Author: Claire
Understanding Anatomy . Why it is Important. The Patellofemoral Joint.
Having recently met for my regular research meeting with an anatomy colleague of mine, it reminded me of the importance of anatomy and why we should understand it.
There has been controversy recently about the need for cadaveric teaching, the need for detailed anatomy, and from some quarters a push for moving right away from this ‘dry’ anatomy. I would like to take this opportunity to argue for its role, certainly with respect to understanding and treating patients with patellofemoral pain.
One of the counter arguments is that we need to consider behavioural response to pain, and not especially the source of the pain, particularly in patients who have central sensitization. However, I would ask how easy it is to understand and spot non-mechanical pain if you do not understand mechanical pain in the first place?
At the recent Patellofemoral Research Retreat that I attended there was a lot of focus on patellofemoral pain as a continuum with patellofemoral osteoarthritis. In line with this question there was interest around dysplasia. I personally am very interested by patellofemoral dysplasia and think that it is seen on a huge spectrum with many patients showing subtle anatomical variation. Dysplasia is such a good example of where understanding the anatomy really helps to alter treatment. So, for example if a patient has a lateralized tibial tuberosity I understand they will find it hard to absorb medial femoral rotation, so I think of particularly addressing horizontal plane control. In contrast someone with a long patella tendon, (patella alta) will take longer into flexion for their patella to engage, and hence receive stability from the trochlea. Understanding this anatomy leads me to focus their dynamic control work in the early ranges of knee flexion.
Understanding anatomy also helps me to understand potential tissue damage after dislocation, and helps me give out realistic prognosis and know when to refer on for a surgical opinion. So, for example take the medial patellofemoral ligament. This poor old ligament doesn’t even get a mention on the physiotherapy degree, and yet it plays a major part in stabilizing the patella. If I suspect a rupture after dislocation, I need to get this looked at.
Anatomy is also at the centre of my current research on the VMO. Our group our looking at the changes in fibre angle and insertion onto the patella, and forming a new paradigm as to what might be happening when we do quadriceps exercises. Understanding the anatomy helps to potentially identify who are good candidates for hypertrophy work.
Understanding anatomy further helps us work out what is the likely dysfunction when structures get tight. So, for example by understanding that the ITB itself cannot be stretched, but its contractile proximal attachments of gluteus maximus and tensor fascia lata can be, and by understanding that the distal ITB attaches to both the tibia and patella, I can understand the potential alteration that can occur if these structures get tight.
I do not for one-minute want to send the message out that understanding pain science and/or the psychosocial part of biopsychosocial is not important. It is very important, as evidenced by blog my on activity modification (http://www.clairepatella.com/activity-modification-in-the-treatment-of-patellofemoral-pain/ ). However, it is my belief that a deep understanding of applied anatomy has a definite place for anyone treating patients with patellofemoral pain.
Ideas para Médicos Clínicos desde el Retiro Femoropatelar, Manchester, 2015
Ideas para Médicos Clínicos desde el Retiro Femoropatelar, Manchester, 2015
Hay un problema inherente con el retiro: solamente puedes participar si estás presente. Por esta razón, he intentado extraer los puntos sobre los cuales los médicos deben desear reflexionar y que puedan auxiliar a evolucionar su práctica.
En mi opinión, el campo está todavía muy limitado en la biomecánica. Por supuesto que esto es relevante, pero todavía hay una división entre los practicantes de esta área y aquellos preocupados con la ciencia del dolor y de la adaptación comportamental. Un ejemplo de esto fue una discusión sobre si el ‘dolor’ debe ser eliminado de la etiqueta diagnóstica. ¡No! Es sobretodo por el dolor y, en última instancia, ¡es por esta razón que los pacientes vienen a batir en nuestras portas!
Andrew Amis hizo una charla inaugural realmente fantástica. Si estás interesado en biomecánica y alguna vez tenga la oportunidad de oír a Amis hablar – ¡ve! Sin ego aquí, realmente él no necesita tener tanta calidad o ser tan prolífico como su trabajo. Amis dijo que nosotros debemos estar conceptualizando el área de contacto, y no el mal encarrilamiento. Mucho antes del mal encarrilamiento, nosotros obtenemos presiones alteradas capaces de generar dolor, y frecuentemente estos resultados serán 30% elevados en PFP. Amis puso mucha atención en morfología anormal, como tendón rotuliano largo, forma tróclea y la distancia TTTG, y afirmó que esto tiene el potencial de alterar presiones de manera más rápida. Yo estoy completamente de acuerdo con esto, y como en muchas ocasiones, observo en clínica que esto ocurre en gran medida en un espectro. Finalmente un desafío para aquellos de ustedes que les gustan: Amis describe que el MPFL se une a la cabeza medial del gastrocnemio. Sin discusiones adicionales, considerando la importancia de esto…
Vincenzino presentó alteraciones en la sensibilidad termal y de dolor en PFP. Busque por pacientes que informen rodilla fría, sin importar el clima. James Selfe descubrió esto hace una década. ¡Es frustrante que nadie más haya realizado pesquisas sobre lo que hacer con estos pacientes! De manera intuitiva, ejercicios CV aparecerían en el topo de mi listado.
