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Ultrasound guided corticosteroid injection for plantar fasciitis

Discussion in 'Biomechanics, Sports and Foot orthoses' started by NewsBot, May 23, 2012.

  1. NewsBot

    NewsBot The Admin that posts the news.


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    Ultrasound guided corticosteroid injection for plantar fasciitis: randomised controlled trial
    Andrew M McMillan, Karl B Landorf, Mark F Gilheany, Adam R Bird, Adam D Morrow, Hylton B Menz
    BMJ 2012; 344 doi: 10.1136/bmj.e3260 (Published 22 May 2012)
  2. Admin2

    Admin2 Administrator Staff Member

  3. drsarbes

    drsarbes Well-Known Member

    Sounds like someone just got a new MSK US machine and wants to use it!

  4. Karl Landorf

    Karl Landorf Member

    Dear Steve,

    Sorry, but I'm going to address this quckly as I am unsure of what your inference is in your post, but it does appear to be quite offhand.

    Anyway, for the record, the ultrasound scans were paid for from research funds from the departments involved in the research. The scans were conducted at a local medical imaging group, who we have had a research relatsionship for about 5 years now. We did not, as you put it, just get a new MSK US unit!

    This article has been published in the British Medical Journal and it is good for podiatry. Please don't bag the research or the investigators through the relative safety of Podiatry Arena. Andrew McMillan, the 1st author on this randomised controlled trial, is a very good young researcher. This trial was the main project in his PhD and he has done an outstanding job. For a PhD student to publish their work in the BMJ is an outstanding achievement and due to the quality of peer-review, is a real vote of confidence in the work.

    Please be supportive of your colleagues.

    Best wishes,

    Dr Karl Landorf
    La Trobe University
  5. Karl Landorf

    Karl Landorf Member

    Can I please request that if people want to post a reply to this thread, that they read Andrew's article closely before doing so. Craig has posted the publication details so everyone should be able to get access to the article.

    By doing so, you will be aware of the justification for the project and methods used. That is, you will make informed comments if you do choose to post.

    Thank you,


    Dr Karl Landorf
    Research Coordinator
    Department of Podiatry
    La Trobe University

  6. Looks like a good study to me. Don't think I remember this type of study being done before so hats off to Andrew and coauthors for producing the type of research that sorely needs to be done in podiatry.

    Now, the question that I would appreciate Andrew, Karl, Hylton and the others to answer for me: many "authorities" say that the condition of "plantar fasciitis" should rather be called "plantar fasciosis" since they site a few studies that showed no inflammatory cells within plantar fascia biopsies as being "proof" of it not being a disease of inflammation but rather a disease of degeneration. In fact some suggest that the term "plantar fasciitis" should be discarded because of these bits of research and Lemont et al (2003) also calls into question the practice of serial corticosteroid injections for this condition. It is also interesting to note that others have found chronic inflammatory changes with plantar fasciitis (Buchbinder, 2004).

    However, certainly with a short acting steroid, I would imagine the main effect of the steroid is anti-inflammatory in nature, rather than anti-degenerative in nature, thereby the relief in pain for approximately four weeks (which correlates with my clinical experience of probably doing over a thousand of these injections over the past 27+ years) seem more likely to reducing the localized inflammation in or around the plantar fascia than some other mechanism.

    Question: Does this study support more that "plantar fasciitis" is a disease of inflammation or rather a disease of degneration of the plantar aponeurosis? What further research could be done to get to the bottom of what causes the pain of plantar fasciitis, if your study does not do so?

    Good job Andrew and Co-Authors!!:drinks
  7. CraigT

    CraigT Well-Known Member

    Outstanding work guys!
  8. Karl Landorf

    Karl Landorf Member

    Apologies, I need to correct an earlier post because I have confused myself with another study that we have been involved in.

    We have conducted two studies, this RCT and another case-control study, where we have utilised ultrasonography for the diagnosis and monitoring of the condition in question.

    In the RCT, we used an ultrasound machine owned (for the past 5 years or so) by La Trobe University and we used it in our clinic to measure the thickness and observe the appearance of the fascia.

    In the other study, the case-control study (still to be published), we used a far more expensive machine at the medical imaging organisation mentioned in my earlier post. We had to do this because we wanted to use power Doppler and our machine did not have this function.


