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Is a calcaneal spur in the plantar fascia?

Discussion in 'General Issues and Discussion Forum' started by Craig Payne, Jul 12, 2005.

  1. Craig Payne

    Craig Payne Moderator


    Members do not see these Ads. Sign Up.
    In a Yahoo Groups Discussion on manipulation, a question was asked:
    to which I replied:
    Needless to say there was some interesting comments that followed, mostly based on what people were taught as students, and NOT on a reading of the research evidence.

    At the end of the day, all the published evidence I have seen, is that the spur is not in the plantar fasica, so how can plantar fasica "traction" cause heel spurs?

    One poster (Peter Morgan) did back up what I said with this:
    THIS WAS PUBLISHED IN 1979!!!! -- why do people still talk about the calcaneal heel spur as being due to traction of the plantar fascia :confused:

    How, I finally found one of the other more recent references showing the same thing:
    That was 3 yrs ago.

    There are other references, I just don't have them handy (does anyone have them?).

    Is it not time to "put this one to bed"? What say you?
    Last edited: Jul 12, 2005
  2. Hylton Menz

    Hylton Menz Guest


    A couple of references to muddy the waters:

    M. Abreu, C. Chung, L. Mendes, A. Mohana-Borges, D. Trudell, D. Resnick. Plantar calcaneal enthesophytes: new observations regarding sites of origin based on radiographic, MR imaging, anatomic, and paleopathologic analysis. Skeletal Radiology 2003;32:13-21.

    Objective. To determine the relationship between sites of calcaneal plantar enthesophytes and surrounding fascial and soft tissue structures using routine radiography, MR imaging, and data derived from cadaveric and paleopathologic specimens. Design and patients. Two observers analyzed the MR imaging studies of 40 ankles in 38 patients (35 males, 3 females; mean age 48.3 years) with plantar calcaneal enthesophytes that were selected from all the ankle MR examinations performed during the past year. Data derived from these MR examinations were the following: the size of the enthesophyte; its location in relation to the plantar fascia (PF) and flexor muscles; and the thickness and signal of the PF. The corresponding radiographs of the ankles were evaluated at a different time by the same observers for the presence or absence of plantar enthesophytes and, when present, their measurements. A third observer reviewed all the discordant observations of MR imaging and radiographic examinations. Two observers analyzed 22 calcaneal specimens with plantar enthesophytes at an anthropology museum to determine the orientation of each plantar enthesophyte. MR imaging of a cadaveric foot with a plantar enthesophyte with subsequent sagittal sectioning was performed to provide further anatomic understanding. Results. With regard to MR imaging, the mean size of the plantar enthesophytes was 4.41 mm (SD 2.4). Twenty (50%) enthesophytes were located above the PF, 16 (40%) between the fascia and abductor digiti minimi, flexor digitorum brevis and abductor hallucis muscles, and only one (3%) was located within the PF. In three (8%) cases the location was not determined. The size of enthesophytes seen with MR imaging and radiographs was highly correlated (P<0.01). The interobserver agreement for all measurements was good (Pearson >0.8, kappa >0.9). Eleven of the 22 bone specimens had plantar enthesophytes oriented in the direction of the abductor digiti minimi and 11 oriented in the direction of the flexor digitorum brevis and PF. The cadaveric sections revealed different types of enthesophytes. Conclusions. Plantar calcaneal enthesophytes arise in five different locations: at the insertion sites of abductor digiti minimi and flexor digitorum brevis muscles; between the PF and these muscles; and, less frequently, within the PF and at the insertion site of the short plantar ligament.​

    Prichasuk S, Subhadrabandhu T. The relationship of pes planus and calcaneal spur to plantar heel pain.Clin Orthop Relat Res. 1994 Sep;(306):192-6.