Michael Rathleff se presentó de manera muy buena en el retiro. ¡Qué pesquisador! Trabajo de alta calidad, en grandes números, céntrase en la población adolescente con PFP en Dinamarca. El trabajo que él presentó fue n=2200 (!!) A pesar del dolor, los adolescentes todavía tienen una frecuencia media de 5 episodios de deportes por semana. ¿Entonces sería un problema de carga excesiva? 55% de los adolescentes con dolor seguían así 2 años después. Más pesquisa es necesaria en este momento sobre los efectos del crecimiento.
Lee Herrington presentó una pieza muy breve sobre la velocidad de la corrida y el momento de aducción de la cadera. En pocas palabras, lo más rápido que corras, más grande es la aducción observada de la cadera. Esto es normal. ¿Podemos entonces utilizar velocidad como una manera de alterar la carga PFJ en rehabilitaciones? – Sí.
Lee también hizo una presentación sobre la utilización de ultrasonido para evaluar la carga de peso de la posición PFJ. Como parte de esto, él nos recuerda el trabajo de 2014 de Peng que muestra que aquellos que pueden reducir la inclinación con una SQC tienen más probabilidad de responder al fortalecimiento cuadrangular.
Matthews mostró una correlación muy útil: Si un paciente con PFP tiene más de 11mm de diferencia en su anchura media del pie en carga de peso de inexistente a completa, entonces un soporte ortopédico artificial es recomendado. Una pinza digital de una tienda de herramientas puede ser utilizada para esto. Bueno.
Otro de mucho peso, Felson (¡más de 500 publicaciones!), presentó un discurso sobre OA. Las mejores correlaciones con dolor en OA son la presencia de edema en medula ósea y sinovitis. Podemos detectarlos en una imagen de resonancia magnética. Esto está de acuerdo con el trabajo de Callaghan mostrando que el uso diario de un aparato ortopédico Q puede reducir el edema en la medula ósea en la tróclea lateral. Van der Hejiden presentó resultados de MRI para toda la populación normal de 14 hacia 40 años, y nos recordó que mismo en esta joven edad, 60% tenían osteofitos.
Hubieron muchas discusiones sobre la cuestión: ¿la PFP está en un continuo con la PFJ OA? Todavía sin conclusiones. Personalmente yo pienso que esto está relacionado con la morfología, y que con el tiempo nosotros seremos capaces de predecir aquellos que estén con un riesgo más grande de desarrollar PFJ OA por medio de su morfología PFJ.
Kay Crossley demostró la pérdida observada en la extensión de la cadera en PFJ OA. Esto encaja para mí y es por cierto algo que yo maximizaría en cualquier persona con PFP. La pérdida de la extensión de la cadera significa una flexión de rodilla más grande en la postura terminal.
Toby Smith presentó la Puntuación de Inestabilidad Femoropatelar Norwich para utilización después de la primera dislocación. En sus palabras, si buscas ‘Puntuación de Inestabilidad Femoropatelar Norwich’ en Google, podrás encontrar este recurso gratuito validado.
Hubo muchas presentaciones sin conclusiones sobre corrida y PFP. Esculier está demostrando hasta hora con su doctorado que la educación solamente ¡es tan eficaz como el fortalecimiento o la reeducación de la marcha en el tratamiento de PFP en corredores! Wow, esto realmente evidencía mi ya fuerte creencia en el poder de la educación.
Al final, ¡mi trabajo propio! Yo presenté un poco de mi trabajo vmo, mostrando simplemente que un programa cuadrangular en casa por 6 semanas en adultos sedentarios va a cambiar el ángulo de la fibra y la cantidad de músculo ligado a la borda mediana de la rótula, de acuerdo a las medidas realizadas con ultrasonido.
Para finalizar..
Se te gustaría aprender más sobre la integración de cualesquiera de los puntos arriba en su práctica clínica, entonces ¿por qué no unirte a mí para un curso de PFJ de 1 día? Si te gustaría un poco más de conocimiento de nicho, entonces busque mis clases magistrales. Y para aquellos que no pueden encontrar un curso próximo de ustedes, tienen dos opciones: Primeramente yo estoy siempre en búsqueda de nuevos lugares, entonces por favor contáctenme para hablar sobre recibir mi curso. En segundo, yo estoy para empezar a grabar toda una serie de webinars. Para todas las informaciones sobre ellos y más, por favor verificar en www.clairepatella.com
Si les gustaría mas blogs en español, por favor me envíen un correo y me lo dejen saber. Si hay demanda suficiente yo haré blogs futuros también en español.
