilage under the patella
-PatellaFemoral tracking problems
-Infrapatellar Fat Pad being impinged (Hoffa's Disease)
This is why I often tell colleagues and those which attend my seminars to not worry about the diagnosis. What you need to find out is WHAT EXACTLY IS CAUSING THIS PAIN?
Originally many used to take a structural approach to PFPS. Measurements of one's Q angle or a patient's knee valgus was observed and often chondromalacia patella was diagnosed. However, if structural abnormalities were deemed the cause how does one explain the benefits from conservative treatment? The patients Q angle has not changed. Furthermore, not everyone with a high Q angle has knee problems?
Researchers are starting to progress away from the structural approach of PFPS and asking what is actually causing the pain?
Ok so what are my options?
A biomechanical fault, muscle imbalance or pathophysiological process which leads to:
1.Inflammation of the synovial lining
2.Inflammation of the fat pad
3.Increase in intra articular pressure
4.Hyperinnervated Lateral Retinaculum
To fully understand you have to address the signs and symptoms
PFPS can be exaggerated with running and climbing up and down stairs. This mechanism of injury is simply due to overuse or excessive force. Such activities as climbing stairs can produce forces 3 times one's body weight. A loss of Tissue Homeostasis occurs and now the joints synovial lining becomes inflamed (#1). This concept is a pretty easy one to understand.
However, how does one explain the movie sign (Pain in the knee with a prolonged period of sitting)? One does not put excessive force through the knee as they sit. There are two leading theories for the movie sign. While sitting we may predispose our knee to change normal position and now structures my impinge a once swollen inflamed synovial lining (#1). The second theory is that as we sit our knee's intra articular pressure increases and thus creates pain (#3). Studies have shown that the knee is an extremely fibrotic and capsular entity. When put in prolonged flexion we may impede venous outflow and increase arterial blood flow to and from the knee. This change in blood flow can increase the pressure within our knee as we sit.
Reasoning for these causes of pain is the popular treatment called McConnell taping. This is a taping method which has shown to relieve pain. However, the results are not always consistent and many wonder why. It can be purposed that by taping the patella in a more neutral position we are preventing it from impinging structures and thus resolving the patient's pain (#1, #2).
Lastly a maltracking patella has also been associated with PFPS. What studies have observed is anatomically those who suffer from PFPS have a hyperinnervated lateral retinaculum. Furthermore, these subjects presented with more nociceptive fibers within the nerves. The theory is the patella tracking medially (usually) will produce tension along the lat retinaculum. Now the nerves are put under traction and start to experience myxoid degeneration. In an attempt to heal itself the body now produces more neural drive and stimulation to that area thus creating a hyperinnervated structure and pain is produced (#4).
Still Don't Believe Me?
Check out the article posted below by Scott F Dye. This is one of the most intriguing and interesting articles I have ever read. Scott which is an orthopedic surgeon (I believe?) has actually been diagnosed with chondromalacia patella in the past. He attempts to cut himself open and inspect the cause of his knee pain. When probing his patella cartilage no pain is felt. However, pain is accentuated when probing his synovial lining and Hoffa fat pad. Furthermore injecting himself with saline increases his intra-articular pressure and produced extreme pain. This article has given valuable premise to support 3/4 theories of what causes PFPS. Imagine... the things we do for science (Left probing cartilage, Right probing synovial lining).
In summary, as professionals we need to steer away from umbrella terms such as PFPS. As a student I found this diagnosis extremely confusing and more so difficult to explain to patients. It wasn't until exploring the mechanism of pain in which I become more inclined to make such a diagnosis. To create consistency in research and amongst colleagues we need to address the actual form of PFPS were discussing. In addition, exploring this notion lays great premise on how we can guide our treatment. This is one condition where the diagnosis may actually be made after treatment is initiated. Dr. Wayne Button, BSc, D.C
What exactly is PFPS?