    A prospective study of pes planus by using calcaneal pitch and calcaneal spur was carried out in 82 patients with plantar heel pain and in 400 normal subjects. The mean normal calcaneal pitch was 20.54 degrees. The mean calcaneal pitch in patients with plantar heel pain was 15.99 degrees, which was significantly lower than in normal subjects. The incidence of calcaneal spur in normal subjects and in patients with plantar heel pain was 15.5% percent (62 of 400) and 65.9% (54 of 82), respectively. Again, this was a highly significant difference. Excessive weight gain, aging, and gender may be important factors effecting the lowering of the pitch and the increasing of spur formation. These factors could lead to the development of plantar heel pain.​


  3. Craig Payne

    Craig Payne Moderator

    Thanks Hylton - the first one was the ref I knew about but could not find or recall.

    The key finding in the second one was 15% prevalance (they called it "incidence" :mad: ) of asymptomatic heel spur in the general population - why do people continue to consider it a problem?
    Last edited: Aug 20, 2005
  4. Don ESWT

    Don ESWT Active Member

    Have you seen the latest CT Light Speed scan images over 900 images in 11 seconds.
    Give A/P and M/L then generates 3D image

    Don Scott
  5. In the patients that I have surgically resected a plantar calcaneal spur in, all of them had their plantar spur just dorsal (adjacent) to the plantar fascia. It was almost like the fascia was lying directly plantar to the spur, with the spur more invested in the origin of the flexor digitorum brevis.

    My surgical observation correlates with the studies listed by Hylton and Craig but I still think the plantar calcaneal spur is a traction spur. It is probably due to increased magnitudes of tensile force within one of the plantar intrinsics instead of due to tensile force within the plantar fascia.

    Even though I only do plantar fasciotomy procedures in the few patient who do not respond to exhaustive conservative care, I still am impressed at how transecting the medial half of the fascia nearly completely relieves the chronic plantar heel pain within two weeks of the surgery. The problem is, as I have lectured on frequently, that these patients have more likelihood to develop other problems due to the partial plantar fasciotomy procedure.

    In this regard, here is my list of the 10 functions of the plantar fascia that I will be lecturing on in seven weeks at the Australian Conference of Science and Medicine in Sport in Melbourne:
    We must remember that the plantar fascia has functional importance in both static and dynamic activities and that, if the decision is made to surgically alter it, then the above ten functions must be considered as possible reasons for any future sequellae.
  6. Simon Smith

    Simon Smith Moderator


    I have just completed a modest histological study on resected heel spur samples from surgical cases. 5 samples, all witihin the 1st layer of intrinsic musculature (notably FDB and Abd Dig Qnt).

    However, studies dedicated to delineating this relationship are:

    Forman and Green (1990) "the role of intrinsic musculature in the formation of inferior calcaneal exostoses" Clin Pod Med Surg Vol. 7, No. 2, p. 217

    Barrett et al. (1995) "Endoscopic Heel Anatomy: Analysis of 200 fresh frozen sepecimens" J Foot Ankle Surg Vol. 34, No. 1, p.51

    Abreu et al. (2003) "Plantar calcaneal enthesophytes - new observations regarding site of origin based on radiographic, MR imaging, anatomic and paleopathologic analysis" Skel Rad Vol 32. p.13.

    You have mentioned other articles. There are, of course, many other authors who relate emphatically, and anecdotely, that the heel spur resides within the musculature.


  7. Craig Payne

    Craig Payne Moderator

    Thanks Simon....I knew there were more references, just did not have them handy.

    I guess this then begs the question, despite all this evidence that we have had for a long time and no evidence to the contrary, why can you read almost daily that its the pull of the plantar fasica is the cause of a heel spur .... don't figure... :confused: :eek: :rolleyes:
  8. summer

    summer Active Member

    It seems to me that due to Wolf's law ( essentially bone responding to stresses and strains caused by outside sources ) that the spur MUST be pulled out by the fascia. Isn't the fascia attatched to the tubercles?

    I routinely perform the endoscopic procedure (300+ plus cases over the past 10 or so years with success in the 90+ percentile.

