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'Inflammatory' vs 'mechanical' plantar fasciitis

Discussion in 'Biomechanics, Sports and Foot orthoses' started by Craig Payne, Jul 18, 2006.

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  1. Craig Payne

    Craig Payne Moderator


    Members do not see these Ads. Sign Up.
    I have always used the term 'mechanical' plantar fasciitis to refer to the 'run of the mill' 'garden variety' plantar fasciitis that we see every day due to mechanical causes.

    I usually use the term 'inflammatory' plantar fasciitis to refer to the much less common enthesitis of the attachment of the plantar fascia that occurs in certain rheumatological conditions (ie the seronegative spondyloarthropathies).

    They are both different beasts. Why is it that when I read in most podiatric texts and articles, especially those from the USA, that the management of the 'inflammatory' type is the same as the 'mechanical' type (ie low dye strapping; stretching; foot orthoses; night splints). My success rate with treating 'inflammatory' plantar fasciitis with these modalities is 100% failure so can not understand why these authors suggest such treatments :confused: - how many cases of this type of plantar fasciitis have they actually seen? ... the best I have been able to achieve with these people is some minor symptomatic relief. They normally respond dramatically to some of the newer drugs aimed at the spondyloarthropathy.

    What brought this up today, was the appearance of this case report that caught my eye:
    What say you?
  2. Atlas

    Atlas Well-Known Member

    It is quite confusing. Your knowlege of inflammatory conditions puts you in a better position to comment.

    From a purely mechanical and musculoskeletal view point, we accepted years ago, that mechanical pain, gets worse with activity...or rather, as the day goes on. Conversely, inflammatory pain gets worse with inactivity...or rather, first thing in the morning.

    The dilemma with that guideline, is that as we know, tendinopathies (shin splints) can peak with initial activity and ease during the warm-up phase...only to peak again at the end of activity and post-activity.

    The other dilemma is that don't NSAIDs relieve both types? They even relieve knee tendinopathy, and Jill Cook (I think) has shown that no inflammatory presence is detected microscopically.

    You would think that tensile stress in the plantar fascia is not 'enjoyed' by both the mechanical variety and the inflammatory variety. I would have thought that a strong application of low dye taping that reduces tensile stress would assist both, at least for the short-term.
  3. Craig Payne

    Craig Payne Moderator

    Ron - the plantar fasciitis I have seen associated with a seronegative spondyloarthropathy just do not seem to repsond to any sort of therapy to off load the plantar fascia (ie low dye strapping), yet the podiatric texts and articles I read say to do this :confused:

    I have now got a full copy of the case above --- he had an undifferentiated form of spondyloarthritis with severe heel pain --- it responded instantly to the adalimumab (anti-TNFapha) injectin.

    There was also this publication I have in my files:
    D'Agostino MA et al: Refractory inflammatory heel pain in spondylarthropathy: a significant response to infliximab. Arthr Rheum 46:840-841 2002
  4. Scorpio622

    Scorpio622 Active Member

    I agree that medical treatment is primary in rheumatologic heel pain, but why not add a low dye taping,or arch support,or shoe modification to decrease the PF tension? Inflammation from any source (rheumo, infection, macrotrauma, microtrauma) would be exascerbated by mechanical forces- unless I'm missing something here. If mechanical offloading is achieved and the pain is unchanged, then I would suspect that the pain generator is elsewhere (bursitis) or the pain has not be decreased to the threshold of perceived improvement.

    Wouldn't you try to decrease the pull on an "inflammatory" achilles tendonitis with heel lifts, etc????

  5. Atlas

    Atlas Well-Known Member

  6. Mart

    Mart Well-Known Member


    Carrying on from your thread regarding Diagnostic ultrasound exam of plantar plates, I had bought up an issue which I have more confidence and experience with when using US and we started the interesting issue of fasciitis vs fasciosis.
    Your reluctance to jump on bandwagons is well taken.

    As a little bit of background, increasingly I am using Diagnostic ultrasound (DUS) with power doppler (PDI) to try and distinguish between “itis” and “osis”.
    This has allowed me to suspect higher incidence of inflammatory MSK disease in the foot than I had before.

    For example I have recently suspected gouty artritis in 2 people previously diagnosed with osteo-arthritis from physical and radiographic exam by primary care physician. They have normal serum uric acid, episodic pain which is not classic podagra, (not hot or swollen with rest pain), demonstrate osteo-arthritic changes with radiographic exam. When I examined them there was evidence of synovitis and flow with PDI, and I saw birifringent needle shaped crystals with artrocentisis and polarisised microscopy.

    This is a bit lengthy but the devil is in the detail and I feel gives weight to my growing conviction that there already is convincing evidence regarding the nature of plantar fascia disease and the means to determine this using DUS.
    If this is true then the implication is that we should be able to design the prospective studies which are lacking using DUS and possibly make better decisions regarding treatment planning and predicting outcomes.

    My impression is that the evidence points to likelihood for the condition to exist as

    one OR other

    rather than

    one NOT ever the other.

    Craig hinted at this in his initial post.

    My experience with diagnostic ultrasound and the plantar fascia is of being able to frequently detect abnormal appearance with grayscale DUS but unable to detect inflammatory hyperaemia of the plantar fascia in cases of long standing plantar heel pain.

    I have been very curious about how to interpret this and it’s implications and last week did a pretty thorough literature study around these observations.

    I suggested that I would attempt to pull together some ideas into a cohesive posting , more has been posted around this subject on the arena than any other and I hope this adds something new and useful; here’s my efforts.

    As a generalization there seemed to be;

    differences from previous individuals in posts regarding treatment plans and the underlying pathology of plantar heel pain attributed to injury/disease of the plantar fascia.

    - a growing trend, to regard inflammation or fasciitis less likely than degeneration or fasciosis.

    A good recent reference along these lines:

    The authors review histologic findings from 50 cases of heel spur surgery for chronic plantar fasciitis. Findings include myxoid degeneration with fragmentation and degeneration of the plantar fascia and bone marrow vascular ectasia. Histologic findings are presented to support the thesis that "plantar fasciitis" is a degenerative fasciosis without inflammation, not a fasciitis. These findings suggest that treatment regimens such as serial corticosteroid injections into the plantar fascia should be reevaluated in the absence of inflammation and in light of their potential to induce plantar fascial rupture. (J Am Podiatr Med Assoc 93(3): 234-237, 2003

    This following article sums up the conundrum:

    Sports Medicine. 36(7):585-611, 2006.
    Wearing, Scott C 1; Smeathers, James E 1; Urry, Stephen R 1; Hennig, Ewald M 2; Hills, Andrew P 1

    Plantar fasciitis is a musculoskeletal disorder primarily affecting the fascial enthesis. Although poorly understood, the development of plantar fasciitis is thought to have a mechanical origin. In particular, pes planus foot types and lower-limb biomechanics that result in a lowered medial longitudinal arch are thought to create excessive tensile strain within the fascia, producing microscopic tears and chronic inflammation. However, contrary to clinical doctrine, histological evidence does not support this concept, with inflammation rarely observed in chronic plantar fasciitis. Similarly, scientific support for the role of arch mechanics in the development of plantar fasciitis is equivocal, despite an abundance of anecdotal evidence indicating a causal link between arch function and heel pain. This may, in part, reflect the difficulty in measuring arch mechanics in vivo. However, it may also indicate that tensile failure is not a predominant feature in the pathomechanics of plantar fasciitis. Alternative mechanisms including 'stress-shielding', vascular and metabolic disturbances, the formation of free radicals, hyperthermia and genetic factors have also been linked to degenerative change in connective tissues. Further research is needed to ascertain the importance of such factors in the development of plantar fasciitis.