  9. Peter

    Peter Well-Known Member

    I remember reading the research protocol in JRES i think, and thought, WOW, these guys have covered evrything!

    Having just finished studying in Med.Ultrasound, I can categorically state that there is so little "evidence" regarding interventional and diagnostic sonography, and this type of research starts to address some of those issues, and pose further questions also.
  10. drsarbes

    drsarbes Well-Known Member

    I was referring to the fact that we are, apparently, losing the ability to inject without US guidance, not the study itself.

    I'm sure I'll get conflicting comments from this, but.................. why do we need US to inject the fascia?
    It's a fairly simple site to inject and why put a patient (or an insurance company or a government agency) through the additional cost of needle guidance when most, if not all of us, are very capable of injecting for fasciitis without it?

  11. Peter

    Peter Well-Known Member

    Hi Dr Arbes,

    I have done quite a few scans and am amazed at the variation in the location of the fasciosis itself, some on the lateral aspect of the medial tubercle, some very posterior on the tubercle, some on the calcaneal surface only, by and large most are in the "traditional" area, the outliers are not. US has shown us the variation in plantar fasciosis to "target" out injection therapy better/safer.

  12. Peter

    Peter Well-Known Member

    pre-rx 2.JPG

    I hope the enclosed Sonogram attaches, it shows the fasciosis occurring on the lateral aspect of the medial tubercle.
  13. drsarbes

    drsarbes Well-Known Member

    Hi Peter:
    Duly noted.
  14. Peter:

    I'm with Steve on this one.

    Here's is what I do when I inject the plantar heel for "proximal plantar fasciitis". I push firmly on the plantar heel and with the patient's help, find the point of maximal tenderness (PMT). The PMT is now marked with an "X" with a pen on the plantar heel.

    The patient is placed prone on the table (i.e. plinth), their knee is extended 90 degrees and their foot is dorsiflexed so that the plantar foot is now facing straight upward. After using an isopropyl prep pad to clean the area of injection, either myself, or my assistant, will get the PMT temporarily frozen with ethyl chloride spray after which I inject directly into the "X" at the PMT with a mixture of local anesthetic and corsitione solution. The plantar fascia is easily felt (as increased resistance in the needle/syringe) and even heard as a "celery crunching sound" as the needle is placed repeatedly plantar and dorsal to the fascia in an area ranging in diameter from 1.0- 1.5 cm at the level of the plantar fascia.

    I have been giving cortisone injections like this for 25 years now, give probably 5 of these injections per week, 250 injections per year and therefore probably have given at least a few thousand cortisone injections into the plantar fascia using this prone-plantar injection technique over the past quarter century. And, amazingly enough, each injection takes less than 60 seconds to give, and has never required an expensive diagnostic ultrasound machine to do so. And I get routinely good to excellent patient pain relief results with these injections.

    Do you really need to use an ultrasound device to know you are accurately injecting the most symptomatic areas of the plantar fascia? I don't think so.
  15. Lab Guy

    Lab Guy Well-Known Member

    I thought it was a very well written paper as well. I also agree with the comments from Kevin and Steve.

    Here in the USA, insurance companies pay about $160.00 for the use of ultrasound (US) for cortisone injections. Some insurance companies have stopped paying for US guided injections for plantar fasciitis but others, including Medicare continue to pay.

    With that being said, I do not think it is a surprise that the US guided steroid injection provided superior results to normal saline. I do think its important to ascertain if it is financially prudent for our health care dollars to pay for a US guided injection versus non-US guided injuections (like Kevin's technique).

    I think if a second paper was written comparing the results of patients given an US guided cortisone injection versus patients giving a cortisone injection without US that the end results would be the same. If they are the same, then we can use that knowledge to not use US for the diagnosis of plantar fasciitis and save our health care dollars for something worthy.

    I think US is necessary for injecting an impinged spinal nerve in the back but in my own opinion, US is simply a billing device when used to administer injections for plantar fasciitis.

  16. I just went to a 2 day Primary care conference in Birmingham UK and am totally blown away by the expertise of the Podiatrist and the level and scope of work they do.
    I am sooooo inspired.
    Check the Primary care 2012 website and you may get all the data from it
  17. Peter

    Peter Well-Known Member

    Hi Kevin, I'm not disputing anybody's technique, I used to undertake blind steroid injections myself, but as I am fortunate enough to have an US machine for diagnostic purposes in my clinic room, is it not feasible to add a few seconds to the injection procedure by using the diagnostic technology for interventional procedures?

