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Hopefully, Dr. Paul Bennett can enter into the discussion to give us some more insight into this topic that he had helped introduce to Podiatry Arena some time ago. Ready for another lively discussion?!
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
96% with rupture?..... hardly a "random sample" of the population,
Post hoc comparision with a 19 year old ..... no suprises here
Corrolation with MRI..........figures
Interesting to view the images, and the ease at identifying in cadavars.... given US relies heavily on hypoechoic signal in the presence of inflammation.
I suppose this study employed someone for a while.
96% with rupture?..... hardly a "random sample" of the population,
Post hoc comparision with a 19 year old ..... no suprises here
Corrolation with MRI..........figures
Interesting to view the images, and the ease at identifying in cadavars.... given US relies heavily on hypoechoic signal in the presence of inflammation.
I suppose this study employed someone for a while.
Kind regards,
PB
I was hoping you might want to comment on any personal experience you may have had of correlating US results to MRI or surgical findings. Is US better than MRI in your experience??
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
I was hoping you might want to comment on any personal experience you may have had of correlating US results to MRI or surgical findings. Is US better than MRI in your experience??
Kevin,
I place most (if not all) weight on the clinical findings rather than US/MRI. MRI commonly misses the plantar plate tear if the slice is not spot on. Also, chronic conditions tend to go undetected more-so. US is highly operator dependant.
Clinically, if there is a positive Lachmans combined with relief with taping/Budin splint- and, no other glaring explanations for the pain (neuroma, friebergs,fracture,etc)- I make the diagnosis with comfort. Actually I use the MRI to r/o other possibilities rather than rule in plantar plate disruption.
I place most (if not all) weight on the clinical findings rather than US/MRI. MRI commonly misses the plantar plate tear if the slice is not spot on. Also, chronic conditions tend to go undetected more-so. US is highly operator dependant.
Clinically, if there is a positive Lachmans combined with relief with taping/Budin splint- and, no other glaring explanations for the pain (neuroma, friebergs,fracture,etc)- I make the diagnosis with comfort. Actually I use the MRI to r/o other possibilities rather than rule in plantar plate disruption.
Nick
I don't use US or MRI either for diagnosing plantar plate pathology, but thought that since Paul strongly advocated the diagnostic benefits of US for these and similar pathologies, he could give us some more up-to-date information.
I just wrote a Precision Intricast Newsletter on metatarsophalangeal joint (MPJ) capsulitis/stress syndrome/predislocation syndrome/plantar plate pathology. I use the following clinical signs/tests (which may or may not all occur) to diagnose plantar plate pathology:
1. Pain with plantarflexion range of motion of MPJ
2. Plantar and/or dorsal edema at MPJ and base of digit
3. Tenderness on plantar plate, especially at insertion onto base of digit
4. Dorsal subluxation and/or pain with Modified Lachman's test
5. Reduced pain during walking with plantarflexion strapping of digit
6. Reduced digital purchase force at affected digit and/or dorsiflexion deformity at MPJ during standing
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
How do you manage these patients with orthotics? For patients that don't want long term taping/Budin splinting, shoe modification or surgery- orthotics are the last resort for me. I typically add a met pad and sometimes pad out the met head area- with mixed results. Any other suggestions?? I find that this is one of the most difficult pathologies to treat.
How do you manage these patients with orthotics? For patients that don't want long term taping/Budin splinting, shoe modification or surgery- orthotics are the last resort for me. I typically add a met pad and sometimes pad out the met head area- with mixed results. Any other suggestions?? I find that this is one of the most difficult pathologies to treat.
Nick
Nick:
On the initial visit of patients with 2nd metatarsophalangeal (MPJ) stress syndrome (i.e. plantar plate pathology, capsulitis, predislocation syndrome), here are the following initial treatments I have found work best for my patients with 20+ years of trial and error treatments:
1. Add accommodative padding (i.e. plantar to 1, 3-5 metatarsal heads) and/or metatarsal pads to shoe insoles/sockliners to reduce ground reaction force (GRF) to plantar plate.
