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Growing pains

Discussion in 'Pediatrics' started by Cameron, Feb 19, 2015.

  1. Cameron

    Cameron Well-Known Member

  2. drhunt1

    drhunt1 Well-Known Member

    Lee Cohen is correct in that shoe "inserts" can stop growing pains in children. But he has the kids lined up with their shoes on, instead referring to genu recurvatum and the alignment of the leg as a potential source of the problem. That is not correct. I might add the genu recurvatum can be a potential indicator of a collagen deficiency disorder, such as EDS. But that is not the source of the problem. Dr. Cohen is focusing on the wrong plane. He ends the segment by discussing getting the heel to vertical by whatever means...a custom orthotic or pre-fab. He is correct there, but not for the right reasons. Help is on the way, folks...come April, the solution to the problem will be revealed.
  3. Admin2

    Admin2 Administrator Staff Member

  4. drhunt1

    drhunt1 Well-Known Member

    Read those articles. The one written by Arthur S. Walters back at Vanderbilt University is a good reference resource. I have talked to him twice. The first time was when I contacted him to perform peer review on the program. First, he refused because he worked for Vanderbilt and they would not allow him to sign the NDA. But second, he's currently being funded by Big Pharma so he wouldn't qualify for peer review due to conflict of interest. The second time I talked with him, I told him what the answer was, how it's diagnosed and treated, and the connection between the two maladies. Some docs have made an entire career off the study and treatment of RLS. Dr. Walters, however, has produced some seriously good research on the connection between the two problems. He should be recognized for his work.
  5. Dananberg

    Dananberg Active Member

    Throughout my career I saw many, many children with growing pains (GP) and spent considerable time explaining to their parents that it really does not hurt to grow! I cannot recall a time when simple orthotic intervention failed to solve this specific issue of GP and I followed many into adulthood and saw them avoid the issues of RLS. In that regard, I am a real proponent of biomechanical treatment of this entity and have learned to viewed GP as overuse syndrome in a child.

    As far as being related to genu recurvatum, this seems to relate to the negative biomechanical influence of equinus on gait style. In practice, these negative effects are usually and immediately alleviated via ankle manipulation and this was an essential part of my exam and treatment. The interesting aspect to manipulation is the co-factor of changing muscular inhibition to facilitation, specifically involving the peroneals. When one of the “pistons” of the engine are lost, the other muscle groups must overwork to compensate for the inhibited state, leading to the marked muscular leg pain associated with GP. While foot orthotics were a very effective tool in managing this condition, the addition of manipulation was as much a factor in positive outcomes as the orthotic device.

  6. drhunt1

    drhunt1 Well-Known Member

    Howard-you're on the right track! Article in April PMM will describe what you've already figured out on your own. The two maladies are "compensatory" but not primarily due to sagittal plane problems. Lee Cohen was focused on that in the video to a certain degree. The answer is forthcoming. Congrats.
  7. Dananberg

    Dananberg Active Member


    Since sagittal plane comprises 80% of the available ROM that the foot uses during the gait cycle, how could it not play a major role? And, as you noted, I "figured this out myself", why did my treatments prove so successful when this was not the answer. In all my years of practice, I have found that when the correct treatment is applied, the response is rather rapid. Since this was the case, not sure what I missed.

  8. Howie:

    Aren't you glad "you're on the right track" after all your years of practice?;)
  9. drhunt1

    drhunt1 Well-Known Member

    Howard-my opinion is that an orthotic is "best" at treating frontal plane deformities...not sagittal plane. In the video above, Dr. Cohen discussed genu recurvatum as a potential source of the problem. Now...can you tell me how an orthotic treats hypermobility of the knee joint in the sagittal plane? The ankle joint is a hinge joint functioning primarily in the sagittal plane. Can you be so kind as to tell me how an orthotic controls ankle joint motion in the sagittal plane?
  10. drhunt1

    drhunt1 Well-Known Member

    All the years in practice, all the dozens upon dozens of lectures you've given worldwide, the hundreds of published contributions you've made, peer reviewed and otherwise...and you've concluded that growing pains is an overuse syndrome. You can take comfort in the fact that the malady is 192 years old and no one else has figured it out either.
  11. Dananberg

    Dananberg Active Member

    If you construct the orthotic appropriately, you can create everion and plantarflexion of the 1st metatarsal head and negate any functional hallux limitus which may develop. Since the hallux never moves once it touches the floor, when a functional limitation exists, then the remainder of the foot and body above must
    adjust. Thus, foot orthotics can have pronounced influence in the sagittal plane.