    I am unsure about the US, but in the UK and Europe, MSK US is gaining popularity due to its real-time imaging modality, portability, cheap to administer and non-ionising radiation, and now Podiatrists are gaining accredited training in this imaging to complement other clinical skills, including injection therapy,

    Respectfully yours,

  18. Peter:

    I'm sure that US is helpful. And I'm sure for someone who has a US unit already, that it could be used to give an injection and that it may be good practice management to do so (more $$$). If you like using US for giving injections, then this certainly seems very reasonable to me.

    However, as the 65 year old orthopedic surgeon I have been working with for the past 26 years just told me when I mentioned this thread we are discussing now, he told me that he also didn't really feel a need to use US to give a good cortisone injection:

    "However, I guess I'm just a fossil and nobody really cares what the **** I think any more."

    That statement just about sums it up for me also when I hear that podiatrists absolutely need to use US guidance to do a good plantar cortisone injection for plantar fasciitis.:cool:
  19. Peter

    Peter Well-Known Member

    Hi Kevin,
    I don't believe anyone in this thread has said the above,

    It appears that I am probably on a different wavelength to everybody else on Podiatry Arena these days, so will take a break:sinking:


  20. Peter:

    I'm sure that many may find that US guided cortisone injections for plantar fasciitis are the way they feel they can best help the patient. The only point I am making is that US guidance is not needed to give effective injections for plantar fasciitis.

    In the study referenced, I think the US guidance helped to strengthen the paper since it offers confirmation that the plantar fascia was indeed injected by the examiners. In my hands, however, I don't think US would help my patients that much since I am sure that by using my knowledge of the anatomy of the foot along with my "feel" for the plantar fascia that I am putting the cortisone in the area that I want it to be in.

    A good followup study would be to see if there is any difference in therapeutic effect of US guided and non-US guided cortisone injections for plantar fasciitis.:drinks
  21. bmjones1234

    bmjones1234 Active Member

    Maybe US is best for student building clinical experience, but once they have a good few years [Say 5yr] then it might not become as 'essential'. And by the time they eventually reach your level of expertise, then it might not be necessary at all. After all - like any career it becomes and Art [Hence Artisan] at its highest levels. I am (Hopefully) a freshly qualified student in Podiatry, we haven't be shown any steroid injections as on yet, but I can see the benefit of improving accuracy using an US machine, yet if I felt that my instincts and results of success were higher without an US then I would only use it on tricky instances or complicated cases.
  22. drsarbes

    drsarbes Well-Known Member

    Hi all

    I do have an MSK US in my office, and I must say it takes (me at least) more than a few minutes extra to us it in order to inject.
    I have not found any benefit from using it for most injections I do, and I refuse to use it just to pad my patient's bill (NO, I'm NOT saying that is what anyone is doing, I'm just saying that I will not)

    I could also see that if you are not on a tight schedule one might be more inclined to use it.

    I do agree that in an educational setting it could help inexperienced practitioners "see" where they are injecting and "feel" the differences of various tissue resistance.

    Jones1234..... I don't think it's a matter of time but rather how many you have done.

  23. Mart

    Mart Well-Known Member

    Karl I understand your indignation; problem with lack of non verbal clues on internet forums and not necessarily knowing the personalities using them . Having talked to Steve a fair bit and "knowing" him somewhat I would say that he was being whimsical rather than insulting. I agree that this purports to be an academic forum and that is sometimes traded for "humour" which doesn't always sit well.

    Notwithstanding the expertise of the person giving the injection the only way anyone can be sure of the deposition of an injected substance is to “see” where it is being put. When I started doing US guided injections for plantar aponeurosis I realized that prior I had not done a reliable job. I lacked the expertise. Having done many now I feel much more adept and simply mark the injection site and depth with US then doing the injection “blind’ but with decent map.

    I can report that I see people with heel pain and recent corticosteroid injection done elsewhere which didn't help who after examining them demonstrated a sonographically normal plantar aponeurosis which suggested that chronic plantar fasciosis was not issue in first place.