    Craig after reading this last year you prompted me to research this further and changed the way I practice on this issue because there was some very interesting detail in the following study utilising ultrasound AND PDI to examine for enthesisitis related to inflammatory disease, to my knowledge this was a new approach.

    For those unfamiliar with Diagnostic ultrasound exam findings of plantar fascia; there are many published studies which use B Mode grey scale imaging, they agree on similar features, the ability to detect hypoechoic fusiform thickening at plantar fascia insertional and distal, possibility to interpret tears , rupture, fibromatosis, examination of superfical plantar fibro-fatty pad, studies to look at visco-elastic compression properties with weight-bearing. Normal thickness is agreed to be in range of 2.5 to 5mm at insertion. This gives us opportunity to confidently and objectively examine “appearance”.

    There were only 2 published studies I could find to date which used PDI adding the important dimension of examination of blood flow associated with inflammation, the plantar fascia was amongst the most frequently examined sites.

    There is also an interesting paper utilizing scintography which I also added.

    Here’s some extracts from these 3 papers


    Assessment of Peripheral Enthesitis in the Spondylarthropathies by Ultrasonography Combined With Power Doppler

    This is the first report of a systematic analysis of peripheral entheses by US examination in B mode combined with power Doppler in a large group of patients with the different SpA subtypes.

    There were several important findings in this study. First, the frequency of abnormal peripheral entheses was very high among Spondylarthropathies (SpA) patients compared with controls.

    Second, abnormal entheses were uniformly found among SpA patients, irrespective of the disease subtype.

    Third, abnormal vascularization of affected entheses was detected EXCLUSIVELY in SpA patients.

    In this study, the high prevalence of peripheral entheseal abnormalities detected by gray-scale combined with power Doppler US in SpA patients further outlines the primary significance of this finding among SpA manifestations. The greater sensitivity of US compared with clinical examination for the detection of SpA enthesitis was previously reported (13,30) and was largely confirmed in the present study. In addition, we have shown that US assessment of inflammation at entheseal insertions could be dramatically improved by combining power Doppler with B mode, resulting in the visualization of a pattern highly specific for SpA. Thus, 98% of the SpA patients had at least one vascularized enthesitic site, compared with NON of the controls.

    So far, MRI has remained the imaging technique most widely applied in the assessment of musculoskeletal inflammatory processes. The MRI pattern of SpA enthesitis has been described as a diffuse bone edema adjacent to entheses, associated with surrounding soft tissue edema (31). However, this technique lacks sensitivity and specificity (8). This is because changes in the fibrous part of the enthesis, where fibroblasts are tightly cross-linked with little capacity for the accumulation of water, cannot easily be detected with MRI (8,32).


    Since MRI is not appropriate and histologic assessment of enthesitis is not practical because of limited access, there is no “gold standard” for validating the US features of enthesitis.



    Thickening of the plantar fascia in patients with plantar fasciitis is a well-established sonographic criteria for the diagnosis of plantar fasciitis and has been previously reported in several studies (Cardinal et al. 1996; Gibbon and Long 1997, 1999; Wall et al. 1993).

    A hypoechoic fascia is also a frequent finding and is related to underlying reparative processes after microtears, fiber degeneration and edema (van Holsbeck and Introcasso 1992). Kier et al. (1991);
    Kier (1994) and DiMarcangelo and Yu (1997) demonstrated an increased signal of the plantar fascia in T2-weighted magnetic resonance imaging (MRI) scans, due to extracellular water found during the inflammatory state.

    Histologic findings associated with plantar fasciitis are collagen necrosis, angiofibroplastic hyperplasia, chondroid metaplasia and calcifications (Snider et al. 1983). LeMelle et al. (1990) investigated tissue specimens of patients with heel-spur surgery. They reported different histologic findings in patients with chronic heel pain. In 1 patient, they found fibrovascular hyperplasia; in another patient, normal blood vessels, no fibrosis and no lymphocytic infiltration.

    Although these findings are limited by the small number of patients, they demonstrate the variability of the disease. results of US examination of the plantar fascia reported by Cardinal et al. (1996), Gibbon and Long (1997, 1999) and Wall et al. (1993) are supported by our findings.

    In all studies, a significant increase of the plantar fascia thickness was found in symptomatic heels compared with the asymptomatic side of the patients. This was also shown when comparing them with the heels of a control group. Martin et al. (1998) recently reported long-term result in 157 patients who were not surgically treated for their plantar fasciitis. In their study, subjects with symptoms of a chronic plantar fasciitis had a poorer outcome than patients who suffered from plantar fasciitis for less han 12 months.

    They concluded that local inflammation and only a few permanent changes of the plantar fascia indicate the acute phase, whereas patients with chronic symptoms show more permanent changes, such as thickening of the medial bundle of the plantar fascia. Intrasubstance signal abnormalities in MRI also indicate changes within the plantar fascia (Theodorou et al. 2000; Yu 2000).

    Power Doppler visualizes blood flow on a microvascular level (Bude and Rubin 1996; Rubin et al. 1995), and has been proven to be a reliable tool in measuring the extend of soft tissue hyperemia. Walther et al. (2001, 2002) could demonstrate a strong correlation between local vascularity and power Doppler signals in synovial tissue. A moderate or marked hyperemia was found in 6 of 8 patients with a history of plantar fasciitis lasting less than 6 months (p _ 0.01) and in no person of the control group (p _ 0.01). Perifascial fluid was found in all 6 with moderate or marked hyperemia. Our results suggest that the moderate or marked hyperemia in power Doppler US indicates an acute-phase plantar fasciitis.
    Power Doppler signals seem to decrease with the development of chronic plantar fasciitis.

    We could not identify hyperemia in patients with a history of plantar fasciitis lasting over 12 months.

    These observations are supported by histologic findings (Snider et al. 1983).

    The acute phase accompanied by high inflammatory activity can be followed by a chronic phase with less or no inflammation (Chandler and Kibler 1993). Plantar fasciitis is classified as a syndrome resulting from repetitive overload of the plantar fascia at its insertion into the calcaneus (Kier 1994; Kwong et al. 1988; Nigg 1985). The development of plantar fasciitis can also be related to improper biomechanics, abnormal anatomy, muscle strength imbalances and range of motion deficits.

    Therefore, there can be quite a period between the onset of the cause and the development of plantar fasciitis (Cardinal et. 1993). Cardinal et al. (1996) reported on one asymptomatic volunteer with sonographic signs of plantar fasciitis. In our series, mild hyperemia was seen in one asymptomatic volunteer. The incidence of hyperemia within a larger asymptomatic population is unknown. Our finding however, can be discussed as reaction to a recent overload or as a subclinical form of plantar fasciitis.


    Bone Scintigraphy Predicts Outcome of Steroid Injection for Plantar Fasciitis
    Clayton Frater1, Dzung Vu2, Hans Van der Wall3, Chandima Perera4, Paul Halasz2, Louise Emmett3 and Ignac Fogelman5

    Plantar fasciitis is a common cause of foot pain and may be disabling. Although localized injection is painful, anesthetics or corticosteroids can relieve symptoms well. Bone scintigraphy can confirm the diagnosis. We hypothesized that blood-pool abnormalities could provide prognostic information on the response to such injections.