The infrapatellar (Hoffa’s) fat pad explained
There are various fat pads, but the one at the knee that causes a lot of problems is the infrapatellar fat pad, also known as Hoffa’s fat pad after the man who first described it.
The fat pad has been shown to be very pain sensitive. It is rich with nerve endings that can fire off messages of pain to the brain, and it is therefore of no surprise that people with fat pad problems are often in a lot of pain.
The fat pad is often overlooked, with clinicians concentrating on joint surfaces, cartilage, ligaments and tendons, and dismissing the patient if these structures appear normal on imaging.
So what can go wrong in this funny pad of fat? There are two very different scenarios. The first is mechanical. The fat pad gets a trauma to it. Now this may be an obvious one off blow to the knee, or where the patient straightens their knee at speed and feels an immediate very sharp pain in the fat pad. Or, as is seen more commonly the fat pad may get nipped between the patella and the tibia, and microtrauma leads to a macro problem. In either of these situations it is common to see an inflammatory response. This is a problem as inflammation leads to swelling, and leads to the scenario where the fat pad gets pinched and caught even more. This feeds into a vicious cycle that many patients get completely stuck in. Furthermore, once the fat pad becomes big it alters the way the kneecap moves, and this in turn can lead to high pressure under the patella, which is also often painful.
Can anything be done? Yes! The first is to try and break the vicious cycle of inflammation and swelling. I often recommend ice massage to oiled skin, right on to the fat pad, (the ice-it-away is really effective for this), and will often tape the kneecap off the fat pad. Wearing a slight heel can help stop the patella knocking onto the fat pad, and most definitely avoiding standing with the knee locked back.
A treating clinician should also be assessing if there are other factors contributing to squashing the fat pad. These may, for example be quadriceps tightness, or poor movement patterns, particularly in people who are hypermobile.
There are also non-mechanical sources of problem in the fat pad, and these should be referred to as metabolic. This is seen with obesity and osteoarthritis of the knee.
Let’s take obesity. When someone is carrying excess fat they will have systemic inflammation. This is one of the reasons for raised cardiovascular risk, but the fat pad becomes inflamed and can hurt. The good news is that weight loss not only reduces load to the knee but also with immediate effect has been shown to reduce the inflammatory state of the knee.
In osteoarthritis it appears that the fat pad changes its state to produce unhelpful pro-inflammatory cells. As the fat pad is housed within the capsule of the knee the fat pad drives further joint breakdown that clearly is undesirable. The good news here is that any efforts to reduce the inflammatory state of the fat pad will have a positive effect on the inflammatory state of the whole knee.
To conclude, as weird as it is, this little pad of fat under the kneecap can be a very painful and persistent source of problem. Make sure you seek the right help to treat the problem, and help you get back to the things you love doing.
If you want to understand this in more depth why not look at my webinar on the fat pad https://t.co/juxILqftIm
Thoughts for Clinicians from the International Patellofemoral Pain Research Retreat, Sep 2015.
2nd – 5th September 2015
Thoughts for Clinicians from the Patellofemoral Retreat, Manchester, 2015.
There is an inherent problem with the retreat: you can only attend if you present. For this reason I have tried to draw out the points that clinicians may want to ponder over and may help evolve their practice.
In my opinion the field is still far too housed in biomechanics. Of course this is still relevant, but there is still a divide between the biomechanists, and those concerned with pain science and behavioural adaptation. An example of this was a discussion around whether ‘pain’ should be dropped from the diagnostic label. No! It is all about pain and ultimately this is why patients come knocking at our doors!
Andrew Amis gave a truly fantastic keynote talk. If you are interested in biomechanics and ever get the chance to hear Amis talk-go! No ego here, in fact he doesn’t need to be as his work is of such high quality and so prolific. Amis discussed that we should be conceptualizing contact area, and not maltracking. Well before maltracking do we get altered pressures capable of creating pain, and often these will be 30% elevated in PFP. Amis put a lot of focus on abnormal morphology, eg long patellar tendon, trochlea shape, and TTTG distance and stated that this has the potential to alter pressures more readily. I fully concur with this, and like most things observe in clinic that this occurs very much on a spectrum. Finally one for those of you that like the challenge: Amis reports that the MPFL attaches onto the medial head of gastrocnemius. No further discussion given re the relevance of this….
Vincenzino presented alteration in thermal and pain sensitivity in PFP. Look out for patients who report a cold knee, whatever the weather. James Selfe found this over a decade ago. Frustratingly no one has researched what to do with these patients! Intuitively CV exercise would feature high on my list.