    Also problem is when we look at most research data for these kinds of interventions they are largely poor quality because there is no indication as to certainty of delivering drug where intended. That is why for research purposes I believe US guidance is vital.

    For those of us using US daily as part of physical exam it makes no sense not to use it. Whether it improves outcomes would depend on skill of clinical at doing blind injections. I have no embarrassment to say that I would not trust my judgment to do most of my injections blind; but I admit to having a bias based on my experience.



    Foot and Ankle Clinic
    1365 Grant Ave.
    Winnipeg Manitoba R3M 1Z8
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    Last edited: May 29, 2012
  24. Martin:

    I have a question for you since you seem to have a great deal of experience with diagnostic ultrasound (US). When giving a plantar heel injection with cortisone, I use a 25 gauge, 1.5" needle and can very distinctly feel when I reach the central component of the plantar aponeurosis (i.e. plantar fascia) by the added resistance encountered while trying to advance the needle. In addition, I can also feel the decreased resistance to advancing the needle once I feel I am completely through the plantar fascia with the needle tip now deep to the plantar fascia.

    Do you think that the US would give a clinician significantly more accuracy with cortisone injection placement if they were to use the tactile feel of the injection process rather than using US? In other words, it would be interesting to see if when you first "felt" the plantar fascia with the needle, that indeed correlated to when the needle was first encountering the plantar fascia and if the feeling of less resistance correlated to when the needle pierced through the fascia. Sounds like a great research project for someone with a diagnostic US machine at their disposal!
  25. Mart

    Mart Well-Known Member

    Hi Kevin

    I think your interpretation of the feel of the needle is correct and useful.

    From discussion we have had in the past I understand that your technique is to palpate medial process of calcaneal tuberosity and take the shortest route via plantar approach.

    This intuitively seems to provide best precision for blind injection.

    I think there may be some limitation to this idea though if wanting to “fan” the injection within the fascia since without US it is impossible to know where the zone of degeneration extends to. For example in some people the degenerated zone can extend 3 or 4 cms distal to the MCT. In others not insertional but somewhat distal to medial process of calcaneal tuberosity though with exam the entire region is tender to palpation.

    As Peter mentioned, uncommonly the lateral band of the plantar aponeurosis is sometimes degenerated; I am unsure how well palpation without US can differentiate this from more usual situation.

    I can tell you that when I started doing guided injections I used my foot as a learning tool (still do) and can recall that I observed (and felt!) exactly what you described but unsure how well this might be generalized, so perhaps your study idea has some merit.

    I believe that the tactile feel may be influenced by needle gauge (I use 27g and this tactile feel you describe is often ambiguous) and also how quickly you advance the needle. Resistance to actually ejecting fluid I think is likely very specific to “being within the fascia”.

    As you know, the problem is that if injecting superficial to fascia the plantar fibro-fatty pad may be adversely metabolized. Also if the needle is too proximal having the cortex insulted might be a bit rich. I wonder if it is possible to disrupt an enthesite with your technique and create some problems.

    I continue to justify using US for chronic plantar fasciosis injections then for a variety of reasons other than my lack of expertise.

    When I started doing guided injections I used same approach as show in this study; it can be quite tricky and time consuming to visualize the oblique needle properly which is why I simply map the zone now with US which is much more convenient and faster. There are special US needles which have highly reflective surface and really easy to see but they are thick and therefore not very kind for this injection.

    Clinical exam doesn’t differentiate neovascularization. The study cited in this thread didn’t use power Doppler imaging to evaluate this. Whilst it is unclear what role neovascularization has in plantar heel pain it may influence outcomes and was not controlled for other than randomizing subjects in this study; it is possible that corticosteroid injection is more effective in presence of true “inflammation” vs degeneration. I think that the results using soluble corticosteroid are somewhat consistent in terms of duration of effect compared to insoluble agent which seems associated with longer pain relief. I thought it was interesting that it was speculated that the insoluble agent might be more risk averse.

    Where I find US extremely useful and would be surprised if anyone could duplicate this blind is with small distal plantar aponeurosis defects. I am not talking about plantar fibromatosis nodules but lesions which appear as tiny expansible voids which I interpret a small none healing tears. Whilst these can be can be palpated as tender areas I think that it would be difficult to know how to inject these properly without US because the fascia is usually less than 2mm thick and lesion similarly around 2mm wide in these zones (typical insertional fasciosis is 5-10 mm).