    Methods: We devised scintigraphic criteria that graded the blood-pool abnormalities as being localized to the plantar enthesis, being localized to half the length of the aponeurosis, or involving the whole aponeurosis. We evaluated 24 patients with an established diagnosis of plantar fasciitis, 8 of whom had bilateral disease, leading to a total of 32 feet injected. Results: After injection, pain was relieved either completely or nearly completely in 20 feet. The other 12 feet had short-term or no improvement, with persistent pain and loss of function at 4–5 wk after injection. Of the 20 feet responding to injection, 14 had focal hyperemia on blood-pool images and 6 had minimal extension into the proximal third of the plantar soft tissues.

    No patient with diffuse hyperemia in the plantar fascia had a response (5/12 feet). On the delayed images of the 20 responders, mild inferior calcaneal uptake was seen in 8 feet, moderate uptake in 6, and severe uptake in 6. These groups did not significantly differ (P > 0.05). The blood-pool studies had good reproducibility, with a -value of 0.64.

    Conclusion: Critical evaluation of plantar blood-pool images provides prognostic information on the response to localized injection into the enthesis. Reporting such studies is simple and reproducible.

    In summary, and not surprisingly, perhaps we need to look at 2 different types and possibly stages for plantar fascia disease, and different treatments. An acute phase which is truly inflammatory and may be caused by trauma or systemic inflammatory disease “plantar fasciitis”, and a chronic phase or fasciosis. Also not surprisingly this is not dissimilar to how we already consider disorders of tendons or even joints.



    The St. James Foot Clinic
    1749 Portage Ave.
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
  7. Martin:

    As far as I'm concerned, Martin, you have made the Top 10 Postings to Podiatry Arena with your latest comprehensive posting on the plantar fasciitis/plantar fasciosis issue. I see this posting as the beginnings of a potentially very valuable article incorporating a comprehensive literature review on the subject of plantar fasciitis/plantar fasciosis that should be submitted for publication to the Journal of the American Podiatric Medical Association.

    I am very impressed with your writing and logic....and I don't say that to many, as you are probably aware. Excellent work!
  8. Craig Payne

    Craig Payne Moderator

    Mart - thanks for good post.

    My original intent was really to ask re the differences between the 'garden variety' 'run of the mill' plantar fasciitis (the mechanical tyoe that we see day in and day out, and is probably not an '-itis' anyway) vs the inflammatory type that is the enthesitis that is common in the seronegative's.

    The conundrum that I have is that almost all the podiatric texts that talk about in the inflammatory one that is common in the seronegatives say to treat it with orthoses, strapping etc etc (ie the same way we should treat the mechanical one we see so often). I can't work out why I get 100% failure when tryin gto treat them ... or is it just another one of those podiatric myths?
  9. Craig, Martin and Colleagues:

    What is interesting is that I often see patients who have been diagnosed with fibromyalgia who also have symptoms consistent with plantar fasciitis. Invariably, treatment with foot orthoses will make their pain improve, but they may still have some pain in their plantar heels when their fibromyalgia flares up. Certainly, since fibromyalgia is considered an inflammatory condition, there must be a mechanical component if orthoses help the plantar heel pain from plantar fasciitis in this inflammatory condition.

    My hypothesis is that nearly all of the plantar heel pain we have called plantar fasciitis for the past two decadesis is actually a variable combination of pathological tearing-degeneration and inflammation either in the fascia or surrounding tissues (i.e. fat pad, muscle, bone) that is caused by both the compression forces of ground reaction force and the tensile forces within the plantar aponeurosis. This hypothesis seems consistent with mechanical modelling of the tissues of the plantar heel and the available literature on the subject.
  10. Mart

    Mart Well-Known Member

    Thanks Kevin and Craig for your gratifying remarks.

    Likewise I have been skeptical regarding the “matter of fact” regard of many podiatric texts and presentations I have sat through which “inform” us about plantar heel pain. Most of the more recent broader texts I have read though seem more well informed or honest.

    My assumption has been that if enthesisitis is coming from some immunological or other physiological defect that has nothing to do with mechanical stress, benefits of foot orthoses would be unexpected given the current opinion about foot orthoses effect. This matches your concerns I think Craig and perhaps the recommended treatment plans should now reflect this. It could skew poorly designed studies which examine foot orthoses efficacy, although I suspect the prevalence of SpA related plantar heel pain might be quite low.

    One problem moving forward is having sensitive and specific tests to explore this further and as you can see there is a coherent pattern emerging which points to using power DUS as a reasonable next step.

    There are issues regarding US interpretation but they are understood in the literature and manageable.

    From my own point of view I am looking for opportunities currently to involve my Ultrasound skills in an MSc research project, I have been offered a post graduate position pending clinical placement in UK but after 6 months searching have found no opportunities anywhere on the planet which is quite disappointing.

    If there is anyone in the academic world out there who might see a way to involve me please let me know "off the forum" I have tons of ideas which I would love to pursue.


    The St. James Foot Clinic
    1749 Portage Ave.
    R3J 0E6
    Phone [204] 837 FOOT (3668)
    Fax [204] 774 9918
  11. drsarbes

    drsarbes Well-Known Member

    "he had an undifferentiated form of spondyloarthritis with severe heel pain --- it responded instantly to the adalimumab (anti-TNFapha) injectin. "
    CP: I'd be interested in how this medication was admisnistered.

    Also: It has been my experience that chronic fasciitis (more than 6-8 months of daily symptoms) will usually not respond to antiinflammatory treatments. I always assumed this was due to fibrosis of the fascia and thus pain not related to inflammation; whether this is some type of transformation of the chronically inflamed fascia or a fibrotic tendency as the original etiology. This has been verified by various studies, whether it is related as "thickening" or "fibrosis" or "hyperplasia"....a rose by any other name......

  12. John Spina

    John Spina Active Member

    I am with you.I see a lot of plain old PF and little of the latter.Inflammatory PF will respond to the newer drugs so I use them.
  13. Mart

    Mart Well-Known Member

    An idea which have had for a while but needs more work revolves around the following case and a couple of similar cases I have had this year, I am curious about others who may be thinking along the same lines and what their experiences are.

    Today I saw a 30 something male for 3rd follow up appt.

    He reports to be in good general health, denies trauma or surgery to lower limbs.

    Hx of bilaterally debilitating plantar heel pain.

    He claims to have seen several podiatrists and orthopaedic surgeons regarding this problem and has very limited improvement only with a medium density EVA foot orthoses with 10mm heel ramp with PPT filled cavity which I fabricated 2 weeks ago. His most effective treatment to date he did himself by literally cutting the heel counter off his shoes so that he only walks on his arch and forefoot, this causes bad arch pain but is preferable to his heel pain.

    He believes that his pain stems from a crash diet losing 150 lbs in six months just prior to onset of pain, he feels, and has had this opinion concurred by several practitioners, that he has some deterioration of functional capacity of plantar fibro-fatty pad under heel, this based on radiographic exam measurement of distance of bone to floor in lateral view, I have not seen the films. He is the only patient in my 20 yrs practice who claims to have had suicidal thoughts because no one is able to help him and he cannot function normally, he feels he might lose his job.

    He is currently medicated with Oxycodone which barely helps.

    Pending are blood workup and radiographic exam results

    He walks with slow antalgic and completely appropulsive gait, almost instantaneous forefoot contact, this being when I ask him to walk with heel contact which normally he would avoid when barefoot. Pain on contact lasting through stance. Pain resolves quickly non weight-bearing, Condition worsens with increased activity and improves with rest, worse towards end of day.