2. Apply and instruct patient on plantarflexion strapping of 2nd digit.
3. Instruct patient on 20 minutes/2x per day direct icing to plantar MPJ area of foot.
4. Avoid running, jumping activities for 2 weeks.
5. Have patient purchase an over-the-counter (OTC) orthosis at local running shoe store.
6. I may prescribe a non-steroidal antiinflammatory medicine if desired.
On second visit, in about two weeks following the first visit, I will then modify the OTC orthosis to add a pad plantar to the distal metatarsal shafts that also extends to the sulcus of MPJs 1, 3-5. In addition, I will continue the patient on icing, taping and may allow gradual return to activities if they are making improvement. If little improvement, then I may evaluate and cast the patient for custom foot orthoses with the following design parameters:
1. Neutral suspension casting
2. Balance positive cast 2-5 degrees inverted with 2-3 mm medial heel skive.
3. Use 3/16" polypropylene with 4 degree/4 degree rearfoot post.
4. Make orthosis anterior edge shape to match parabola of each metatarsal neck (i.e. orthosis will be longest at 2nd metatarsal neck). I call this modification the "capsulitis modification" and this is the subject of my latest Precision Intricast Newsletter.
5. Make anterior edge of orthosis 3/16" (i.e. 5 mm) thick with abrupt drop off at anterior edge (i.e. anterior edge full thickness).
6. Use full length neoprene topcover with forefoot extension of 1/8" korex to sulcus plantar to metatarsal heads 1, 3, 4 and 5 to accommodate 2nd metatarsal head.
This prescription may be later modified with a soft metatarsal pad added between the neoprene topcover and orthosis plate and/or a further layer of 3 mm thick korex to the anterior orthosis edge to further reduce GRF plantar to 2nd MPJ (i.e. "float the 2nd MPJ off the ground").
Icing is critical in treating 2nd MPJ stress syndrome since the icing will reduce the plantar swelling that is so common with this condition. Since plantar swelling will increase the GRF plantar to the plantar plate area due to the alteration in soft tissue contour at the plantar forefoot (i.e. the 2nd MPJ area is more plantarly prominent both visually and via palpation), by reducing the plantar swelling with icing, not only is the pain from the inflammation reduced but, I believe, GRF and localized plantar pressure on the plantar plate is also reduced. Therefore, unless the plantar edema is reduced locally at the 2nd MPJ with icing, patients do not seem to respond nearly so readily as they do as when they regularly use ice therapy to reduce their swelling, inflammation and pain.
If the orthosis does not completely resolve the pain, then careful extra-articular injections of cortisone solution (generally no more than one) into the plantar MPJ area will generally help resolve the remaining pain and swelling from the condition.
Hope this helps.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
I see quite a lot of metatarsophalangeal joint pathology in racquet players - especially badminton and squash - and concur with your management. Interested in your modified Lachman's test - but I'm only aware of this with ACL injuries - could you explain further with regards to plantar plate tears?
Thanks
Mark Russell
__________________
"citing an indisposition due to special circumstances"
I see quite a lot of metatarsophalangeal joint pathology in racquet players - especially badminton and squash - and concur with your management. Interested in your modified Lachman's test - but I'm only aware of this with ACL injuries - could you explain further with regards to plantar plate tears?
Thanks
Mark Russell
The Modified Lachman's Test and Dorsal Drawer Test are the same tests. Basically, grasp the distal metatarsal firmly with one hand (i.e. examiner's fingers stabilizing the distal metatarsal dorsally and thumb stablilizing distal metatarsal plantarly) and with the other hand (i.e. examiner's thumb at proximal-plantar base of proximal phalanx of digit and examiner's forefinger on distal-dorsal head of proximal phalanx of digit) attempt to dorsally translate the proximal phalanx base relative to the metatarsal head. In plantar plate tears, the base will significantly sublux relative to the metatarsal head and the patient may have pain with the maneuver. It is recommended to practice on normal feet to feel the normal range of motion at the MPJ with the Dorsal Drawer Test so that the increased range of motion indicating plantar plate tear may be better appreciated by the examiner.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
I read this paper a few weeks ago and was surprised that almost every sample had significant plantar plate tears IE 2.2mm x 3.4mm mean. Even tho this was not a good statistical representation of population the bias of the findings were so large as to make them clinically significant at least for further investigation. Do you think it is likely that asymptomatic plantar plate tear is a normal finding amongst the population and if it is what makes a plantar plate tear symptomatic? Maybe this is similar to the old heel spur misinterpretation. IE Pain in heel – x-ray = heel spur –therefore- Dx = heel spur causes pain – but most people have heel spurs but no pain?? The results of ultrasound were backed up by physical examination in this study, which would seem to validate the experiment. I’m not knowing much about the limitations of u/s examination so perhaps Paul you could elaborate on your first post to this thread.