    Now, think about knee function. Its primary motion is flexion-extension, both which are sagittal plane motions. Genu recurvatum is not necessarily a primary laxity issue, but rather a proximal manifestation of an ankle equinus the presence of ligament laxity. When the equinus is reduced by manipulation the effect of the recurvatum is negated. If you have no experience with manipulation, you can go to youtube and check out ankle manipulation. Don’t know how I would have practiced without it. The funny thing about high ROM patients, is that they have the highest propensity for developing Functional hallux limitus. So, with this inability to raise the heel without compensating in either the MLA or ankle or knee (or all) in a lax patient will be evident as extreme foot pronation, genu recurvatum, etc. Since the equinus is most often related to a loss of fibula translation and not gastrox tightness, manipulation becomes a very viable option.

    That all said, I don’t generally respond to smug comments. As long as we keep this truly professional, I would be happy to offer a deeply thought through perspective on these issues. I come with the experience of reviewing thousands and thousands of pressure analysis F-scans, I have learned a great deal about the implications of sagittal restrictions within the foot and their more proximal postural manifestations.
  12. drhunt1

    drhunt1 Well-Known Member

    Howard-I didn't mean to be smug, (at least not with you)...just generally inquisitive. Patients that have a genu recurvatum, (at least in my experience), do not demonstrate an equinus deformity. They are hypermobile. This can be easily determined by ROM of other UE joints. Two "syndromes" that come to mind are EDS and Marfans. There are many different types of EDS, spanning the gamut from mild to severe:


    I don't think I've ever seen a patient with genu recurvatum, and with hypermobility of other joints, that also presented with an equinus deformity...they are, after all...hypermobile. I would agree, however, that many of these patients present with a hallux limitus deformity...most of them secondary to a MPE deformity. Because they are hypermobile, this deformity can be "casted out" at the time a neutral impression is taken. This is one of the very few instances where an orthotic can successfully treat sagittal plane deformities. For those patients I see that present with a non-reducible FF varus, I suggest rocker soled shoes in combination with an orthotic to treat the frontal plane forefoot problem.

    Now...let's revisit the above video where Lee discusses Christina's genu recuvatum as a potential source of "growing pains"...he discusses aligning the leg with the upper body to solve the problem. Great concept, but not accurate, (I can almost guarantee that she has a mild form of EDS). This will be made more clear after the article I wrote is published this April linking GPs in children to RLS in adults. The answer to solving both medical conditions is the same, because they are a continuum of the same problem.
  13. Jeff Root

    Jeff Root Well-Known Member

    In a triplane joint, when you have motion in one body plane, you have motion in the other two body planes. FHL is a clinical sign that has a mechanical cause. It is a limitation of motion in the sagittal plane but can have a triplane influence on the STJ and most likely, at the MTJ as well. FHL can be primary (the cause of compensation at other joints) or secondary (the result of forces/motion or lack of motion at other joints). Metatarsus primus elevatus is one cause of FHL. A long 1st met can also be a cause of FHL. I believe it is important to try to determine any structural/mechanical cause of FHL when there is one. By that, I'm not referring to structural hallux limitus at the 1st MTPJ, I'm referring to other structural conditions that can produce FHL like a long 1st met. In addition, there can be functional causes of FHL that originate somewhere else in the foot, ankle, knee and hip that result in FHL. That's why a triplane approach, like the use of an orthosis may be necessary in treating a sagittal plane condition like FHL.

  14. Dananberg

    Dananberg Active Member

    One of the tenants of manual medicine, is that when something can’t move, something else will move in its place. In this regard, genu recurvatum can be a saggital compensation IN THE PRESENCE of lax ligaments, thus making it quite profound but hidden as a compensatory result vs a primary issue. Functional hallux limitus is very similar. When the 1st MTP joint doesn’t dorsiflex at the time when heel lift begins, the other sites are capable providing at least some of the motion lost in the sagittal plane. (This has been confirmed in other published papers.)
    So, when Functional hallux limitus is present, the knee can hyperextend as the CoM advances but the foot fails to move sagittally. (Above the waist, the torso flexes via the same mechanism.)