    Static biomechanical exam is unremarkable. No signs of swelling, erythema, heat or skin lesions at affected sites, no pain with palpation, compression, windlass operation, no tinel sign. No trophic signs to suggest Complex regional pain disorder type 1.

    Diagnostic ultrasound exam is unremarkable, normal plantar fascia thickness and contour, no flow with power doppler. Fibrofatty pad seems to be more compliant than I am used to seeing with compression but I am aware that I am expecting this and probably biasing my judgment.

    Barefoot FMat exam showed peak pressures and force/time integral at heel were marginally elevated above normal, synchronized video showed no evidence of “targeting”, and hip and knee flexion at HS were normal despite almost instant forefoot contact and rapid offloading of plantar calcaneal area, stance phase was prolonged because of slow velocity which likely explains elevated force/time integrals.

    A tricky case, I was wondering initially if he might be a narcotic abuser looking for prescription, but think it unlikely given consistent gait exam and very keen to try “anything” which might help.

    I suspected possible neurogenic pain and today infiltrated left foot tibial nerve at med mal with 10 mls of mixture of 9:1 sterile normal saline: 1% plain lidocaine. I did this with US guidance so I know the Post Tib nerve was surrounded (with 10mls swimming!).
    I sat him down for 30 mins, he had taken Percocet 2hrs previous.

    I then asked him to walk along a carpeted walkway for 10 minutes. He had no pain left foot and normal level of pain right foot, he was convinced that I had anesthetized his foot, I tested it with needle prick, sensation was unimpaired.
    I explained the implications of this and am now his hero (despite lack of assurance of long term effective treatment).

    I have seen 4 patients this year with similar although not such desperate histories, all were negative for any reasonably identifiable mechanical or systemic problems. 3 responded similarly to diluted tib nerve blocks, one not. One completely recovered following 5 serial marcaine post tib nerve blocks, another I am about to try this after failure going the magic laser/steroid injection/accupunture route and and one I lost to follow up.

    Perhaps it is a bit of a stretch of the imagination


    I have treated dozens of chronic plantar heel pain patients with evidence of plantar fascia thickening on diagnostic ultrasound exam and NEVER flow with power doppler, most resolve within three months with “normal” conservative approach.

    Craig Payne pointed out a while ago in one of his posts that the cause(s) of plantar heel pain has never been properly established.

    This blinding fact is easy to overlook.

    Most practitioners I have talked to believe that they treat plantar heel pain by eliminating edema, inflammation, tensile stress of plantar fascia, reducing heel impact, etc. Non of us really know how our treatment effects the pain, and all that we really know when people get better is that we have effected pain.

    I used to believe that my foot orthoses fixed the chronic long standing plantar fascial injury until I recently started looking at Diagnostic ultrasound exams before and after treatment with custom foot orthoses designed to influence autosupport mechanism. What I found was – no inflammation before or after, various degrees of plantar fascia insertional thickening sometimes calcified, which RARELY CHANGED and never back within normal range after pain resolved.

    So how could this be explained?

    Why would the enthesis be tender with palpation and no inflammation?

    One idea I find convincing is that of Kevin’s, that the visco-elastic nature of the plantar fascia is modifiable therapeutically so that tensile strain is reduced below injury threshold. Likewise well designed foot orthoses could work by reducing strain. Ditto stretching exercise regimen for soleus and gastocnemius, elevating the heel, night splints, plantar fascia resection.

    The question still haunts me and is so fundamental; why pain with palpation and NO inflammation.

    Allodynia has been discussed in relation to peripheral nerve sensitization for a while amongst pain specialists and progressive physiotherapists.

    It makes perfect sense to me that people with long standing chronic plantar fasciosis could develop localized peripheral nerve sensitization. Lower the pain threshold and normal stress becomes painful that is what allodynia seems to be about.

    Since all our therapies are designed, probably, to lower in various ways, the stress, then is the effect simply to alleviate pain by bringing the stress level below that which provokes an allodynia response rather than, as we might assume, from an injurous level to a below injury threshold?

    To date I have only tested for neurogenic pain in a few people whose histories cry out for this to be investigated much like the case I saw today.

    I have never tried treating people for peripheral nerve sensitisation BUT NOT tensile stress.

    A small study which I shall try an locate demonstated that serial post tib nerve blocks were as effective as steroid infiltration,


    Treatment of chronic plantar fasciitis with botulinum toxin A:
    an open case series with a 1 year follow up

    It is not yet clear whether treatment of chronic plantar
    fasciitis with botulinum toxin A (Btx-A) works by causing
    muscle paresis or by analgesic/anti-inflammatory effects, or
    both. A combined effect may occur—namely, (a) induction of
    paresis of the muscles originating at the medial calcaneal
    process and (b) occurrence of direct analgesia owing to its
    anti-nociceptive and anti-inflammatory properties.7–10
    Our results thus suggest that a single injection of
    200 units Btx-A (Dysport) may be a possible treatment
    for patients with chronic plantar fasciitis. This level IV
    study may yield the database for a power analysis of a
    double blind, placebo controlled multicentre study (in

    this study ignores possiblity of neuropathic pain but could this also be non nociceptive effect?

    A bit of a ramble but would love to discuss this further.

    is this idea flawed?

    Since this is likely not an abnormality caused by sympathetic involvement (or could it be?) how might be go about trying this, or could lidocaine and botox be having this effect?

    is it a non starter with no realistic approach?


    Last edited: Oct 3, 2007
  14. Kent

    Kent Active Member


    This is somewhat similar to what I've found in some Achilles tendinosis patients. Baseline ultrasound shows changes consistent with tendinosis (i.e. no inflammation, fusiform thickening, hypoechoeic areas, many have neovessels under colour Doppler). After treatment, the patient is completely pain free - some running marathons. BUT at 12 month ultrasound, the tendon looks exactly the same as at baseline. In some cases, it actually looks worse. This contradicts what Alfredson and Ohberg have reported - most of their patients have normal tendon structure after treatment.

    A couple of theories as to why this may be occuring:
    1. It takes the tendon longer than 12 months to return to normal structure
    2. The tendon will never return to a normal structure. Treatment is changing the PNS (which in turn changes the CNS), therefore the patient can exercise pain-free (ie we're changing the pain threshold).

    So when we're treating non-mechanical / inflammatory plantar fasciitis, is it a similar scenario to what I've seen in some of my Achilles patients - just changing the PNS/pain threshold???

  15. Lawrence Bevan

    Lawrence Bevan Active Member

    Please, can someone give me a brief lesson in neurogenic pain and pain thresholds so I can better follow this discussion??
  16. Mart

    Mart Well-Known Member

    Hi Lawrence

    See if you can track down a book called

    Moving in on Pain
    ed Michael O Shacklock

    Butterworth-Heinemann Autralia 1995

    It is a collection of presentations from the Physiotherapy Research Foundation 1st annual conference April 1995

    My podiatric education 22 yrs ago only taught me about nociception as a pain generator. Pain seems to be way more interesting, complex and mysterious to me after reading this book which covers the different broad facets of pain without on the whole getting too bogged down in the technical details of neurotransmitter terminology and it defines pain jargon sensibly.

    I'll try and get time to OCR a couple of paragraphs to inspire anyone to go and get this book.