    Foot and Ankle Clinic
    1365 Grant Ave.
    Winnipeg Manitoba R3M 1Z8
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    Last edited: May 30, 2012
  26. toomoon

    toomoon Well-Known Member

    Now, the question that I would appreciate Andrew, Karl, Hylton and the others to answer for me: many "authorities" say that the condition of "plantar fasciitis" should rather be called "plantar fasciosis" since they site a few studies that showed no inflammatory cells within plantar fascia biopsies as being "proof" of it not being a disease of inflammation but rather a disease of degeneration. In fact some suggest that the term "plantar fasciitis" should be discarded because of these bits of research and Lemont et al (2003) also calls into question the practice of serial corticosteroid injections for this condition. It is also interesting to note that others have found chronic inflammatory changes with plantar fasciitis (Buchbinder, 2004).

    Question: Does this study support more that "plantar fasciitis" is a disease of inflammation or rather a disease of degneration of the plantar aponeurosis? What further research could be done to get to the bottom of what causes the pain of plantar fasciitis, if your study does not do so?

    Anyone game to have a shot at Kevin's question? Seems to have been lost in other discussions but is highly relevant.
  27. Peter

    Peter Well-Known Member

    I have only seen Power doppler signal in 2 cases of plantar fasciitis, and would be more than happy to call it fasciosis instead. For what its worth, both cases had abnormal bloods at the time of scanning, and when blood work restored to normality, the inflammation resolved too.
  28. toomoon

    toomoon Well-Known Member

    Very interesting Peter.. my take on it is that it is probably inflammatory early.. but no-one is insane enough to biopsy it at this stage. For us.. it usually presents as a chronic condition and since chronic conditions have no inflammatory infiltrate, primary inflammation is no longer the major factor and degeneration is.
    Thus I propose the condition most podiatrist treat is indeed not 'plantar fasciitis' (especially given the structure involved is an aponeurosis and not a fascia), and therefore the correct term should either be plantar fasciosis or plantar fasciopathy, but given my remark in parentheses, it really should just be called chronic plantar heel pain until such time as an absolute diagnosis can be made.
  29. Simon:

    Then, if your hypothesis is correct that primary inflammation is no longer the major factor in what we call plantar fasciitis or plantar fasciosus, why would a short acting corticosteroid injection (an anti-inflammatory agent) cause such signficant decrease in foot pain in the subjects in this study?

    See you next week, Simon. I'll be flying into Manchester on Wednesday, the 20th. Bring your guitar...I'll buy the beers.:drinks
  30. Mart

    Mart Well-Known Member

    I think this is an interesting question.

    We know that inflammation is a complex process part of which involves up and down regulating gene expression via numerous different mediators.

    My understanding is that during wound healing there is a normal sequence of cell activity and chronology to the cell signalling.

    With impaired healing there is a different pathway and this is regarded as pathological. with chronic plantar fasciosis there seems consensus that there is a problem where healing rate is less than injury rate. Hence the degenerative nature.

    I think that it is unclear what specific mediators are active through the natural history of this complaint.

    I have noticed, as Peter mentioned, that neovascularisation with chronic plantar fasciosis detectable with power Doppler imaging is uncommon.

    It also raises possible diagnosis of a reactive arthritide as cause as opposed to mechanical trauma, an important distinction because it needs a different approach.
    s a generalization it does seem most common early in presentation of plantar heel pain and most people don't seem to seek help at this stage unless very painful.

    I think it is likely that corticosteroids have capacity to down regulate pain inducing inflammatory modulators - this can happen in absence of mediators which might upregulate vascular growth and this may explain pain reduction in absence of neovasularisation.

    In that sense we might want to reconsider what the term inflammation means since generally it is associated with increased vascularity.

    Being a pedant, I tend to use the description chronic plantar fasciosis (and tendonosis) with or without out neovacularisation in my reporting.



    Foot and Ankle Clinic
    1365 Grant Ave.
    Winnipeg Manitoba R3M 1Z8
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
  31. toomoon

    toomoon Well-Known Member

    hmm.. depends. Are you exclusively infiltrating CS or are you injecting a cocktail?
  32. Mart

    Mart Well-Known Member

    Assuming that you are thinking of local anesthetic as the other component; just wondering why would that make any difference to CS effect on "inflammation" other than if using same dose increasing volume and diluting concentration of CS?