    If one carefully transects only the medial third of the fascia, then the results are reproducable. One does have to be careful to assess whether or not there is a coexistence of tarsal tunnel syndrome as well.

    The EPF procedure has been a saving grace for plantar fascitis, athough it must be performed correctly in order to work. If performed incorrectly, the results can be a disaster.
  9. pablo2081

    pablo2081 Member

    Heel spur formation at the medial condyle/calcaneus occurs in reaction to the weight overload suffered by the musculature that attaches at the calcaneus. The tissue had suffered excess plantar spasm which prevented normal elongation of the hind foot. This Plantar spasm often results from Posterior Calcaneus Subluxation and/or loss of normal independant joint motion at the subtalar and tarsal articulations which prevents normal hindfoot elongation. The cerebellum created the autonomic contraction which serves to "splint" the foot. Having treated 100's of recalcitrant cases using joint specific manipulation, I authored an examination procedure which can image and identify mechanical stress at the calcaneus that was previously unobserved..(PubMed: Kell PM "A Comparative Radiologic Examination for Unresponsive Plantar Fasciitis") Bilateral Lateral Wt. Bearing radiographs are taken. A line is constructed on both feet at like points from the medial condyle/calcaneus and extending anteriorward to the base of the 5th metatarsal. A 3mm shift or greater identifys the posterior calcaneus subluxation. Anterior manipulation is performed using either an Activator Instrument or a Thompson Drop Piece Table in a series of treatments until the pain is relieved at which time a Post Radiograph is taken. Approximately 70% of patients will show a 40 to 100% improvement in calcaneus alignment. My next two sequel papers will follow in 2006. Paul M. Kell DC San Diego
  10. eddavisdpm

    eddavisdpm Active Member

    Anatomical position of infracalcaneal "spurs"

    My experience is similar to Kevin Kirby. A more cost effective manner to conduct further studies may be via sonography. There appears to be considrable variability in "spur" location within the origin of the plantar fascia or even the origin of the first layer of plantar musculature. One could argue that if a spur or plantar fasciitis is severe enough to warrant surgical intervention then that is most likely a traction "spur" in the plantar fascia. As such the surgical approach will be biased toward spurs that are indeed within the plantar fascial origin. Sonography can provide a relatively inexpensive tool to examine and document locations of both symptomatic and asymptomatic infracalcaneal spurs.

    Ed Davis, DPM
  11. NewsBot

    NewsBot The Admin that posts the news.

    Anatomic relationship of heel spur to surrounding soft tissues: Greater variability than previously reported.
    Li J, Muehleman C.
    Clin Anat. 2007 Oct 18;20(8):950-955 [Epub ahead of print]

  12. Scorpio622

    Scorpio622 Active Member

    Thought question.....

    Is it at all possible that the distal edge of the spur irritates the plantar fascia when the foot pronates???

    With reduction of the calcaneal inclination angle, the angle between the calcaneus and plantar fascia also decreases. The spurs lies directly over the fascia and is rotated downward.

    Could this be a source of irritation in severely pronated feet just like a haglunds irritates the achilles???

  13. Bruce Williams

    Bruce Williams Well-Known Member

    So Craig, does this mean you cannot have traction spur formation from muscle orgins?:confused:

    Either way, it seems it is probably a traction spur, just not purely from traction of the plantar fascia.

    I still think the fascial tension has something to do with it, but then I think that the swing limb helps pull the body forward in walking and running... Shows what I know!:pigs:

    Thanks for messing up my usual PF patient discussion! Now I have to say its from the muscles!:bang:

  14. I concur! Its always annoying when a conveniant lie is killed by an ugly truth!

  15. Bruce Williams

    Bruce Williams Well-Known Member

    Thanks for making me smile today Robert! I very much was in need of it!
  16. Craig Payne

    Craig Payne Moderator

    It was TH Huxley that said "The great tragedy of science is the slaying of a beautiful hypothesis by an ugly fact" .... I have this quote on my office wall.
  17. Cameron

    Cameron Well-Known Member

    Very interesting thread and a superb example of the worth of Podiatry Arena, if ever one was needed.