    The other issue is the true ROM of the ankle joint. Even with ligamentous laxity, ROM of the fibula can be restricted. It normal becomes restricted at the proximal end, and loses its ability to translate cranially and laterally. Several problems then develop. First, the peroneals become inhibited and lose the ability to stabilize the 1st ray against the support surface, further exacerbating the Functional hallux limitus. Second, the ankle does not fully dorsiflex as the loss of translation prevents the wider anterior talar dome from fitting into the ankle space. Combined, they make stepping over the foot a challenge, with the body essentially bending backwards as the step progresses.

    One of the things I learned in all my years to clinical case management, was that mechanical issues can often co-exist in the presence of other organic disease. So, for instance, why do the fingers and thumbs dislocate as they do in the presence of rheumatoid arthritis? The answer lies in the action of gripping and opposing digits. When the ligamentous structures are destroyed by the rheumatic disease, they are incapable of supporting the opposing structures, and thus deform in a rather predictable fashion. So too with ligament laxity. I have learned to view genu recurvatum in the context of sagittal plane restriction. While the laxity can and does exist, the deformity relates to the abnormal motion against the background of ligaments incapable of supporting and protecting the surrounding joints. Solve the motion dilemma, and the laxity has a far less deleterious effect.

  15. Dananberg

    Dananberg Active Member

    One more item in regards to the link you provided. This patient is standing with obvious hallux rigidus and ankle equinus. Ankles are actually plantarflexed, so in order to stand without falling over, the knees MUST bend backwards.
  16. Jeff Root

    Jeff Root Well-Known Member

    Hi Howie,
    Nice to see you involved in a Podiatry Arena discussion. At several podiatry conferences I have heard some prominent podiatrists talk about fusing the 1st MPTJ in runners and how well they do with it. I know my father wasn't a fan of fusing the 1st MTPJ. What are your thoughts on this?
  17. drhunt1

    drhunt1 Well-Known Member

    Howard-I believe that genu recurvatum is an anatomic anomaly, not a compensatory one...at least in re to this discussion...which was growing pains. I have witnessed several patients that I believe have a mild form of EDS, and there is a pattern of anatomic differences between them and "normal" patients. [Normal patients rarely complain about mechanical problems, so I see these patients secondary to other maladies, such as ingrown toenails, etc.] However, I have seen plenty of patients with an equinus deformity that do not demonstrate recurvatum.

    Your suggestion that genu recurvatum is a compensatory result of hallux limitus doesn't follow what I've witnessed in my office. Further, I have not witnessed a patient with genu recurvatum that demonstrates an equinus deformity. At the time that the patient enters into forefoot loading in preparation for the propulsive phase, their heel is off the ground, so motion at the MT or STJ is something I'll have to pay closer attention to while watching them walk.

    Your paragraph on RA is an interesting one. I have always considered the hands being more deformed than feet in these patients a result of less activity, not, as you stated, due to flexion activity of gripping. Not enough info to extrapolate. Now...back to the topic at hand, (pardon the pun), which was growing pains. I certainly hope Dr. Cohen reads my article this April, as it might help him to determine a treatment protocol that makes better sense. Viewing patients from the side in order to assess LE alignment is not the answer, it's just a singular component of a more complete biomechanical evaluation.
  18. Dananberg

    Dananberg Active Member

    Hi Jeff,
    Always good to hear from you. Your dad and I had some very interesting discussions many years back. These were some of the most stimulating biomechanical talks of which I have ever had the privilege of being engaged.

    As far as fusing the 1st MTP joint, this is a very tricky subject. Some of the worst postural pain patients I ever treated developed after fusion of this joint. But then, I have seen others who have done quite well, provided there was adequate flexion of the joint designed into the fusion technique. The real way to look at this is over long periods of time, ie, decades. How do this patients fare over time? What are the long term issues which develop both in the foot and posturally as well.