    Foot and Ankle Clinic
    1365 Grant Ave.
    Winnipeg Manitoba R3M 1Z8
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
  33. toomoon

    toomoon Well-Known Member

  34. Mart

    Mart Well-Known Member

  35. Mart:

    Good posting.:good:

    My belief that is we are just don't sufficient knowledge yet to know, for sure, how much of "plantar fasciitis" is inflammatory and how much of "plantar fasciitis" is "fasciosus"to some extent and that not all cases of "plantar fasciitis" should be called "plantar fasciosus". I'm not for making wholesale changes in diagnostic names unless there is concrete evidence that the name change needs to occur. Short acting cortisone's main effect on the human body is a reduction in inflammation. Patient after patient after patient get good temporary relief of less chronic cases of plantar fasciitis with cortisone injections...most likely by reducing inflammation, whether it is within the actual substance of the plantar aponeurosis or within the tissue that surrounds the plantar aponeurosis. Until someone can conclusively prove to me that all cases of what we currently call plantar fasciitis are non-inflammatory in nature, then I will not start making a wholesale change in calling all conditions of this nature "plantar fasciosus".

    Maybe the term plantar fascial dysfunction would be a better.
  36. toomoon

    toomoon Well-Known Member

    Thanks for the posting Martin.. this is such an interesting topic.

    I do not think there is any great surprise that once there has been change to the fascia, it will not revert even in the absence of pain. This is exactly what we see with tendinopathy, and the plantar fascia behaves in a similar manner. I suspect that more than anything this has to do with the relatively greater concentration of Type 3 collagen vs the normal Type 1, with Type 3 collagen being very unlikely to remodel after it is established since it is not designed as much as stress or load accepting material. By far the most abundant collagen in human tissue is type I which accounts for between 65 – 95% of the total collagens. Type I collagen is the major protein of tenon, ligament, bone, skin and intramuscular connective tissue, with small amounts of other types of collagen (types V, III, VII and XIV). Type I collagen is found predominantly in these tissues because it tends to form into parallel fibres which produce high tensile strength and limited elasticity. In tendons and the plantar fascia the fibres are also arranged horizontally and transversely to form spirals and plaits along their course. This type of tissue therefore is eminently suited for force transmission.

    In terms of quantity, type III collagen ( or more properly labelled Collagen alpha-1(III) is the second most prevalent. In adult tissue its proportion ranges from 5 – 30% but high proportions exist in foetal and granulation tissue. So, when the ratio of Type III to Type I collagen is abnormally high, the normal parallel bundled fibre structure is disturbed; the continuity of the collagen is lost with disorganized fiber structure and evidence of both collagen repair and collagen degeneration.
    Microtears and collagen fibre separations are seen. Many of the collagen fibres are thin, fragile, and separated from each other.
    The number of fibroblast cells is increased; the tenocytes look different, with a more blast-like morphology (the cells look thicker, less linear). These differences show that the cells are actively trying to repair the tissue.
    Perhaps the major reason for the phenomenon you observe is that when tenocytes are cultured from tendinosis they continue to produce abnormal collagen outside of the body; the tenocytes produced collagen with abnormally high Type III to Type I ratios (as compared to collagen produced by tenocytes cultured from normal tendon). This observation is significant because it shows that the tenocytes have been altered and continue to produce abnormal collagen even when the repetitive or injurious motion is no longer present.
    Check out: Maffulli N, Ewen SWB, Waterston SW, et al. Tenocytes from ruptured and tendinopathic Achilles tendons produce greater quantities of Type III collagen than tenocytes from normal Achilles tendons. Am J Sports Med 28(4):499-505, 2000.

    Interesting discussion..
  37. toomoon

    toomoon Well-Known Member

    Well Dr. Kirby, it does not happen often, but I am afraid I must put forth an opposite view (as distinct from a disagreement). I put forth the following with input from my friend Scott Wearing

    I have not looked specifically at corticosteroids for a long time and am probably not the best person to comment.. but I will anyway (;.
    Having said that, I seem to recall that generally, they show a positive effect but one that is short lived (~1month) and is often confounded by a powerful response to placebo. For instance, it seems that "needling" without injection may be as effective as injection with corticosteroids in tendinopathies.

