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What is the best treatment for plantar fascitis induced heel spurs...
to which I replied:
Quote:
Since when did heel spurs have anything to do with the plantar fascia?
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:
Quote:
McCarthy DJ, Gorecki GE. The anatomical basis of inferior calcaneal lesions. JAPMA 1979;69:527
This is quoted as finding the spur in the origin of the flexor digitorum brevis. ALSO, they asserted "the origin of flexor digitorum brevis, quad. plantae, long plantar ligament, abductor hallucis muscle and abductor digiti minumi are all sites of potential spur formation.
THIS WAS PUBLISHED IN 1979!!!! -- why do people still talk about the calcaneal heel spur as being due to traction of the plantar fascia
How, I finally found one of the other more recent references showing the same thing:
Quote:
Heel Spur Formation and the Subcalcaneal Enthesis of the Plantar Fascia
TSUKASA KUMAI and MIKE BENJAMIN
Objective. To describe the structure and significance of subcalcaneal heel spurs associated with the plantar fascia.
Methods. The enthesis of the plantar fascia was removed from 17 elderly cadavers by sagittal saw cuts either side of the medial tuberosity, radiographs were taken, and the tissue was processed for routine histology. Sagittal sections were stained with toluidine blue, Masson's trichrome, or alcian blue, and sections were matched with the corresponding radiographs.
Results. Spurs develop on the deep surface of the plantar fascia but their formation is heralded by degenerative changes that occur within it. According to differences between small and large spurs, we propose that there are 3 stages in their development: (1) an initial formation of cartilage cell clusters and fissures at the plantar fascia enthesis; (2) thickening of the subchondral bone plate at the enthesis as small spurs form; (3) development of vertically oriented trabeculae buttressing the proximal end of larger spurs. The spurs grow by a combination of intramembranous and chondroidal ossification.
Conclusion. Contrary to popular belief, subcalcaneal heel spurs cannot be traction spurs as they do not develop within the plantar fascia itself. They are thus fundamentally different from heel spurs in the Achilles tendon. We suggest instead that they develop as a consequence of degenerative changes that occur in the plantar fascia enthesis. (J Rheumatol 2002;29:1957-64)
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?
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.
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" ) of asymptomatic heel spur in the general population - why do people continue to consider it a problem?
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:
Quote:
Ten Biomechanical Functions of the Plantar Fascia
1. Serves to support the medial and lateral longitudinal arch in a higher arched position.
2. Assists in resupination of subtalar joint (STJ) during propulsive phase of walking.
3. Assists the deep posterior compartment muscles by limiting STJ pronation.
4. Assists the plantar intrinsic muscles in preventing longitudinal arch flattening.
5. Reduces tensile forces in plantar ligaments.
6. Prevents excessive interosseous compression forces on dorsal aspects of midfoot joints.
7. Prevents excessive dorsiflexion bending moments on metatarsals.
8. Passively maintains digital purchase and stabilizes proximal phalanx in sagittal plane.
9. Reduces ground reaction force on metatarsal heads during late midstance and propulsion.
10. Helps to absorb and release elastic strain energy during running and jumping activities.
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.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
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
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.
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...
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.
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
The Following User Says Thank You to pablo2081 For This Useful Post:
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.
The stimulating factor for the development of heel spur (calcaneal exostosis) is controversial. In a sample of elderly cadaveric specimens, using radiographic, gross morphological, and histological investigation, we demonstrate that heel spurs are generally not found in the trajectory of traction from the plantar aponeurosis enthesis or plantar muscles. Rather, they are variably associated with soft tissues including loose connective tissue, fibrocartilage, muscle, and aponeurosis. Furthermore, the bony trabeculae of the spur are not aligned in the direction of soft tissue traction, but rather in the direction of stress on the calcaneus during walking and standing. These results substantiate the view that the heel spur may be a skeletal response to stress and may serve to protect the bone against the development of microfractures.
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???
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...
So Craig, does this mean you cannot have traction spur formation from muscle orgins?
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!
Thanks for messing up my usual PF patient discussion! Now I have to say its from the muscles!
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.
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.
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?
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?
Ha! Craig is now proven wrong!
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!
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?
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.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
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...
Quote:
Originally Posted by Kevin Kirby
The plantar intrinsics certainly have enough tensile force at their origins at the plantar calcaneus to cause a spur formation.
How do you know that these traction forces (in the intrinsics) aren't generated or transmitted from the plantar fascia?
How do you know that these traction forces (in the intrinsics) aren't generated or transmitted from the plantar fascia?
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.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
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.
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."
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?
I talked about this in an earlier post a few days ago:
Quote:
Originally Posted by Kevin Kirby
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.
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?!
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
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)?
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)?
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.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
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..
So...............
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
musmed
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
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
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
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.
Cheers
Martin
The St. James Foot Clinic
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Is a calcaneal spur in the plantar fascia?
) of asymptomatic heel spur in the general population - why do people continue to consider it a problem?
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