    Initially I was very skeptical regarding the idea of neurogenic pain. I remember being at a weekend presentation by Howard Dannenberg in Boston 15 years ago when he talked very matter of fact about something which I had never heard of "neurogenic pain" and thinking "this sounds like a bit of flakey pseudoscience, just like this FHL stuff " duh!!!:eek:

    The case I described in my last post I hope dramatically illustrated why these concepts need to been added to our "paradigm tool kit".

    Anecdotal as it is, I don’t believe, as it may have been, that this was a placebo effect . After explaining the rational for this diagnostic test to the patient, it will be interesting to repeat the block (dilute and only likely effecting the sympathetic nerves) and see if it has same effect.

    Any other recommendations for reading on neuropathic pain relevant to this thread?


    Last edited: Oct 3, 2007
  17. Mart

    Mart Well-Known Member

    Hi Kent

    my experince with US and TA/posterior heel pain is less than PHP.

    However, similarly, the few cases I have followed are exactly as you described which is an interesting and I feel relevant analogue.

    your theories

    1 - I have no experience yet to support or refute this


    2- what makes you think we are changing pain threshold when conventional wisdom of our therapy suggests to me that we are likley changing the structural loading to bring it below the established pain threashold?

    simply based on this idea and the possibility of nerve sensitisation and theoretical effects of long term nociceptic bombardment that using our established therapies, pain may be relieved by reducing the amount of sensory stimultation rather than lowering the sensory responce. Perhaps as you infer this may also "retrain" the system. I am intersted in your responce to this because I think it may be crucial if not too big a generalisation.

    I am reading a bit around this again and when I get time I'll try and post some papers.

    BTW I have been unable to upload files this past few days anyone else having the same problems?


    Last edited: Oct 3, 2007
  18. drsarbes

    drsarbes Well-Known Member

    Hi Mart:
    Just a thought re: your 30 something male patient with "debilitating" plantar heel pain.
    I have seen this a few times over the years where a relatively young, even very "fit" young patient, will have varicosities within the Tarsal tunnel. This may or may not give a tinel's sign and is almost always worse when dependent. It defies clinical diagnosis alone and Venogram is needed for verification.
    I have seen the symptoms isolated to the heel area and even present pain on direct palpation of the medial plantar tubercle. A cuff around the lower leg raised to bewteen systolic and diastolic will often duplicate the pain.
    Just a thought
    Good luck
  19. Mart

    Mart Well-Known Member

    Hi Steve

    Thanks for your suggestion and test.

    Could you suggest why the dilute tibial nerve block would have worked for this pain if it was caused by varicose vein related nerve compression?

    Also would you expect that the pain would resolve immediately with rest and that the probability of simultaneous bilateral onset would be reasonable if this was cause?

    Do you use US to examine for tibial nerve compression in tarsal tunnel? I would imagine this would image rather well and have looked out for varicosities with cases of +ve tinel sign. Not seen this yet but I'd imagine pretty rare.



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  20. drsarbes

    drsarbes Well-Known Member

    Hi Mart:
    Patients normally do not appreciate immediate relief with elevation. I would assume this is because any irritation to the nerve would continue for a time even though the venous congestion has been decreased.

    I cannot recall simultaneous onset. I have seen a few that have been bilateral, but some months or even years later.

    I don't regularly us Dx US

    I was not really suggesting that your patients symptoms pointed to this as a diagnosis, just one more item to add to your DD.
  21. Mart

    Mart Well-Known Member

    Thanks for that, it had not occured to me use a cuff to artificially elevate venous pressure, I guess on US this might make defect more obvious too.


  22. One explanation is that diagnostic ultrasound is not sensitive enough or is the wrong diagnostic test to detect tissue damage/healing and/or the presence/absence of inflammation. MRI scan may show increased bone edema in plantar medial tubercle in these patients indicating the inflammation is inside the bone, not in the soft tissue. Bone and bone-plantar fascial origin biopsy would be the test of choice in my opinion.

    Injury can occur without inflammation, but not generally in an individiual with normal healing potential. Like I said, if the patient has chronic heel pain, but you are using diagnostic US to look at anything other than the plantar fascial insertion into the calcaneus, or are taking your biopsy from the plantar fascia distal to the medial calcaneal tubercle, and are not considering the possibly intraosseous plantar calcaneal bone edema and inflammation that may be occurring that may not be able to be visualized with US, radiographs, or with distal plantar fascial biopsies, then you may be missing the actual anatomical site of the inflammation....THE BONE!! Bone Edema at Plantar Calcaneus in Chronic Plantar Fasciitis

    Increased tensile loads on the plantar aponeurosis will increase the tensile strain (i.e. stretching of fascia) and tensile stress (i.e. stretching force per unit cross-sectional area of plantar fascia) on the plantar aponeurosis. Reducing tensile strain in the fascia likely reduces the stimulus to pain-sensing elements at the plantar fascial origin which may be located within the plantar fascia itself, located at the plantar fascial-bone junction or located within the bone itself. My guess, is that most of the pain-sensing elements that are responsible for the plantar medial calcaneal tubercle pain seen in "plantar fasciitis" are at the plantar fascial-bone junction, with the inflammation manifesting itself as subcortical bone edema at the medial calcaneal tubercle on MRI.
  23. Mart

    Mart Well-Known Member

    Hi Kevin

    I agree with your proposition regarding US sensitivity.

    The problem I encounter (this is well documented in the literature) is with motion artifact where even the slightest probe motion causes same effect as the red blood cell motion which is what is being looked for.

    To compensate for this manufacturers have some tricks which average adjacent captured samples and other algorithms which clamp down the signal.

    When I use PDI for plantar fascia exams I set the setting at most sensitive level I can, the sites which tend to show motion artifact most are bone surfaces and enthsesis, obviously this is a consideration during the exam.

    My problem in having sense of a comparative sensitivity is that the only inflammatory pathology I have seen which compares in terms of intensity is tendo-achilles. I can say that I have detected flow in insertional tendo-achilles painful sites confident that I am not seeing motion artifact with my sensitivity above the threshold I use when checking for plantar fascia. This is I feel a reasonable basis for comparing sensitivity but am unable to substantiate this other than it seems a plausible anologue. Synovitis is much less subtle I have found quite obvious.

    Please correct me if I am wrong but I understand that bone inervation is primarily from the periosteal membrane, this is visible on US.

    If you are unfamiliar with MSK use, cortical surfaces are usefully investigated and examination of periostium is performed for as evidence for recent fracture and osteomyelitis in a US bone exam.

    Agreed that sub cortical reaction will be invisible to US unless there is an erosive window.

    Would you expect to see deeper bone reaction without enthesis/periosteal reaction from a tensile stress problem with plantar fascia?

    How could that happen?

    Compression injury I could see causing isolated bone inflammation.

    As regards enthesis being root of pain.

    Here’s my experience and I suspect most of us with physical exam.

    Usually pain with palpation, most often very specific at medial calcaneal insertion, but quite often less localized.

    Relatively less common is pain with increasing tensile stress of the plantar fascia by dorsiflexion of Hallux and applying force in more distal plantar fascia which I would assume creates equal ormore tensile stress along plantar fascia as palpation of enthesis site.

    This site will not be painful with palpation in a normal exam.

    Agreed that pain sensing elements within the plantar fascia could signal pain with excessive stress but palpation is not creating excessive structural stress unless the cross sectional area has been severely compromised. I

    n which case would the pain not be constant when standing and not dissipate after short period as in pain on rising from bed in morning then improving?

    I am enjoying thinking this idea of possible peripheral nerve sensitization as root cause through, and look forward to making some progress at least in terms of logical deduction.