    In the absence to evidence to the contrary, I assume the pathological pathway to PFitis is probably similar to that of tendinopathy.

    So, if I assume that steroids work in some people at least some of the time; then it is possible that PFitis may have a local inflammatory component (at least in some phase(s) of the disease).

    Certainly, corticoid steroids are potent anti-inflamm agents that act directly on nuclear steroid receptors to control rate of synthesis of mRNA and proteins. This has a number of consequences, including changes in T and B cell functions, changes in white cell traffic, alterations in levels of cytokines and enzymes, and inhibition of phospholipase A2 resulting in a reduction in proinflammatory derivatives of arachidonic acid (everyone seems to be pinning their hopes on PGE2). Some of these derivatives, such as bradykinin or histamine, can stimulate nociceptive fibres directly while others (prostaglandins, leukotrienes, and interleukins 1 and 6 may sensitise nociceptives to mechanical or other stimuli.

    However, based on findings in tendinopathy, it is possible that pain may not be mediated via prostaglandins (ie chemical inflammation). I think it was Alfredson that first demonstrated PGE2 levels were not elevated in tendinopathy but rather neurotransmitters (that were previously thought to be found only in the CNS), such as Glutimate were elevated. Interestingly, glucocorticoids have also recently been shown to suppress synaptic glutamate release (albeit in other tissues), so it is possible that corticosteroid injections may act via this pathway instead via their perceived anti-inflammatory role.

    As for the changes in plantar fascial dimensions that have been observed with steroid injection over the short term, these are generally modest (witihin measurement error) and, if I was a betting man, probably related to tissue fluid levels rather than alterations in collagen1.

    I tihnk I should probably stop my tirade now - sorry!
  38. Good posting, Simon.:good:

    How about "plantar fascial dysfunction" since we really don't know how much of what we currently call "plantar fasciitis" and/or "plantar fasciosus" is inflammatory in nature and how much of it is degenerative in nature?

    About time you started contributing more here on something other than barefoot running.....:wacko::cool::drinks
  39. toomoon

    toomoon Well-Known Member

    Haha.. yeah.. I am preparing myself for the day ASICS sacks me and I have nothing to do. I used to be a podiatrist once you know, and plantar heel pain was always my... "Achilles Heel".. boom boom.. because in so many ways what was being taught and the treatment methods never made sense to me.

    I still am not sure about the term plantar fascial dysfunction because it really IS the plantar aponeurosis. Seems nitpicking I know, but how come we have to accept this misnomer? If it makes sense to everyone else, then I am ok with it, and it seems that we just cannot shake the global acceptance of the involvement of the "plantar fascia"... maybe I should just conform! I have always just been happy with chronic plantar heel pain. Accurate and descriptive in the absence of an absolute diagnosis.
    Guitar tuned, packed and ready to accompany your dulcet tones next week my friend!

  40. Simon and Colleagues:

    Even though when I do my lecture on the "Ten Functions of the Plantar Fascia" I go into great detail that what we commonly clinically call the "plantar fascia" is actually the "central component of the plantar aponeurosis", I have decided that sometimes I should call this structure the plantar fascia since most clinicians use this term "plantar fascia" to describe the central component of the plantar aponeurosis (CCPA).

    However, now having slept on my suggestion of "plantar fascial dysfunction" for one night, I think I will change my mind and suggest that the term "plantar fascial stress syndrome" may, perhaps, be a better name for the myriad of tension stress-related and compression stress-related conditions of the CCPA.

    Plantar fascia stress syndrome would include the conditions of:

    1. Proximal plantar fasciitis (i.e. plantar heel pain syndrome)
    2. Distal plantar fasciitis (i.e. no heel pain, only arch pain)
    3. Chronic plantar fasciosis

    and possibly also include:

    4. Plantar fascial pain due to partial ruptures of the CCPA.

    Creation of a new term that included both the inflammatory, more acute condition of "plantar fasciitis" and the degenerative, more chronic condition of "plantar fasciosus", since we really never know how much inflammation vs degeneration is the cause of the pain in these patients, would make sense to me clinically.

    What say all of you?

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