Like Scorpio I find this one of the most difficult pathologies to treat successfully, But yesterday I had a very pleased customer who had the pain for many months before seeing me and this had now resolved after treatment very similar to that which you describe above, Kevin. However, she had elevated 1st ray after bunion sugery and a compliant lateral column, which left a relatively non compliant 2nd MPJ / ray to bear the main stress of GRF reactions. The orthosis was made to relieve the 2nd MPJ pressure but now she has plantar digital neuroma pain 2nd and 3rd interspace. To relieve this I need to raise the met transverse arch, which may in turn increase 2nd ray GRF. What do you suggest?
On a second pair of orthoses I’m trying a lower profile to the forefoot balancing and adding a met raise biased to the 3rd ray.
Like Scorpio I find this one of the most difficult pathologies to treat successfully, But yesterday I had a very pleased customer who had the pain for many months before seeing me and this had now resolved after treatment very similar to that which you describe above, Kevin. However, she had elevated 1st ray after bunion sugery and a compliant lateral column, which left a relatively non compliant 2nd MPJ / ray to bear the main stress of GRF reactions. The orthosis was made to relieve the 2nd MPJ pressure but now she has plantar digital neuroma pain 2nd and 3rd interspace. To relieve this I need to raise the met transverse arch, which may in turn increase 2nd ray GRF. What do you suggest?
On a second pair of orthoses I’m trying a lower profile to the forefoot balancing and adding a met raise biased to the 3rd ray.
Dave:
These pathologies are difficult to treat when the clinician uses only traditional functional foot orthoses without the specialized modifications to the forefoot region of the orthosis listed above. Unfortunately, very few podiatrists are aware of these modifications since most podiatrists still believe that a functional foot orthosis ends proximal to the metatarsal heads!
Neuroma/neuritis-like symptoms, with burning and/or tingling in the distal-plantar digit, are often experienced by patients with 2nd MPJ capsulutis, probably due to irritation of the adjacent plantar nerve from the localized swelling of the plantar joint area. Also, when doing these forefoot extension modifications, keep track of the tightness of the upper of the patient's shoe around their forefoot while the patient is standing with the orthosis inside the shoe. Increased orthosis forefoot thickness will take up more room inside the shoe which may, in turn, cause increased external forefoot pressure from the shoe upper and increase neuroma/neuritis-like symptoms due to increased internal intermetatarsal pressures.
In the patient described above, try increasing the forefoot extension thickness plantar to the 1st MPJ, removing the forefoot extension plantar to the 2nd and 3rd MPJ, so that the forefoot extension is only now under metatarsal heads 1, 4 and 5. In addition, try adding a 3 mm piece of korex/EVA plantar to the distal orthosis edge to increase the GRF plantar to all the distal metatarsal shafts. Alternatively, a metatarsal pad placed on the distal orthosis edge may be used to increase the GRF proximal to the symptomatic area.
Glad to hear that you have had some initial success with my orthosis modifications for MPJ capsulitis on your patient.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
Do you think it is likely that asymptomatic plantar plate tear is a normal finding amongst the population and if it is what makes a plantar plate tear symptomatic? Maybe this is similar to the old heel spur misinterpretation. IE Pain in heel – x-ray = heel spur –therefore- Dx = heel spur causes pain – but most people have heel spurs but no pain?? The results of ultrasound were backed up by physical examination in this study, which would seem to validate the experiment. I’m not knowing much about the limitations of u/s examination so perhaps Paul you could elaborate on your first post to this thread.
Cheers Dave
Hi Dave
My main interest in adding to this thread concerns your point regarding explaining “abnormal” imaging findings in asymptomatic subjects. This ties in quite nicely with some of the other threads currently regarding chronic plantar fasciosis.
I certainly wouldn't regard myself as an expert using Diagnostic ultrasound, but am currently using it frequently to investigate a variety of MSK structures and usually look at the integrity of the plantar plate during my exam for metatarsalagia. I use a high res machine at 13 Mhz and get good quality images but find being certain of identifying plantar plate tears difficult and have a way to go before I feel that I have enough experience to have an opinion as to the value of doing this.
I am attaching a paper on this subject which I feel is more interesting than the one Kevin cited from a users perspective because it investigates living subjects and includes power Doppler which is very useful to determine the presence of increased vascularity which might be assumed present with inflammation. Conclusions are consistent with the cadaver study in identifying a large number of asymptomatic tears.