    As to PF and heel spurs I still maintain these are, quite obviously Alien implants. :wacko:

  18. admin

    admin Administrator Staff Member

    Me thinks you need to check this: Research into 'tin foil' hat wearing
  19. Kent

    Kent Active Member

    I might be missing something here... I'm not a surgeon so I can't comment on what these spurs look like in vivo but when I was studying anatomy, we learned that all three muscles in the 1st or most superficial layer of the plantar intrinsics (abductor hallucis, flexor digitorum brevis and abductor digiti minimi brevis) all attach to the medial tubercle and the plantar fascia. Could it be that the traction/tightness comes from the plantar fascia which in turn pulls on the 3 intrinsics listed above causing damage (muscles are more vascular than fascia) at their origin (the medial tubercle) which leads to spur formation in the direction of the traction??? Any thoughts?
  20. Bruce Williams

    Bruce Williams Well-Known Member

    Ha! Craig is now proven wrong! :dizzy:

    I don't have my anatomy text handy Kent, but I think you are correct?

    The plot thickens, or is it the plantar calcaneal spur!:wacko:

  21. Kent:

    When viewing these surgically, plantar calcaneal spurs are always deep to the plantar aponeurosis, with the plantar aponeurosis almost laying on top of the spur, at least the ones I have done surgery on. They are sharp, to a point almost, but ridge-like in nature, extending from medial to lateral for probably 2 cm on average.

    The plantar intrinsics certainly have enough tensile force at their origins at the plantar calcaneus to cause a spur formation. The plantar aponeurosis probably is subjected to much more magnitude of tensile force than any of the plantar instrinsics. However, the plantar aponeurosis wraps all the way around the plantar calcaneus from the anterior-plantar calcaneus to the posterior-plantar calcaneus at its origin, whereas, the plantar intrinsics insert more on the anterior leading edge of the plantar calcaneus only. It is likely that the plantar intrinsics have a smaller magnitude of tensile force but have a much smaller cross-sectional bone-soft tissue interface at its origin than the plantar apeurosis, which has a larger magnitude of tensile force and a much larger cross-sectional bone-soft tissue interface at its origin. Therefore, the tensile stress at the bone-soft tissue interface of the plantar intrinsics at the location of the spur may be much greater than that present at the relatively broad origin of the plantar aponeurosis (Stress = force/cross-sectional area). Increased magnitude of tensile stress at the bone-soft tissue interface is the likely cause of "traction spurs". This is my hypothesis for why the plantar calcaneal spurs occur where they do on the plantar calcaneus.
  22. Kent

    Kent Active Member


    I think you may have misunderstood what I was trying to say. I agree with what you have said. I'm not saying that these traction spurs develop in the plantar fascia. What I meant was that the much greater tensile forces through the plantar fascia are transmitted through to the plantar intrinsics (via their direct attachment), thus causing a traction spur at the origin of the intrinsic muscles. We both agree there is a greater magnitude of tensile force through the plantar fascia but...

    How do you know that these traction forces (in the intrinsics) aren't generated or transmitted from the plantar fascia?
  23. Kent:

    Which plantar intrinsic muscle do you think receives enough tensile force from the plantar fascia to significantly increase its own tensile force at its origin. In addition, can you propose a mechanism by which this event occurs? I tend to doubt this mechanism is a significant factor.
  24. Kent

    Kent Active Member

    3 plantar intrinsics have an attachment to the plantar fascia. If I had to guess which was the most significant, I would say flexor digitorum brevis. Can you explain how you think enough tension is generated by flexor digitorum brevis (or one of the other 2 intrinsics which attach to the medial tubercle) alone to cause a traction spur?