    What is missing when fusion is performed is the effect of the VARIABLE tension within the fascia network as the digits dorsi and plantarflex during the course of any single step. Recent work by Helene Langevin, MD at University of Vermont Medical School demonstrates the effects of acupuncture needle twisting on this same connective tissue network. Her work has clearly shown that this connective network extends to within the intracellular binding structures and that this actually has an effect on fibroblastic activity within the body. This article was linked in a prior PA posting on Acupuncture by Leah Claydon. A very interesting read, particularly in light of the fascia connection to the digits and particularly to the hallux.
    Fascia is continual within the body, and there is a growing consensus that this is essential for proper function of the musculoskeletal system. The anchors of this system are the jaw proximally and the foot distally (although other “floating” structures such as the fibula and clavicle serve this same purpose). This is why TMJ, for instance, has been implicated in many chronic postural ailments. There is an ability to vary the tension within the system when movement of this structure is optimized. So too with the foot. Fusion of the 1st MTP joint should really be the last step in a process of trying to resolve intractable hallux limitus pain. I have had many, many successes with conservative management of hallux limitus utilizing orthotics and manipulation as the core method of treatment. Unfortunately, an insufficient number of podiatrists take this course of action, and feel as though fusion is the only way to solve chronic hallux limitus. When one takes the Hippocratic Oath, they swear “above all, to do no harm”. While fusion may be well intended and work well for some, for those with a bad outcome, the disaster is 100%. Considering the intricate anatomy of the 1st MTP joint and its elaborate attachment to the connective tissue system, it would seem that trying to avoid fusion would be the appropriate step in any truly appropriate care model.
  19. Dananberg

    Dananberg Active Member

    If you do not see the connection between hallux limitus, equinus and genu recurvatum….you are simply not looking hard enough. It is painfully obvious in the patient video YOU posted! She is standing in 5-8 degrees of plantflexion, with a large dorso-medial 1st MTP joint deformation consistent with hallux limitus.
    There was a time when it was believed that the sun revolved around the earth, as we saw sunrise and sunset and could not comprehend what was vs what was not moving. Many of the pedal motions occur far too fast to observe with the naked eye. Pronation, ie lowering of the MLA does appear as a primary motion, but when viewed with in-shoe pressure measuring systems in 10ms increments, what is moving vs. what is not becomes far clearer. As I earlier wrote to Jeff Root, motion at the MTP joints is extremely important in understanding the fascia banding which occurs with digital dorsiflexion. Compounding this support feature, this joint further represents the fulcrum about which body weight is lifted efficiently during any step. When MTP motion is lost, the ability to lift body weight is compromised, and it falls at the same time it should be rising. The visible effect of this “falling body weight” is evident as LATE MIDSTANCE PRONATION. This failure creates stress on the secondary support mechanism, the musculo-tendonous system, which attempts to “catch” body weight while it is falling. It has also become my view that it is at this temporal period when the subtalar joint contributes the most to the visible pronation. Since the subtalar joint is screw-like, as the tibia (which sits atop the talus) falls, it MUST internally rotate, and hence the medial talar bulge associated with a hyperpronated foot. It is also the repetitive strain of this fall-catch action which results in the eventual symptoms. Any co-existing myofascial or muscular systemic pathology will serve to further exacerbate these symptoms. When one treats any issue, not all the pathology needs to be managed. Often, care of one of these will reduce sufficient stress to reduce or resolve the pain associated with this overuse.
  20. drhunt1

    drhunt1 Well-Known Member

    Howard-the example I used was an extreme case, probably the "Classic", Type II form of EDS...not all genu recurvatum presents itself as such. In the case that Dr. Cohen used, Christina, hers was not an extreme case, probably a Type III...but the deformity was there. [Jeff Root was correct, and I omitted the long first ray as a subset of deformities that leads to hallux limitus]. But since you want to focus on this pathology as "an end all" to other mechanical problems...let's explore that further. First, the ROM in a limitus deformity is sufficient to allow for "some" dorsiflexion at that joint...certainly enough to allow the heel to come off the supporting surface as the patient enters the propulsive phase of gait. According to Merton Root, late midstance is when you'll witness maximum pronation of the normal foot, right before the heel rises and the foot enters forefoot loading, so I'm not sure what you really meant by that. In other words, the heel's already off the ground before limitation of motion restricts further 1st MPJ dorsiflexion, so the effect on structures more proximal seems like less of a concern.