I have examined hundreds of plantar heel pain patients with diagnostic ultrasound exam and feel pretty confident at interpreting what I see in this region. The plantar fascia is one of the easiest structures to explore because of its size and location.
The observations I have made so far which I feel are worthy of generalization are these:
Most people with the classic features from history and physical exam for chronic plantar fasciosis show fusiform hypoechoic thickening greater than reported norms described in the literature.
Most with unilateral pain will have a normal exam for the asymptomatic plantar fascia.
Some will have abnormally thickened plantar fascia bilaterally with unilateral pain, the painful side usually being thicker.
I have NEVER seen any signs of motion with power Doppler (= blood flow) in a normal or abnormal image.
Most people when examined after resolution of pain have a slight reduction in measured abnormal thickening, some no change and a few worsening, but NEVER have I seen a case return within normal limits even when completely pain free.
Some have concurrent signs of calcific insertion of plantar fascia which is nearly always deep to the plantar fascia insertion.
People with a thickening greater than 10mm have low success with foot orthoses designed to influence autosupport function and/or decrease tendo-achilles tension.
My concerns from these observations are:
As others have been suggesting for a while, acute inflammation of the plantar fascia seems a rarity, we should be thinking about chronic plantar fasciosis.
What are the pain generators in most cases of chronic plantar fascia injury?
Could it be a result overload of the healthy portion because of inadequacy of the damaged region?
Is there a contribution of the calcification in injury or pain generation?
The so called “tissue stress” model describes that when a threshold is passed where applied force exceeds the elastic deformable properties of issue pain will likely result because of the effects of derangement. I am curious about the mechanism of pain since it seems unlikely that inflammation plays much of a role. Power Doppler is very sensitive indicator of motion and if I examine an actively inflamed portion of tendo-achilles or synovium it is unambiguous.
This leads me to suspect that pain generation is in the healthy tissue at that instant when being over stressed to the point of derangement, at least in part, because adjacent chronically damaged tissue has lost it’s load bearing integrity. Most people with this kind of injury report pain on rising from bed in morning, and condition worsens with increased activity and improves with rest. Kevin pointed out in one of his intricast newletter essays that, a small linear short axis defect would have considerable cross sectional impact and shift injury threshold.
Considering that most of the chronic non articular musculo-skeletal injuries we see in the foot and lower limb are concerned with tensile stress problems this makes sense. It seems also consistent to me that diagnostic imaging might detect structural but asymptomatic derangement . I often find patient reports episodic pain which resolves without intervention. This could be self limiting derangement which might only ever be detected with imaging unless at some point another episode occurred at an adjacent site which lead to a chronic injury.
As to the value of Diagnostic ultrasound exam or other imaging for chronic musculo-skeletal injury?
I have yet to make up my mind. Certainly it gives me useful clues with people who give poor history or who have no pain on examination or infrequent episodes. I feel it is akin to using plantar pressure measurement. Isolated abnormal measurements are not that useful because so many other factors determine if the “abnormality” or injury will be problematic.
I’d be interested in comments regarding the pain generators.
This leads me to suspect that pain generation is in the healthy tissue at that instant when being over stressed to the point of derangement, at least in part, because adjacent chronically damaged tissue has lost it’s load bearing integrity. Most people with this kind of injury report pain on rising from bed in morning, and condition worsens with increased activity and improves with rest. Kevin pointed out in one of his intricast newletter essays that, a small linear short axis defect would have considerable cross sectional impact and shift injury threshold.
Considering that most of the chronic non articular musculo-skeletal injuries we see in the foot and lower limb are concerned with tensile stress problems this makes sense. It seems also consistent to me that diagnostic imaging might detect structural but asymptomatic derangement . I often find patient reports episodic pain which resolves without intervention. This could be self limiting derangement which might only ever be detected with imaging unless at some point another episode occurred at an adjacent site which lead to a chronic injury.
As to the value of Diagnostic ultrasound exam or other imaging for chronic musculo-skeletal injury?
I have yet to make up my mind. Certainly it gives me useful clues with people who give poor history or who have no pain on examination or infrequent episodes. I feel it is akin to using plantar pressure measurement. Isolated abnormal measurements are not that useful because so many other factors determine if the “abnormality” or injury will be problematic.
I’d be interested in comments regarding the pain generators.