  24. Martin:

    You, like most other clinicians, seem to be assuming that proximal plantar fasciitis is caused only by excessive tensile stress on the plantar fascia. However, if you consider the more likely mechanical etiology, as I have said many times on this forum, that proximal plantar fasciitis is caused by both tensile stress on the plantar fascia combined with compression stress from ground reaction force (GRF) acting on the plantar medial calcaneal tubercle at the site of the origin of the central component of the plantar aponeurosis, then all your observations make complete sense. Therefore, the compression stress from GRF combined with the tensile stress in the same little area of the medial calcaneal tubercle which serves as the attachment point of the plantar fascia causes inflammation of the subcortical areas of the medial calcaneal tubercle and probably, early on, to the periosteal area also.

    1. Why do patients feel better with low-Dye strapping?
    Because the plantar fascia pulls less on the inflamed area of the medial calcaneal tubercle.

    2. Why does the heel hurt to direct palpation? Because the subperiosteal bone is inflamed (with MRI subcortical edema being the evidence).

    3. Why do patients often get better with a well-made foot orthoses? Because the foot orthosis not only decreases the compression stress on the medial calcaneal tubercle from GRF but also decreases the tensile stress at the site of origin of the plantar fascia.

    4. Why do patients often feel somewhat better with simple foam cushions or gel cushions plantar to their heels? Because the compression stress on the medial calcaneal tubercle is decreased with these pads and possibly also because the increased heel height differential decreases the tensile force on the plantar fascia.

    5. Why does the heel hurt often after stepping up out of bed or from a sitting position (post-static dyskinesia)? Because of the well known, time dependent viscoelastic phenomena of stress relaxation and creep phenomenon where the plantar fascia shortens with the decreased tensile loads of the non-weightbearing foot and then is violently stretched upon the first few steps from a non-weightbearing position that causes increased magnitudes of tensile stress on the inflamed calcaneus and increased pain perceived by the patient.

    Of course, this does not cover all cases of plantar heel pain, but probably covers about 90-95% of what I see in my office on a daily basis.
    Last edited: Oct 4, 2007
  25. Mart

    Mart Well-Known Member

    Hi Kevin

    Thanks for your detailed response, you have nicely and succinctly clarified some important clinical reasoning for me. The thrust of my questioning was focused on the idea that palpation pain may be result of localized allodynia rather than inflammation (as opposed to assumption of purely tensile injury, which I do not hold, I should have made this clearer but your point is well taken).

    Your defense of the possibility of bone inflammation in absence of plantar fascia inflammation as cause of palpation pain I cannot flaw.

    However I remain a little skeptical based on the reported nature of bone pain from attached paper and I need to study this further. Correlative studies with amount of force required to cause bone pain with palpation might be revealing, I’ll see if I can find anything!

    Also your suggestion from some past post of patient questioning of heel contact vs heel lift pain during gait as an important clue on this issue. I find this worthwhile in differentiating the balance between the aggravating factors.

    My observations with ultrasound remain difficult to evaluate partly because of the issue you raised of PDI sensitivity (I need to go and do some deeper reading on this) and also as you say bone inflammation is invisible to US and may play an important role.

    My comments before regarding periosteal origins of pain were over simplistic and I am attaching a reference which is a nice overview of nociceptic and non nociceptic bone pain and also touches on bone edema and fluid dynamics of haversion canals

    Although your explanation of palpation pain as explainable by bone inflammation works nicely, it doesn’t exclude the equally plausible theoretical explanation of allodynia.

    Do you have any thoughts on this?

    If, as I suspect, we don’t have any unequivocal evidence to look at, how might we go about logically considering this right now?



    Damm still cant upload files I'll see if Craig can help out:bang:

    Bone pain differs in many respects from other types of pain (Mercadante 1997).

    While skin pain is characterized as sharp, pricking, stabbing or burning, bone pain is frequently perceived as aching.

    It may be accompanied by referred pain and muscle spasm which hardly ever occur with skin pain.

    The response to treatment with opioids and prostaglandin inhibitors often differs between skin and bone pain. The mechanisms of bone pain are obscure in several respects.

    It is difficult to explain why some disease processes of bone cause pain while others, very similar, do not. It is well known that even the same pathology—e.g., cancer metastases in bone— may give rise to pain at some locations but not in others (Front et al. 1979, Patt 1993).

    It may be asked whether the central processing of nociceptive information is different for bone pain.

    Bone nociception is probably processed by the CNS in a way similar to that in other tissues of the same mesodermal origin as joint and muscle.

    Of particular interest is the recent finding that a change in CNS behavior (central sensitization) can be seen as a consequence of strong and/or long lasting nociceptive C-.fi ber input from skin, joint and muscle (Ma and Woolf 1996). This phenomenon is due to the plasticity of the CNS in the same way as the wind-up phenomenon that gives rise to a gradual increase in dorsal horn neuron activity in response to repetitive stimuli (Mendel and Wall 1965) and frequently outlasts the noxious stimuli in both time and response-amplitude (Woolf 1986, 1996).

    Furthermore, central sensitization appears as secondary hyperalgesia and allodynia (Woolf 1996)—e.g., drilling a hole in the tibia of the rat results in secondary hyperalgesia and allodynia (Houghton et al. 1997), suggesting central sensitization.

    Morover, some clinical evidence indicates that central sensitization is involved in human pain mechanisms (Arendt-Nielsen and Petersen-Felix 1995), including bone nociception (Mercadante 1997). Osteophytes and pain in osteoarthrosis are common (Spector et al. 1993).

    It has been suggested that pain is caused either by stretching of nerve endings in the periosteum or by microfractures in the fragile bone in the spurs (Brandt 1999). A correlation between microfractures and bone pain has been suggested in a series of other clinical

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  26. Mart

    Mart Well-Known Member


    I OCRed some selected paragraphs for you from "Moving in on pain", there's a few little blemishes but I dont have time to tidy it up - should be easy to figure true meaning.

    hope this helps



    Due to the fact that pathology frequently does not account for pain, there is a growing migration of attention toward pain as an entity in its own right. After all, pain is the most common reason for seeking help from the physiotherapist.

    However, physiotherapy research into pain is lacking. For example, little is known of what physiotherapy actually does for pain in terms of outcome or of the biological effects of physiotherapy on pain. The challenge is for therapists to
    conduct research into the nature of pain and its assessment and treatment. I have positioned the Images of Pain art exhibition early in this book to illustrate the multidimensional experiential nature of pain and that pain is a Pandora's box, into which this book is a fleeting glimpse. The papers which follow cover various aspects of pain and its causes and management. All health professionals who deal with the person in pain should have a good working knowledge of this subject.

    WE do not yet speak the language of pain. The two most common
    words used in the pain sciences arena are allodynia and hyperalgesia. It is
    rare to find clinicians who know what these words mean. And yet, they have
    been in widespread use for many years and they relate to well documented
    pathobiological changes in nociception. Allodynia is simply pain experienced
    from a stimulus that would not normally hurt, such as cold or light touch.
    Hyperalgesia is increased pain experienced from a stimulus that would
    normally be painful. Links to other professions require a common languague.

    An understanding of the issue of centrally based allodynia and hyperalgesia should make obvious and clear, one of the

    greatest clinical reasoning errors that we may perpetrate in the clinic. For example, when a patient with chronic

    low back pain is examined, very often, many tests can be painful -joint tests, rnuscIe tests, pelvic girdle movements,

    straight Ieg raises, trigger points. It creates a dilemma for the examiner trying to make some sort of working diagnosis.