    Second, in all the years of practice, I have never seen an acquired genu recurvatum as compensation for an equinus or a hallux limitus deformity...either the motion is available at the knee joint, or it is not. Kids that have milder forms of EDS, (Type III), for instance, have hypermobility long before they begin to ambulate as an adult ~ 3 years of age.

    Third, it has been my experience that patients whom present with hallux limitus deformities, whatever the cause, were fast runners in high school, either in track in sprints or on the football field...which makes sense when you think about it. It's when they get older that the problems associated with this foot type begin to cause them pain.

    Again...back to the original video of Dr. Cohen, his assessment and association of growing pains with sagittal plane deformities is not correct, as soon shall be revealed.
  21. Dananberg

    Dananberg Active Member


    The fact that you see some amount of motion at the MTP joint when you examine it off weight bearing, doesn’t mean that it actually moves at the time it is most required while weight bearing. This is what in shoe pressure analysis demonstrates. A 100ms change in the timing of heel lift can be the difference between treatment success and failure, yet be invisible to your eye. I’m afraid your description of the midstance phase is too basic to conceptualize the principles I am trying to convey. The real key is to view weight transfer during single support phase, but this can be a discussion for another day.

    Good luck with your paper. Where will it be published?

  22. drhunt1

    drhunt1 Well-Known Member

    Howard-I actually load the foot while dorsiflexing the hallux, watch the patient walk and compare with WB plain film radiographs. Typically, I see a hallux that looks like a thumb, because the IPJ needs to dorsiflex in compensatory fashion. Further, when I see these patients ambulate, they typically swing their foot "out and around" in egg beater fashion...pretty much a hallmark sign.

    At this point, I don't think luck has much to do with my paper, or acceptance of the information I'm offering...but thanks anyway. April edition of PMM. I had the information/manuscript peer reviewed by Valmassy and a local Vascular/Thoracic Surgeon who became CEO/President of the largest hospital system in central California. That was an extra step I took, because I don't believe PMM is peer reviewed...I just wanted the info out there quickly.

    You'll be amazed just how simple the answer really is and why hasn't someone else figured this out before. But alas...this is just the first of several "projects" that I'm working on. I wouldn't want to be considered a "one hit wonder"...ya know? :D
  23. Dananberg

    Dananberg Active Member


    Peer reviewed actually means that the individual who reads your paper doesn't know who wrote it and the author doesn't know the reviewer! Less than that.... is not considered a true peer reviewed paper. That said, how many subjects were included in your study?

  24. drhunt1

    drhunt1 Well-Known Member

    Howard-you can attempt to throw "volleys" across my bow all you want, I really don't care. If you know/knew Dr. Valmassy, you would know he's a straight shooter, and if he didn't believe the material I presented, he would say so. Are you now attacking Ron's credibility as well? How very generous of you.

    17 patients in the study...twice as many as Angela Evans had in her "landmark" 2003 article. I concluded that portion well over two years ago. Since that time, probably two dozen more. I'm more convinced now then ever of the connections between the two conditions. I predicted serious push-back from a LOT of people in my profession as well as others that will attempt to downplay, denigrate, demean, minimize and refute my findings. Are you one of those?
  25. Howie:

    By the way, good to see you still putting up the good fight here on Podiatry Arena. Looking forward to seeing and lecturing with you and Simon in South Africa in August!:drinks

  26. drhunt1

    drhunt1 Well-Known Member

    South Africa in August? Considering my article will be published in April, you, Howard and Simon will have something important to discuss. BTW...the statute of limitations on libel and defamation of character is now two years in California. Tread lightly, Kevin. Really looking forward to meeting you in person at the Western.
  27. Seriously, Matt, I am looking forward to reading your paper since it sounds very interesting. Ron Valmassy is a good friend of mine so if he liked your paper, that should be a good thing. Unfortunately, I probably won't be able to attend the Western this year due to prior lecture commitments elsewhere. Maybe I'll see you at next year's Western. Looking forward to it.
  28. drhunt1

    drhunt1 Well-Known Member

  29. Dieter Fellner

    Dieter Fellner Well-Known Member

    Hi Matthew,

    I've been following the GP thread for a little while and have read the article. I'm just curious to know, what aspect of your findings you believe to be new. The association of abnormal STJ / foot pronation and GP was taught to our class in 1987. Controlling abnormal pronation with CFO seems to me the standard of care. Perhaps I missed something?