Cheers
Martin
Martin:
Thanks for the article. I agree, it was much better than the one I mentioned earlier in this thread.
This article points to the fact that there are many asymptomatic plantar plate tears in the population and that diagnostic ultrasound was better able to detect plantar plate pathology than was MRI.
In regards to "plantar fasciosis", if the plantar fascia and/or its surrounding structures are not inflamed then why do cortisone injections (anti-inflammatory injectable medicine) and NSAIDS (anti-inflammatory oral medicine) help so much with the pain of "plantar fasciosis"?? Could it be that the plantar aponeurosis itself does not show signs of inflammation but the surrounding tissues are inflamed in response to trying to repair the tissue damage to the plantar aponeurosis??
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
In regards to "plantar fasciosis", if the plantar fascia and/or its surrounding structures are not inflamed then why do cortisone injections (anti-inflammatory injectable medicine) and NSAIDS (anti-inflammatory oral medicine) help so much with the pain of "plantar fasciosis"?? Could it be that the plantar aponeurosis itself does not show signs of inflammation but the surrounding tissues are inflamed in response to trying to repair the tissue damage to the plantar aponeurosis??
Kevin,
Don't NSAIDs have a pain modifying/analgesic effect which explains why they can help with non-inflammatory conditions such as fasciosis and tendinosis?
Don't NSAIDs have a pain modifying/analgesic effect which explains why they can help with non-inflammatory conditions such as fasciosis and tendinosis?
Kent
Yes, NSAIDS do have an analgesic effect, but do we know it is not inflammation within or around the fascia that is causing some of the pain? Why would cortisone injections help relieve the pain for 1-4 weeks if it was not inflammation causing the pain? I have a difficult time believing that the body doesn't respond to a damaged plantar aponeurosis with some form of inflammatory process since a normally functioning body responds with an inflammatory process to all other insults that cause damaged tissues.
Before we all jump on the bandwagon that plantar fasciitis is not an inflammatory condition and ride the wagon shouting it should be called "plantar fasciosis" not "plantar fasciitis", it would probably be prudent to become familiar with the histological literature on plantar fascial pathology that does show inflammation in all the cases examined surgically. As far as I'm concerned, plantar fasciitis is still sometimes an inflammatory condition, caused by intrasubstance derangement of some of the fibers of the plantar aponeurosis, until proven otherwise.
Quote:
Degenerative lesions of the plantar fascia: surgical treatment by fasciectomy and excision of the heel spur. A report on 38 cases.
Acta Orthop Belg. 2003; 69(3):267-74 (ISSN: 0001-6462)Jarde O; Diebold P; Havet E; Boulu G; Vernois J
Service d'Orthopédie-Traumatologie, Hôpital Nord-Amiens, France. jarde.olivier@chu-amiens.fr
The authors studied 38 cases of degenerative lesions of the plantar fascia which were treated surgically between 1989 and 1999. MRI showed chronic fasciitis in eight cases and an old rupture of the plantar fascia in 30 cases. Surgical treatment, which was performed in all cases after failure of conservative treatment of several months duration, combined excision of the fascia with resection of the heel spur. Histological examination found inflammation in all cases (fasciitis or rupture), calcification of the aponeurosis in four cases, cartilaginous metaplasia in four and fibromatosis in four. Patients were assessed a minimum of one year and a maximum of seven years after operation. The postoperative results were assessed using three criteria: resolution of pain, results on the static foot and patients' functional activity. Overall there were 24 very good and good results, nine fair and five poor. MRI performed at the time of follow-up revealed good healing of the plantar fascia in 16 cases, defects in two cases, inflammation in seven cases and defects associated with inflammation in 13 cases. Surgical treatment may be considered in cases where conservative treatment of talalgia has failed. Symptoms originating from degenerative damage to the plantar fascia, such as rupture or fasciitis, may benefit from fasciectomy. Short-term results show resolution of pain in 75% of cases, and a slight sagging of the plantar arch. Pre-operative MRI study is useful to determine the exact location of the lesions.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
Yes, NSAIDS do have an analgesic effect, but do we know it is not inflammation within or around the fascia that is causing some of the pain? Why would cortisone injections help relieve the pain for 1-4 weeks if it was not inflammation causing the pain? I have a difficult time believing that the body doesn't respond to a damaged plantar aponeurosis with some form of inflammatory process since a normally functioning body responds with an inflammatory process to all other insults that cause damaged tissues.