    What are your thoughts on the antaomical paper by Li and Muehleman published earlier? They say that "the stresses placed upon the heel spur are the result of vertical load rather than horizontal strain" and "heel spurs are not traction bony outgrowths as are seen with retrocalcaneal Achilles tendon spurs, but rather are a skeletal response to load/stress, and may be a response, or serve, to protect the bone against the development of microfractures. Thus, the stimulus for heel spur development may be due to repetitive stress, in the form of ground reactive force and microtrauma, causing a periosteal reaction with subsequent pathophysiological bone growth."

    If this is the case, then we're both wrong!
  25. I talked about this in an earlier post a few days ago:

    As far as tension vs compression, when you see a spur that is parallel to the pull of the fibers of the plantar fascia and is nearly 10 mm in length, why would one think this is caused by a compression force by GRF?!
  26. Kent

    Kent Active Member


    Why does transecting the medial half of the plantar fascia relieve pain in people with chronic plantar heel pain? Using your theory of traction plantar heel spurs, can I infer that you are saying that plantar fasciitis is completely independent of plantar heel spurs (i.e. some people can have pain as a result heel spurs in the absence of plantar fasciitis)?:confused:
  27. Transecting the plantar fascia eliminates the tensile force from the plantar fascia on the medial calcaneal tubercle and eliminates the force that causes the pain in the plantar calcaneus. My "theory of traction plantar heel spurs" does say that:

    1. most plantar heel spurs are asymptomatic;
    2. not all people with proximal plantar fasciitis have plantar heel spurs; and,
    3. plantar heel spurs, like most ectopic calcifications in the body, often develop independent of any noticeable symptoms.
  28. musmed

    musmed Active Member


    I cannot believe you wrote that.

    If one was to have a rope of 1 inch wide pulling 1 pound of pressure....OK

    Then the pressure per 1/10inch is a 1/10 of a pound pressure.. agree..


    Cut the planter fascia as per operation say 50%..

    Thus the loading on the remaining plantar fascia is now doubled.. and it does not hurt

    yet it hurt when 100% was taking the load...

    I thinks a rethink is needed..

    If not please explain

  29. Paul:

    Yes, believe it, I wrote it.

    The fibers of the plantar aponeurosis that cause the pain from plantar fasciitis, in the vast majority of cases, are the medial fibers of the central component of the plantar aponeurosis. This is likely because these are the fibers that are subjected to the most tensile forces during weightbearing activities since they are the fibers that help prevent the medial column of the foot from dorsiflexing under the effects of ground reaction force. Cutting the medial half of the central component of the plantar aponeurosi, which I just did in a patient last week, simply eliminates the pull on the fibers of the plantar aponeurosis that are causing the symptoms. This is why cutting them relieves the pain in the medial calcaneal tubercle.

    By the way, in your example of the rope above, the proper term would be "tensile stress", not "pressure". Also both stress and pressure are measured in similar ways: Pressure = force/surface area, Stress = force/cross-sectional area
  30. Mart

    Mart Well-Known Member

    Hi Kevin

    Careless use of terminology aside I wonder if this seems counter intuitive for the following reason;

    If you partially resect the most stressed part of the plantar fascia, (assuming you are correct, then the medial segment of the central band) then the stress remaining on the remaining fibres will increase.

    From your formula the total force ie combination of effects of gravity, body weight and combined functional characteristics during weight-bearing will remain constant, the c/s area reduced (effects of resection) therefore stress increases .

    However if you totally resect the segment so that c/s area = zero then stress will likewise be zero.

    I am very curious about this notion.

    Whilst I do not doubt the clinical end result (this is well documented in the literature) I am wondering if surgical resection is able to be so specific regarding which fibres are cut. Kevin I do not perform this surgery and would appreciate your observations.

    Suppose partial resection causes the remaining fibers to be so overloaded that they subsequently rupture with weight-bearing (I suspect this is what Paul may intuitively be feeling :)).

    This would have same effect as an accurately performed resection. If ramaining fibres did not rupture and pain was generated because remaining ones were consequently more overloaded, the outcome would be a worsening of pain. My recollection of pain scale classification of post surgical outcomes is that some subjects do actually get worse.