    What usually ensues is that therapists leap to their favourite clinical hypothesis, or the in vogue diagnosis or the first

    thing that was examined. If only there were adequate attention to and knowledge of the pain, the reasoning errors could be minimised.


    We have been dominated for too long by the idea that injury means pain and that pain means injury and that a single line connects the two. That simplistic proposal joes not fit the facts, does not explain pain as we and our patients experience it and does not generate useful therapies. The classical theory sees a single pain xschanism which consists of a line-labelled, modality-specific, function-dedi- :ated, hard-wired system of nerve fibres and cells running from the periphery to :he cortex. The classical line begins with tissue damage exciting fine nerve fibre nociceptors and has to ignore the poorly observed correlation of pain with .mpulses in peripheral nociceptors and the production of pain by impulses in normal large fibres in conditions of tenderness. It then concentrates on nocicep- :eek:r-specific cells in the spinal cord which has to ignore that the response of such .,ells is too sluggish to correlate with aversive behaviour. Next the classical line ;saps to the thalamus and cortex where the nuclei and cells are labelled "pain L,slls" in spite of the failure of surgical lesions in these areas to cure pain.

    The classical single rigid system is replaced by three systems.

    First, a plastic Censory pathway continually modified by circumstances, particularly in.jury. Beginning with tissue injury itself with its elaborate restorative inflammatory changes, the nerve fibres change their properties. The central cells stimulated by the input change their excitability partly as a result of nerve impulses and partly because chemicals that are transported to them.

    Second, the sensory pathway is under massive control which can exaggerate or diminish the messages. Some of these controls are operated by the convergence of other inputs from the periphery and from surrounding nerve cells. Some controls originate in the brain itself selecting those messages which are passed on. Movement strongly influences these controls both from the periphery and the brain.

    Finally, the classical sequence of sensation followed by perception followed by action is being ques- tioned within initial doubts. The separation of pure sensation from subsequent perception may be an intellectual artefact. Furthermore the input may be perceived in terms of the motor action which is appropriate. This would imply that sensory and motor control are two sides of the same coin.


    Woolf (1987) has proposed a distinction between physiological pain and clinical pain experienced after hank tissue or nerve injury, such as that associated with trauma or surgical operations. Physiological pain has a high threshold, is well
    localised and transient, has a stimulus response relationship similar to that of other sensations, but is associated with fine A-delta and C-fibres, whereas normal touch sensation is associated with A-beta fibres.

    Clinical pain can be broadly divided Into that associated with inflammatory changes elicited by tissue damage (inflammatory pain) and that associated with nerve damage (neuropathic pain). However, this distinction is probably artificial since it is to carry out any surgical procedure without producing some damage to nerve tissue, which then becomes sensitised by he release of inflam- matory mediators. Clinical pain is characterised by both 'peripheral sensitisation' and also 'central sensitisation'.

    The end result of both of these processes is as follows:

    1. An exaggerated responsiveness to noxious stimuli (primary hyperalgesia

    2. A spread of hyper-responsiveness to non-injured tissue (secondary hyperal- gesia)

    3. A reduction in intensity of stimuli necessary to initiate pain so that stimuli that would normally never produce pain now do so (allodynia)
  27. How much force does the plantar calcaneus need to be subjected to with each step before we start considering the possibility that compression forces from ground reaction force (GRF) can cause direct bone injury? For example, if you took your elbow (olecranon), padded it with 1 cm of cushioning material, and then hit it on a hard surface with about 75 pounds of force every 3 seconds for about 2,500 times a day, this would be the equivalent force of what the calcaneus is subjected to on a daily basis. Do you think your olecranon would be sore to touch at the end of the week? You bet it would. And I'll bet that not only will the olecranon have localized edema, signs of inflammation, but also will have MRI evidence of subperiosteal bone edema. And it will be this subperiosteal bone edema which will make the olecranon sensitive to touch for about 2-4 weeks after you pound on it for a week, even when the visible edema and soft tissue inflammation have subsided.

    I tend to doubt that allodynia is a major cause of plantar heel pain, but may play a minor role. I estimate that 95% of all plantar heel pain is mechanical in origin and has purely mechanical explanations. The problem is that 95% of physicians don't know enough about biomechanics to be very successful in treating this very common condition. ;)

    Martin, here is another article supporting my contention that many patients with proximal plantar fasciitis have calcaneal edema, which may not be detectable as inflammation by diagnostic US or by biopsy of the more distal portions of the plantar fascia:

    Last edited: Oct 5, 2007
  28. Mart

    Mart Well-Known Member

    Hi Kevin

    I have absolutely no problem with this, but I appreciate your MRI references supporting likleyhood.

    My issue is with the palpation pain, perhaps I am flogging a dead horse here, and this doesnt really constitue allodynia, no one else seems to be getting too excited about it :empathy:

    Craig said that he would post bone pain article since I cannot seem to upload anything, I found it filled in some gaps in my knowledge and would recommend it to those intersted in the nature of pain.

    I am out of town for while but when I get back would like to pick your brain on your time spent examining the relative depths of the medial calc tubercule cf lateral side, seem to recall you mentioned this in Intricast esssays......

    I have a coronal section on US which I saved of a guy who seemed to have hugely prominent medial prominences bilaterally which I measured at 6mm depth. I could not find any normative data and have no self reference since never done this before, perhaps this is normal but am curious.


  29. drsarbes

    drsarbes Well-Known Member

    "I tend to doubt that allodynia is a major cause of plantar heel pain, but may play a minor role. I estimate that 95% of all plantar heel pain is mechanical in origin and has purely mechanical explanations. The problem is that 95% of physicians don't know enough about biomechanics to be very successful in treating this very common condition."

    I estimate that 89% of all statistics are made up on the spot!

  30. Stanley

    Stanley Well-Known Member


    I have had rheumatologist refer me patients for years, and what I find may help with what Criag has found.
    The patients I get usually have multijoint arthritic conditions, and I find out what other joints are involved besides the calcaneus. If the hands (or any other non weight bearing joint) are involved, I use this as a control to find out the status of the patient. If the hands hurt, I am not going to be able to help the patient with biomechanical therapy, as this is the inflammatory situation-they need pharmaceuticals from the rheumatologist. If the hands are not hurting at this visit, then this is a podiatric biomechanical component that needs addressing, and these patients respond extremely well.

    Regarding the pain of plantar fasciitis (and not a partial tear of the plantar fascia), not all non arthritic patients respond to orthotic therapy. Other factors that should be addressed are not limited to the following (After balancing of the ASIS and correcting the equinus):
    1. Atypical neurogenic pain in which the patient does not report burning, stinging, or numbness; but a positive Tinel's sign can be elicited (anywhere on the 1st &/or second branches of the medial calcaneal nerves).
    2. Periosteal injury to the calcaneus
    3. Trigger point of the soleus
    4. Weak Abductor Hallucis (Strain-Counterstrain or Reverse Strain-Counterstrain injuries)
    5. Posterior calcaneus and the associated injury to the posterior talocalcaneal ligament and stretch injury of the FDB (Reverse Strain-Counterstrain)
    6. Subluxation of the 3rd metatarsal cuneiform joint
    7. Lateral talus and the associated injury to the lateral talocalcaneal ligament.
    8. Periosteal injuries to the metatarsals


  31. Scorpio622

    Scorpio622 Active Member

    This is a very interesting thread that brings up great points. All points made by Kevin, Mart, and Stanley make sense to me. But the bottom line is that I will be treating my next case of "plantar fasciitis" not much differently than I did 15 years ago with subtle differences- less inclination to inject, and facilitating the windlass mechanism with orthoses.