Michael Rathleff featured highly at the retreat. What a researcher! High quality work, on big numbers, focuses on the adolescent population with PFP, in Denmark. The work he presented was n=2200 (!!) Despite pain adolescents still have a mean frequency of 5 episodes of sport per week. Is this all about excess load then? 55% of adolescents with pain still had it 2 years later. More work now needed on the effects of growth.
Lee Herrington presented a very succinct piece on running speed and hip adduction moment. In a nutshell, the faster you run, the more hip adduction seen. This is normal. Can we therefore use speed as a way of altering the PFJ load in rehab-yes.
Lee also presented on using ultrasound to assess weight bearing PFJ position. As part of this he reminds us of Peng 2014 work that shows that those who can reduce tilt with a SQC are more likely to respond to quads strengthening.
Matthews showed a very useful correlation: If a patient with PFP has more than 11mm difference in their midfoot width from non to full weight bearing then an orthotic is indicated. A digital caliper from a hardware shop can be used for this. Nice.
Another heavyweight, Felson, (over 500 publications!) presented a keynote on OA. The best correlates with pain in OA are the presence of bone marrow oedema and synovitis. We can see these on MRI scan. This fits nicely with Callaghan’s work showing that daily use of a Q brace can reduce bone marrow oedema in the lateral trochlea. Van der Hejiden presented MRI findings across the 14-40 year normal population and reminds us that even at this young age, 60% have osteophytes.
There was a lot of chat around the question: is PFP on a continuum with PFJ OA? No conclusions yet. Personally I think it is linked with morphology, and that with time we will be able to predict those who are at higher risk of developing PFJ OA by their PFJ morphology.
Kay Crossley demonstrated observed loss of hip extension in PFJ OA. This fits for me and is certainly something I would look to maximize in anyone with PFP. Loss of hip extension means greater knee flexion in terminal stance.
Toby Smith presented the Norwich Patellofemoral Instability Score for use after first time dislocation. In his words if you Google ,’ Norwich Patellofemoral Instability Score’ then you should find this free validated resource.
There were lots of inconclusive presentations around running and PFP. Esculier is demonstrating so far with his PhD that education alone is as effective as strengthening or gait re-education in the treatment of PFP in runners! Wow that really emphasizes my already held belief of the power of education.
Finally my own work! I presented some of my vmo work quite simply showing that an easy home quads programme for 6 weeks in sedentary adults will change both the fibre angle, and the amount of muscle attached to the medial border of the patella, as measured on ultrasound.
To finish..
If you would like to learn more on integrating any of the above into your clinical practice then why not join me for my 1 day PFJ course? If you would like a bit more niche knowledge then look out for my master classes. And for those of you that can ‘t see a course near you there are two options: Firstly I’m always looking out for new venues so please do approach me about hosting my course. Secondly I’m about to start recording a whole array of webinars. For all info on these and more then please look at www.clairepatella.com
Thanks! Any thoughts/comments very welcome!! Claire
A quick infographic to explain my recent vmo research
Click here to watch:
https://www.facebook.com/profile.php?id=100009872164024
You are more than welcome to email me if you would like more details!
Activity Modification in The Treatment of Patellofemoral Pain
Activity modification plays a vital part of my recommendations. Whilst the vast majority of PFJ problems should be classed as a nuisance but not a worry, activity modification is extremely useful. Why do I recommend activity modification? In a nutshell it changes the stress placed on the joint hence allowing the pain to settle, and can also buy a little time for treatment. Let’s examine this a bit closer:
There are any parameters involved with exercise. For example, take running. There is overall distance, speed, hills, and terrain to name but a few. So it may not be a case of stopping running, but altering some of the aforementioned parameters to decrease the load on the PFJ. Sometimes there may need to be a requirement to have a temporary cessation of running, and I am most likely to recommend this in the presence of inflammation and or bone oedema.
I would never recommend no exercise and so in this situation I am looking to work with the patient to help them find an alternative. In this situation I will be exploring aspects such as whether they like exercising in or outside, alone or in a group etc.
Activity modification does not always relate to sport. Hobbies such as gardening often require activity modification. In this instance I would be suggesting that the patient looks at all the jobs they want to do and with my facilitation work out which are highest stress for the PFJ, and then spread these tasks out. Everything still gets done, but perhaps in a different order, and ultimately in a way that reduces stress to their knee.
Finally stairs are a frequent aggravating factor for patients with PFP. Whilst I thoroughly commend people for using the stairs for exercise, if this genuinely is a clear aggravating movement then the pros of doing repeated stairs may be outweighed by the negatives. In this instance I would look to help the patient re-evaluate how they are getting their exercise.
To summarise, the measures outlined above are not rocket science, but must not be overlooked. With clever activity modification, (often only temporarily) a patient will have quicker resolution of their problem, will hopefully not have had the negative experience of just being told to ‘not’ do something, and ideally will be more understanding about the effects of their daily life on their joint.