When you think about it what exactly does this diagnosis tell you? Essentially all that this means is we know there is pain and we know it has something to do with the Patella-Femoral Joint. In my opinion this is not a real diagnosis. What if we made clinical conclusions like this for everything? Chronic Neck Pain Syndrome or Sore Elbow Disease?
In reality, PFPS is an umbrella term to describe any possible causes of pain which can be attributed to the Patella-Femoral Joint. Such as:
-Chondromalacia Patella - Softening of the cartilage under the patella
-PatellaFemoral tracking problems
-Infrapatellar Fat Pad being impinged (Hoffa's Disease)
This is why I often tell colleagues and those which attend my seminars to not worry about the diagnosis. What you need to find out is WHAT EXACTLY IS CAUSING THIS PAIN?
Originally many used to take a structural approach to PFPS. Measurements of one's Q angle or a patient's knee valgus was observed and often chondromalacia patella was diagnosed. However, if structural abnormalities were deemed the cause how does one explain the benefits from conservative treatment? The patients Q angle has not changed. Furthermore, not everyone with a high Q angle has knee problems?
Researchers are starting to progress away from the structural approach of PFPS and asking what is actually causing the pain?
Ok so what are my options?
A biomechanical fault, muscle imbalance or pathophysiological process which leads to:
1.Inflammation of the synovial lining
2.Inflammation of the fat pad
3.Increase in intra articular pressure
To fully understand you have to address the signs and symptomsPFPS can be exaggerated with running and climbing up and down stairs. This mechanism of injury is simply due to overuse or excessive force. Such activities as climbing stairs can produce forces 3 times one's body weight. A loss of Tissue Homeostasis occurs and now the joints synovial lining becomes inflamed (#1). This concept is a pretty easy one to understand.
However, how does one explain the movie sign (Pain in the knee with a prolonged period of sitting)? One does not put excessive force through the knee as they sit. There are two leading theories for the movie sign. While sitting we may predispose our knee to change normal position and now structures my impinge a once swollen inflamed synovial lining (#1). The second theory is that as we sit our knee's intra articular pressure increases and thus creates pain (#3). Studies have shown that the knee is an extremely fibrotic and capsular entity. When put in prolonged flexion we may impede venous outflow and increase arterial blood flow to and from the knee. This change in blood flow can increase the pressure within our knee as we sit.
Lastly a maltracking patella has also been associated with PFPS. What studies have observed is anatomically those who suffer from PFPS have a hyperinnervated lateral retinaculum. Furthermore, these subjects presented with more nociceptive fibers within the nerves. The theory is the patella tracking medially (usually) will produce tension along the lat retinaculum. Now the nerves are put under traction and start to experience myxoid degeneration. In an attempt to heal itself the body now produces more neural drive and stimulation to that area thus creating a hyperinnervated structure and pain is produced (#4).
Check out the article posted below by Scott F Dye. This is one of the most intriguing and interesting articles I have ever read. Scott which is an orthopedic surgeon (I believe?) has actually been diagnosed with chondromalacia patella in the past. He attempts to cut himself open and inspect the cause of his knee pain. When probing his patella cartilage no pain is felt. However, pain is accentuated when probing his synovial lining and Hoffa fat pad. Furthermore injecting himself with saline increases his intra-articular pressure and produced extreme pain. This article has given valuable premise to support 3/4 theories of what causes PFPS. Imagine... the things we do for science (Left probing cartilage, Right probing synovial lining).
In summary, as professionals we need to steer away from umbrella terms such as PFPS. As a student I found this diagnosis extremely confusing and more so difficult to explain to patients. It wasn't until exploring the mechanism of pain in which I become more inclined to make such a diagnosis. To create consistency in research and amongst colleagues we need to address the actual form of PFPS were discussing. In addition, exploring this notion lays great premise on how we can guide our treatment. This is one condition where the diagnosis may actually be made after treatment is initiated. Dr. Wayne Button, BSc, D.C