    If patients have first step pain and other signs that hint of a mechanical dysfunction- stretching, biomechanical treatment, shoe education, and medication if ADLs affected.

    Those presenting with inflammatory or local neuritic symptoms are treated primarily with meds with mention of proper shoes, maintaining flexibility, and arch support.

    This is certainly a simple approach to a complex problem- and I suspect that this is not much different than what most of us have been doing for quite some time. It's like many dermatological conditions that have interesting histologic findings and great debate as to etiology that are ultimately treated with a steroid cream, just like 50 years ago and possibly the next 50 to come.

    Is there any other proven (or semi-proven) treatment that I can offer my next patient with heel pain, be it -itis or -osis ??????

  32. musmed

    musmed Active Member


    I have been smiling reading all these responses to this listing.

    None make much sense until yours.

    You are so close.

    I am taking most of next year off work to publish 7 papers on foot mechanics.

    I have nearly330 gigs of foot images in static and under loading.

    I will show that and things that have been published as gospel are not.

    I will be publishing data from CT,MRI and ultrasound,using the latest machinery eg a 1.5 tesla MRI and the latest software costing 150000 US.

    Just give me time and what you have written will be proven correct.

    Have a happy Break over Christmas and the data will turn up.

    musmed. www.musmed.com.au
  33. Mart

    Mart Well-Known Member

    Hi musmed

    sounds like you have some kind of revelation :dizzy:

    I am curious to understand what you feel makes not much sense :confused:

    please give us a bit more to think about than this teaser of a post :)



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  34. musmed

    musmed Active Member

    Dear Martin

    Sorry for not replying sooner. I have holidays from the computer. It keeps one on a different plain.

    The study has been in progress for nearly 2 years now.

    I can say the commonest cause for the diagnosis of PF plantar fasciitis is a short Fl. Hall. longus muscle, followed by an immobile lateral cunieform cuboid joint.

    These two causes are in the home straight while everything else is still at the barrier.

    The thickness of PF matters nothing in the majority of patients. Thickness, age, time to cure rates matter (only to the geeks). One year follow ups make for interesting reading.

    Hope this will keep you interested in this study.

    Regards from a wet Sydney (hooray!!)

  35. Stanley

    Stanley Well-Known Member


    I also find the lateral cuneiform is a common cause of plantar fasciitis. I see this restriction/subluxation on the side with equinus and a low ASIS on stance.
    There are other confirmations also, and as you fix one, it becomes another.
    Could you expound upon the short Fl. Hall. longus muscle?


  36. musmed

    musmed Active Member

    Dear Stanley

    One of the functions (I believe) is to help raise the medial side of the foot at the time the sesamoids hit the ground. That is to cushion the hit by the sesamoids as thewy are driven into the ground.

    When its co-helper the abductor hallucis cannot fire ( the muscle will not work in any one with PF) the Fl Hall longus has now got an extra job. The muscle fires for a much longer period and with time becomes chronically shortened.

    In each of these patients the FL. Hall Longus tendon is easily palpable and if you slightly dorsiflex the foot (that is put the PF on Slack) and dorsiflex the great toe, the tendon again is easily palpable.It is NOT the PF, yet I see many who have this problem and when I asked them how much time was spent looking at the foot, the patient mostly says nil to 20 seconds.

    I use a Travell and Simons spray and stretch technique with great results.

    If this is their ONLY problem, (rare to have one foot problem), it will solve their painful foot then and there.

    Trust this helps.


  37. Mart

    Mart Well-Known Member

    Thanks for posting more info on your ideas;

    several questions regarding this:

    My understanding of normal neuromuscular control of forefoot loading is that the deceleration is principally supplied by Tib Ant and toe extensors and that FHL action is primarily eccentric deceleration and stabilization of forward effects of body momentum on the foot after heel rise. I’d be glad if you would comment on this.

    I am curious about your comment regarding abductor hallucis not firing in those with chronic plantar fascia injury, what makes you think this?

    If I understand you correctly you feel that if you dorsiflex the foot (at ankle?) and dorsiflex the Hallux the plantar fascia will be “put on slack” and “ the tendon is easily palpable” (palpable where?). My understanding is the opposite to this


    1st metatarso-phalangeal joint dorsiflexion and to lesser extent ankle dorsiflexion will load plantar fascia (windlass mechanism). Perhaps I am misunderstanding you.



    The St. James Foot Clinic
    1749 Portage Ave.
    R3J 0E6
    Phone [204] 837 FOOT (3668)
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  38. musmed

    musmed Active Member


    I agree with you regarding the deacceleration part using ext. and tib ant, but when the Abd hall is not working, something has to come to the rescue for the distal foot and this is the Fl. Hall Longus.

    I have an interesting case where a 'mad' 72year old walker =20miles + per day for several years managed to turn off her abd hall and has caused herself 2 lovely 1st MET head osteochondral lesions that lie exactly over the sesamoids.

    The role of the sesamoids, according to me (study under way) is to purely reduce the size of the great toe and increase the ground force and they work like two ball bearings and this allows you to enter the coronal plain what Serge Gatovesky says in his spinal engine theory.

    How do I know the and hall does not work. Simply get them the resist you pulling their great toe laterally while palpating the muscle belly, doing the same while ultrasounding the muscle and finally EMG. I have done the lot. Got heaps of data on this.

    The Fl hall longus can easily be palpated through the PF. As I said slightly doresiflex the foot and great toe. Palpate the tension in the PF all over, then raise the great toe slowly. Suddenly there will be pain in a narrow band ie the FHLongus. The rest of the PF is still slack. The important thing is to do it slowly and gently a hard thing to teach people in this ever speeding world.


  39. Mart

    Mart Well-Known Member

    Sorry . . . . I am a little unsure of your use of terminology.

    Are you suggesting using other words that the sesamoids reduce surface area of ground contact of the prox phallanx with the ground, increase GRF (by improved mechnical advantage of flexors) and reduce friction (by providing a synovial articulating surface between flexor tendons and Met head. These characteristics then facilitate pivoting of the foot in saggital plane at what Perry descibed as the "3rd Rocker" If so, although I have never thought about the prox phallanx contact area, this strikes me as consistent with conventional ideas of functional anatomy.

    How do you see this as different to the current established ideas?

    Abductor hallucis strain and possible impingement on branches of calcaneal nerve are on most peoples radar screen as possible DD for heel pain.

    Compensatory increased use of FHL in responce to AB Hal deficit I have negelected to think about, and appreciate you theoretical concern about this and look forward to your research findings.

    What to you see as the pain generator in this phenomenon which you have considered?

    I will prepare and post some annotated US images of the plantar fascia which I would be curious for to you to comment on in relation to plantar heel pain.


  40. Paul:

    I don't understand what you are talking about here. When the foot and hallux are simultaneously dorsiflexed, the medial band of the plantar fascia becomes tight, not slack. In addition, the flexor hallucis longus tendon is deep to the plantar fascia and deep to the flexor hallucis brevis muscle, in the 2nd space of the central compartment of the plantar foot (Sarrafian SK.: Anatomy of the Foot and Ankle, J.B. Lippincott Co., Philadelphia, 1983, p. 357). Therefore, I don't see how you can "easily palpate" the flexor hallucis longus tendon through a tightened plantar fascia and through the flexor hallucis brevis muscle belly??
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