    Coupled with this notion is my observation with US measurement of fasciosis, that most subjects with typical thickened hypoechoic changes with no flow with PDI (suggestive of degenerative rather than inflammatory changes) show little or no measurable change with resolution of pain and presumed reduction of Force applied to plantar fascia from effects of foot orthoses.

    This suggests to me that possibility pain is generated not in the degenerated portion but the remaining healthy portion which then becomes overloaded.

    I feel given our existing evidence this may be major source of pain, which is consistent with the considerations of this thread.

    Can anyone find fault with this reasoning?

    If not then I think it would be interesting to test this idea with site specific local anesthetic infiltration to the “healthy” segment as a diagnostic test.

    I have not tried this, am not sure how realistic it would be to perform, however with US guidance it might be a practical possibility.

    As usual look forward to responses.



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

    The tensile stress remaining in the central component of the plantar aponeurosis (CCPA) of the untransected fibers after a partial plantar fasciotomy will, of course, increase some. However, here some possibilities: 1) either these lateral fibers of the CCPA may become plastically deformed and elongated over time which will gradually reduce their tensile stress over time, 2) the lateral fibers may rupture later post-surgically (this happened to one of my patients 4 weeks after her partial plantar fasciotomy) or 3) the lateral fibers may remain at their same length but the increase in their tensile stress is not enough to generate symptoms. There is also a possibility that since the foot will pronate more after a partial plantar fasciotomy, that the lateral fibers of the CCPA will have less tensile load than expected since the medial metatarsals are now being more loaded by the increased pronated position of the foot (the remainder of the structures which can generate a medial forefoot plantarflexion moment are now under greater tensile stress since the medial half of the CCPA can now no longer generate forefoot plantarflexion moment).

    Doing this surgery with a plantar arch incision (in-step fasciotomy) allows direct visualization of the whole width of the CCPA so that all fibers can be seen to be transected as required. I normally transect only the medial half of the CCPA.

    If the pain in the subperiosteal area of the medial calcaneal tubercle is being caused by both the tensile stress from the CCPA and the compressive stress from ground reaction force, would you expect healing of plantar heel pain to show a change in the US appearance of the CCPA? I wouldn't. I would suspect that serial MRIs of the healed plantar heel pain of plantar fasciitis would show decreasing subperioteal edema over time, with no change in the thickness of the CCPA.

    Good discussion. This talk ties in very nicely with my lecture this Sunday at the PFOLA meeting in San Diego on Rotational Equilibrium Across the Medial-Lateral Axis of the Midtarsal Joint.
  32. Stanley

    Stanley Well-Known Member


    I also have manipulated a posterior calcaneus and/or lateral talus, but I did it after I corrected the equinus, and/or asymmetry, as the previous dysfunctions do not seem to effect the pelvis and/or ankle joint. On the other hand I find the cuneiforms will result in equinus and pelvic asymmetry.
    Regarding the musculature, I find the Flexor digitoum brevis develops a Reverse strain-counterstrain injury.
    If you noticed I used the past tense when I talk about manipulations. I just work the posterior talo-calcaneal ligament, and the posterior calcaneus is corrected. Likewise the lateral talocalcaneal ligament controls the lateral talus.


  33. Mart

    Mart Well-Known Member

    I have to agree that your alternative post surgical effects seem plausible.

    Given the consistency in the literature from many studies with defining abnormal US findings correlated with symptoms I feel it important to determine if these findings are truly indicative of causes of pain or simply related but otherwise insignificant observations as seems likely with the single study of US findings of plantar plate tears.

    Without access to MRI to further study correlation with symptoms, coupled with comparative imaging with US it would seem difficult to answer this question.

    This is one reason why I am looking forward to Paul's study regarding role of FH Longus and results of his MRI/US studies because he claims, at least in his cohort, a low incidence of sub periosteal edema on MRI.