    The article is heavily invested in Rootian-type theory and, I suspect, you can expect some pressure from tissue stress theory, to explain how mechanical therapy works.

  30. drhunt1

    drhunt1 Well-Known Member

    Good morning, Dieter. While many Podiatrists understand that orthotics are effective in treating GPs in children, before this article we didn't know why. Now we do. Now we have evidence, even though many may view it as anecdotal, as to why they work, and perhaps, why they didn't. Further, prior to this article, no one has been able to suggest the anatomic/pathologic connection between GPs and RLS. I can tell you now that I have successfully treated several patients with complaints of RLS that did not have GPs as children, although I have seen them after I had concluded the pilot study. The connection between the two maladies is stronger, at least in my mind, then before. The notion that RLS should be treated with heavy metal therapy and/or neuroleptic medications, forwarded by Sleep Disorder docs and Big Pharma, can now be challenged.

    Actually knowing the source of these problems is therefore new. The anatomic connection between GPs and RLS is also new. The simple diagnostic test of pressing on the sinus tarsi and posterior facet from laterally and medially is new. Providing a forefoot varus extension to the end of the toes, while having been discussed before, is an additional "new" concept which was confirmed when I called the biggest orthotic manufacturer in the US. They confirmed I was the only Podiatrist ordering orthotics with that request. If the TST crowd can provide me with another, equally effective manner to Rx orthotics to treat a structural forefoot varus deformity that doesn't leave the hallux "dangling" in the air, I'm all for it. So then, perhaps, the importance of Hallux purchase, while also not "new", will be discussed more vigorously.

    In my original 10K word manuscript which I pared down to 3K words for PMM, I wrote that this article is not an end point. Further research needs to be conducted, that I know. But I believe this article is the road map which can guide us all in successful treatment.
  31. Jeff Root

    Jeff Root Well-Known Member


    Although the association between growing pains and pronation has been suggested before, I don't believe the mechanism that creates this leg pain has been described like Dr.Sciaroni did:
    Dr. Sciaroni described the nerves that he believes are involved in this condition.

    Many people who pronate do not develop "growing pains" and not everyone who is maximally pronated necessarily has growing pains. What is new is the suggested correlation between chronic subtalar joint end range pronation and possible STJ subluxation and the referred pain that is a result.

    Many people treat growing pains with orthoses and many report good success. But far too often parents and children are told the child will outgrow this condition but as a result, may suffer needlessly in the process. If the etiology of growing pains can be better understood as a result of Dr. Sciaroni's work, then perhaps the justification for orthotic therapy will be become better accepted by the greater medical community. If one goal of medicine is to reduce pain and suffering, then perhaps Dr. Sciaroni's work will contribute to that objective. It seems to me that this article paves the way for further research on his hypothesis and into the methods used in the successful treatment of growing pains.

    Although this article is invested in some Rootian-type theory, this seems like an excellent example of how Root theory (structural conditions and alignment) and Tissue Stress theory (the forces casing the symptoms) can both be used to explain pathology.

  32. toomoon

    toomoon Well-Known Member

    I hate the term "growing pains". What does it mean? It has always seemed to me to be a lazy descriptor and an attempt to normalize one of the most important neural signals we have.. pain. It also seems to encourage a lack of investigation into what it might really be. Kids do get aching legs.. sometimes unilateral.. and they also get osteogenic sarcomata..it would be a huge pity to fob that one off as "growing pains".
  33. drhunt1

    drhunt1 Well-Known Member

    The presentation of LE cancer in these patients, is quite rare, but beyond that, it would appear quite differently in comparison to referred pain from the STJ. Your view is also shared by Angela Evans in her reply to my article, yet she never brought these issues up in her 2003 and 2008 articles. She also mentions infection, (I'll assume by a hematogenous source), although she never really mentions that, either.