Before we all jump on the bandwagon that plantar fasciitis is not an inflammatory condition and ride the wagon shouting it should be called "plantar fasciosis" not "plantar fasciitis", it would probably be prudent to become familiar with the histological literature on plantar fascial pathology that does show inflammation in all the cases examined surgically. As far as I'm concerned, plantar fasciitis is still sometimes an inflammatory condition, caused by intrasubstance derangement of some of the fibers of the plantar aponeurosis, until proven otherwise.
Hi Kevin
I understand your reluctance to jump on bandwagons.
Suggestions made that NSAIDs may have analgesic effect rather than anti-inflammatory seem plausible to me but I am likewise unaware why steroid infiltration might be analgesic (with Lidocaine mixed in I guess it might be for a few hours but there are more likely explanations).
My experience with diagnostic ultrasound is of being unable to detect motion which might be anticipated with increased blood flow caused by inflammation not only at site of hyperchoicity/thickening of the plantar fascia but in the surrounding tissues. I am very curious about how to interpret this.
There some stuff to mull over which I have not seen mentioned in previous threads on plantar heel pain.
Since we are off topic from “plantar plate” exams I will add some comments to the “Plantar Fasciitis Discussions “thread later.
There’s a fair amount of work for me to add something useful which is new so will spend a bit of time preparing this and continue in a couple of days.
This article points to the fact that there are many asymptomatic plantar plate tears in the population and that diagnostic ultrasound was better able to detect plantar plate pathology than was MRI.
In regards to "plantar fasciosis", if the plantar fascia and/or its surrounding structures are not inflamed then why do cortisone injections (anti-inflammatory injectable medicine) and NSAIDS (anti-inflammatory oral medicine) help so much with the pain of "plantar fasciosis"?? Could it be that the plantar aponeurosis itself does not show signs of inflammation but the surrounding tissues are inflamed in response to trying to repair the tissue damage to the plantar aponeurosis??
Hi Kevin
I saw a patient last week who I was able to be fairly certain had both a PP rupture and a PP tear on adjecent joints. Thought you might be interested to see how this manifested itself.
I think I probably see a lot of PP tears and have been a bit reluctant to feel sure of my intrerpretation because of seeing so many, I shall start using PDI to evaluate for inflamatory signs too because this is more likely to indicate a pain generating lesion than simply a common but irrelevant finding.
Our discussion on plantar fascia I have added to in some detail and put into the planatar fascia inflamation vs degeneration thread.
Please let me know what you think about that when you get time.
I tried to attatch the papers but they were too large for the arrena server and just tried attatching compressed images too which were less than max allowable size - perhaps there's a server problem will try again later .
regards
Martin
The St. James Foot Clinic
1749 Portage Ave.
Winnipeg
Manitoba
R3J 0E6
phone [204] 837 FOOT (3668)
fax [204] 774 9918 www.winnipegfootclinic.com
I saw a patient last week who I was able to be fairly certain had both a PP rupture and a PP tear on adjecent joints. Thought you might be interested to see how this manifested itself.
I think I probably see a lot of PP tears and have been a bit reluctant to feel sure of my intrerpretation because of seeing so many, I shall start using PDI to evaluate for inflamatory signs too because this is more likely to indicate a pain generating lesion than simply a common but irrelevant finding.
Our discussion on plantar fascia I have added to in some detail and put into the planatar fascia inflamation vs degeneration thread.
Please let me know what you think about that when you get time.
I tried to attatch the papers but they were too large for the arrena server and just tried attatching compressed images too which were less than max allowable size - perhaps there's a server problem will try again later .
regards
Martin
The St. James Foot Clinic
1749 Portage Ave.
Winnipeg
Manitoba
R3J 0E6
phone [204] 837 FOOT (3668)
fax [204] 774 9918 www.winnipegfootclinic.com
Looks like the glitch is fixed - here's a couple of images from the same patient which might be regarded as textbook, they are from adjacent MTHs from the same foot.
I thought those not familiar with US would enjoy how nicely these structures can be visualised, bear in mind too that you can see them moving during the exam.
Just thought I would let you know that I have just reviewed a patient who I feel has a plantar plate rupture which I was kind of helping with traditional orthotics and toe taping. After reading the description of the modified orthotic you have used for these types of problems I decided to try it out using the formulae you plotted out. She recieved them 2 weeks ago and I just carried out a phone review in which she is very happy - reports an 80% reduction in her symptoms and no longer needs to tape the toe. Thank you.