    Too bad I won't be in San Diego I would be interested to see your presentation.

    I know a couple of other Winnipegers who plan to go so I'll quiz them when they get back.



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

  34. Martin:

    As we learn more about the tissue mechanics behind the diagnosis we currently call "plantar fasciitis", I think we will be able to better differentiate this very broad diagnosis into 3-4 more accurate diagnoses which better correlate with the type of stresses causing the injury, whether the painful pathology originates from within the calcaneus, within the fascia, between the calcaneus and the fascia, or adjacent to the fascia.

    It is my contention that if the plantar calcaneus, at the origin of the central component of the plantar aponeurosis (CCPA), was not subjected to repetitive increased magnitudes of compression stresses occurring due to its mechanical interactions with ground reaction force (GRF) during weightbearing activities, that the rate of "proximal plantar fasciitis" within the population would decrease by at least 75%. In other words, if people walked only on their forefeet, without contacting their heels with the ground (as do most mammals, except bears, apes and humans) then plantar fasciitis would be greatly reduced within the human population.

    However, this is not to say that tensile forces arising, especially, from the medial fibers of the CCPA are also not responsible for the pain of proximal plantar fasciitis, since certainly they are. As I have stated many times before on this forum, it is the combination of both the compression stresses from GRF and the tensile stresses on the medial fibers of the CCPA that are the main mechanical causes of proximal plantar fasciitis. It is precisely for this mechanical reason why this small area of the foot is so commonly injured within the human population.
    Last edited: Nov 14, 2007
  35. musmed

    musmed Active Member

    Dear Martin

    I like your thinking.

    An example:

    Patient has classic symptoms of PF.

    HAS U/S shows some PF thickening..ho hum.

    The develops severe increase in pain and describes a tearing / rupture feeling and the pain has gone to an 11/10

    New U/S shows a tear in the PF.

    no tear some pain

    tear pain +++

    Pre surgery pain

    cut PF and no pain???

    who is lying????????????

    or look outside of the box.

    what has happened?
    1. patient sees surgeon... ? quick fix..
    2. goes to hospital.... ? placebo

    but more importantly

    has a general anaesthetic

    has a muscle relaxant

    muscle spindles RESET

    pain goes

    Methinks that if there was a study on this where some had cut PF and some had a cut skin to show everyone, I bet the outcomes will be the same.

    There again PF is known to get better on its own... maybe a general anaesthetic accelerates the 'get better time'.

    Just a thought but an important one.


    Paul Conneely aka musmed
  36. Paul:

    The surgical results I see with plantar fasciotomy are not with general anesthetic, they are with local anesthetic with monitor anesthesia care (Versed). The same surgical results occur with no intravenous sedatives, and with local blocks only, plantar fasciotomy decreases heel pain....read the literature....it is not a lie.
  37. musmed

    musmed Active Member


    I stand corrected but over here the few people I have seen have had a general anaesthetic.

    Is the local anaesthetic causing necrosis or apotosis and thus the outcome you want?

    Paul C

  38. Paul:

    It sounds to me like you need to do a little research on the efficacy and safety of local anesthetics. I have given probably over 10,000 local anesthetic injections during my practice career and have never seen any tissue necrosis from my injections. Also, I know of no significant apoptosis from my injections either in any of my patients.

    Have you ever given a local anesthetic injection, Paul??
  39. musmed

    musmed Active Member

    Dear Kevin

    The new data is out that Lignocaine in less than 0.5% is an apoptotic and in greater doses is an accelerant of necrosis.

    I started using local anaesthetic in 1969.

    Hope that is long enough.

    Poor old Paul. musmed
  40. Paul:

    I use Marcaine (bupivicaine) for my local anesthetic injections. Since you have been using local anesthetics for at least a decade before I started using it, Paul, certainly you would know if bupivicaine causes tissue necrosis when 10 cc of 0.5% solution is used to anesthetize the foot for a plantar fasciotomy. Please provide references.

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