    I agree about the term "growing pains"...therefore my title to the article. Still today, we have Pediatricians and Podiatrists telling patients and their family that they "will grow out of the pain", and that a certain level of pain is normal. Hopefully, that 192 year old misinformation ends.
  34. NewsBot

    NewsBot The Admin that posts the news.

    Christchurch girl struck by rare, incurable disease
  35. drhunt1

    drhunt1 Well-Known Member

    "One in a million" being the crux of the article...that, and the sentence that described her as a normal child, running around without any problems before symptoms surfaced. Although the age of presentation is correct, the article doesn't discuss the other relevant findings that could've/should've alerted practitioners to "dig a little deeper". If they had read my article, perhaps the diagnosis would've been made sooner.
  36. Jeff Root

    Jeff Root Well-Known Member

    Why did she (mum) suspect growing pains? This is not a classic presentation for growing pains.

    I'm not sure what the point of posting this article here is other than to encourage parents to first search Google before making assumptions about their potential child's illness.
  37. drhunt1

    drhunt1 Well-Known Member

    The other "nugget" of info in this article, is that the other daughter experienced "growing pains" and the girl experienced pain, not at rest, (which is one of THE important presentations with GP's), but while bending over...ie., not at rest. Transient synovitis/inflammation of the STJ occurs after the patient is NWB.
  38. Sorry I'm late to the party on this one. I was invited to comment on this article on growing pains.

    My thoughts.

    1. Its not research. There is no reseach question, no falsifiable hypothesis, no control group, no methodology, no statistical analysis, no clear outcome measures etc etc. At a real stretch one might describe it as a case series, but its better described as an exposition.

    2. There is a huge disconnect between the clinical outcome "data" (such as it is) and the discussion / conclusion. The one does not support the other. Neither is it incompatible, they are simply unconnected.

    3. There are large unaswered questions which make this very hard to follow up on. For eg, it states
    (emphasis mine) but does not state what criteria were used to define abnormal subtalar joint pronation. Is this based on Roots criteria for normalcy? Redmonds normative data set? Static wb? Dynamic range? Eversion velocity? Kinematics? Kinetics? If one wished to repeat this "study" there is nowhere near enough data to do so.

    4. There is a substantial paucity of citations. To take the pertinant example
    It would be standard in an academic text to cite a reference for this definition. Definitions do vary considerably, and this definition differs from, for example, the definition found in valmassey, which reads "An inverted position of the forefoot relative to the rearfoot at the level of the mid tarsal joint.... due to inadequate frontal plane torsion of the head and neck of the talus during normal development of the foot".
    Where does the author get his definition from? We don't know, its not been stated. That's just one example. Makes it very hard to read as at every step one has to stop and question the terms of reference.

    This, the nub and crux of the whole piece, is bald assertion. It simply does not follow from the cases collected. One could, as well, say that growing pains are caused by compensatory myalgic stabilisation for ligamentous hypermobility. Or inflamation in long bones from bending moments. Or an imbalance in the Chi! This is opinion and nothing more.

    6. The other comment I would make is that this paper leans rather heavily on some rather shaky concepts. The nature of forefoot and rearfoot varus for one. The whole concept of drawing lines and measuring angles from RF to FF, and RF to ground is suspect in the extreme given the repeatability issues which have be demonstrated ad nauseum in the literature. There seems to be a lot of credence given to static measurments in general, the emphasis is very strongly on kinematics, kinetics getting nairy a mention.

    Then there are the elephants in the room which are not mentioned at all. Forefoot supinatus, the far more common explanation for inverted forefoot. The windlass, and how one can discuss forefoot angles and function without mentioning the windlass is a head scratcher. Gave me a pang of nostalgia actually, for the days when forefoot and rearfoot varus and valgus were the key points in how one made an orthotic. Good times. Or perhaps, not so much.

    It's an interesting piece, but at best if forwards a hypothesis. There is no evidence here to support said hypothesis. If that was the intention of the article, it served well, and was published in an appropriate format. It may, indeed, inspire somebody to design a genuine research study to test it. If however it aspired to provide evidence to support this hypothesis, or to classify as evidence OR research, then no, not at all. The first line of the discussion belongs in the abstract as a hypothesis, not at the end as a conclusion.
  39. Griff

    Griff Moderator

    Good to have you back Rob.
  40. Why Thankyou sir.

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