__________________
Mark Egan
Absolute Podiatry
331/33 North St
Spring Hill, Qld
4000
Just thought I would let you know that I have just reviewed a patient who I feel has a plantar plate rupture which I was kind of helping with traditional orthotics and toe taping. After reading the description of the modified orthotic you have used for these types of problems I decided to try it out using the formulae you plotted out. She recieved them 2 weeks ago and I just carried out a phone review in which she is very happy - reports an 80% reduction in her symptoms and no longer needs to tape the toe. Thank you.
I'm glad to hear my 20+ years of trial and error experimentation with different foot orthosis designs for plantar plate injuries/MPJ capsulitis has helped your patient, Mark. You made my day.
__________________
Sincerely,
Kevin
**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
Hi,
I know this is an old post - but very informative.
I would, however, like your opinion on Matt Dinot's article in the Australasian Journal of Podiatric Medicine
2003; Vol 37, No.2 : 43-46. That states:
"Importantly, it should be noted that based on the biomechanical
underpinnings of this condition, pads or orthoses that
incorporate a U-shaped design to balance the metatarsal head, may actually hasten the progression of the digital deformity.
Allowing for plantarflexion of the metatarsal promotes the
dorsiflexory action of the intrinsic muscles (interossei and
lumbricals) hence worsening the hammering of the digit and
further opening up the plantar plate rupture."
This appears to be in conflict with
"then modify the OTC orthosis to add a pad plantar to the distal metatarsal shafts that also extends to the sulcus of MPJs 1, 3-5".
Hi,
I know this is an old post - but very informative.
I would, however, like your opinion on Matt Dinot's article in the Australasian Journal of Podiatric Medicine
2003; Vol 37, No.2 : 43-46. That states:
"Importantly, it should be noted that based on the biomechanical
underpinnings of this condition, pads or orthoses that
incorporate a U-shaped design to balance the metatarsal head, may actually hasten the progression of the digital deformity.
Allowing for plantarflexion of the metatarsal promotes the
dorsiflexory action of the intrinsic muscles (interossei and
lumbricals) hence worsening the hammering of the digit and
further opening up the plantar plate rupture."
This appears to be in conflict with
"then modify the OTC orthosis to add a pad plantar to the distal metatarsal shafts that also extends to the sulcus of MPJs 1, 3-5".
????
SRD
Mr./Ms. SRD:
Accommodating the metatarsal head with a foot orthosis will not "hasten the progression of the digital deformity" or "worsen the hammering of the digit" as is claimed below.
Quote:
"Importantly, it should be noted that based on the biomechanical underpinnings of this condition, pads or orthoses that incorporate a U-shaped design to balance the metatarsal head, may actually hasten the progression of the digital deformity. Allowing for plantarflexion of the metatarsal promotes the dorsiflexory action of the intrinsic muscles (interossei and lumbricals) hence worsening the hammering of the digit and further opening up the plantar plate rupture."
Plantar plate tears are not caused by a plantarflexed metatarsal. Plantar plate tears are caused by increased magnitudes of tensile stress and increased magnitudes of compression stress within the plantar plate. Patients with plantar plate tears are always more comfortable once the foot orthosis is designed to adequately reduce the ground reaction force plantar to the affected metatarsophalangeal joint, which will in turn reduce both the tensile stress and compression stress within the plantar plate. If stress is taken off the joint for a long enough period of time, then the symptoms from a plantar plate tear can resolve and become asymptomatic, as long as the plantar plate tear is not too severe. Joint position does not cause pathology, abnormal tissue stresses cause pathology.
__________________
Sincerely,
Kevin
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Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College
Accommodating the metatarsal head with a foot orthosis will not "hasten the progression of the digital deformity" or "worsen the hammering of the digit" as is claimed below.
Do we actually know this? Can allowing a metatarsal to plantar flex in relation to the others create a tendency for increased clawing/hammering of the toe?
I also use a met head accommodation with a gel fill.I will also add a first ray cut away to allow sagittal motion through the first mtpj hopefully reducing abductory twist on the 2nd mtpj. The accommodation for the 2nd mtpj is made in the reverse morton's extension. Seems to work well.
Regards
__________________
Graham Curryer
None of us know what we are doing, but some of us know more about what we are not doing than others!::
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Plantar Plate Sonography and Histology
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