A recent kerfluffle between several clubbies on a to-be-left-unnamed group site showed how once again, there is a conflict between what we clubbies have come to know as the truth about our situation, and what the medical profession continues to misrepresent to the parents of children born with talipes. In their continuing effort to a) not upset the parents, and b) to keep the parents believing that the medical profession has all the right answers, they would have all believe that they can "correct" and "cure" club feet. This is such an insidious construct that even when such parents hear from us, people who have had to endure the weight of that lie all our lives, they react with sometimes angry responses, telling us that we are lying. Even in the face of those who have had to live with post-CF all their lives, such parents cannot abide hearing anything that contradicts the lies they are being fed.
Even with the application of Ponsetti treatment, there remains a failure rate of about 20%. But this, too, is misleading. Failure rate, as measured by both traditional and Ponsetti-focused practitioners, is based on how far the feet remain deviated from positional "norms". This is an important distinction: it affirms that the entire medical establishment focused on talipes remains convinced that positional deviation is the entirety of the talipes condition. The first clue is in the descriptive term itself - talipes equino varus/valgus - each word describes a positional aspect of the foot. Nowhere is there acknowledgment that the condition is other than positional. Yet there is substantial research showing that there are other elements, most notably, the distortion of the muscle fibers of the lower leg, that contribute to, attend, and potentially point more concretely to a more accurate etiology. The continual willful ignoring of this and other issues that are raised by both research, and by the actual life experiences of post-club feet sufferers by the medical establishment speaks volumes, and merely makes the divide between truth and fiction ever larger.
While I do not in general blame parents for wanting something positive to anticipate for their child, I find it beyond bizarre how, once faced with this new information, there remains a desperate desire to remain ignorant of the truth. However, it is their problem to deal with, not mine. I will continue to shake the trees of the medical profession until at least one reasonable professional emerges to start facing the realities we clubbies face, and who is willing to begin grappling with the true nature of club feet.
As for those who feel insulted by the use of the term "clubby": I will continue to use it, as a reclamation of the truth of what I endure. Those who object to this term are free to not use it. It is basically that simple.
The following is an excerpt from a publication in the © 1981 British Editorial Society of Bone and Joint Surgery 0301 -620X181/30S6-0417
A HISTOCHEMICAL STUDY OF MUSCLE IN CLUB FOOT
D. H. GRAY, JUNE M. KATZ
From the Departments of Orthopaedic Surgery, Middlemore and Auckland Hospitals, and the Department of Surgery, University of Auckland, New Zealand
Abstract
A histochemical analysis was made of 103 muscle biopsies taken from 62 patients with idiopathic club feet. Any reduction in the diameter of the muscle fibres associated with wasting of the calf muscle was recorded. Histochemical abnormalities existing in these biopsies were revealed by comparison with normal biopsies obtained from the normal legs of 13 children with unilateral deformities. No significant difference was found between the diameter of the muscle fibres taken from normal and affected legs aged under six months. This indicates that wasting ofthe calfmuscle is due to a reduction in the number of fibres rather than their size. The muscle structure was normal excluding denervation and reinnervation. The soleus muscle in patients aged under six months contained 61 per cent Type 1 fibres in the affected legs, compared to 44.3 per cent in normal legs. Similar values were found in the normal and abnormal tibialis posterior muscles, long flexors of the toe and peroneal muscles. The change in composition of the soleus
muscle and the reduction in the number of fibres may be caused by a defective neural influence on the development of the limb in club foot.
The next is the last paragraph of the Discussion:
The development of a full complement of fibres is under neural control in all types of muscle. Therefore defective neural influences on the development of the limb could account for the wasting of the calf and the maturation peculiar to the soleus. It is unknown whether this latter abnormality is an aetiological factor in the generation of the club foot, or merely concomitant with the primary genesis of the deformity in the bones of the feet. Isaacs et a!. (1 977) have also suggested that idiopathic club foot may have a neurogenic basis. There appears to be increasing evidence that the nervous system is involved in the genesis of club foot, and we suggest that the result of such involvement is defective myogenesis.
It should be noted that this is merely one of 11 such studies I have located so far. There is nearly always a speculation as to the role played in the etiology of talipes, yet there is no parallel response from the same medical community as to how these factors might actually shift thinking, how they might cause some reconsideration of treatment, and most importantly, how they might re-shape how and what doctors tell parents about the true nature of talipes as it may affect their child. The silence, one might be pressed to say, is deafening.
Even with the application of Ponsetti treatment, there remains a failure rate of about 20%. But this, too, is misleading. Failure rate, as measured by both traditional and Ponsetti-focused practitioners, is based on how far the feet remain deviated from positional "norms". This is an important distinction: it affirms that the entire medical establishment focused on talipes remains convinced that positional deviation is the entirety of the talipes condition. The first clue is in the descriptive term itself - talipes equino varus/valgus - each word describes a positional aspect of the foot. Nowhere is there acknowledgment that the condition is other than positional. Yet there is substantial research showing that there are other elements, most notably, the distortion of the muscle fibers of the lower leg, that contribute to, attend, and potentially point more concretely to a more accurate etiology. The continual willful ignoring of this and other issues that are raised by both research, and by the actual life experiences of post-club feet sufferers by the medical establishment speaks volumes, and merely makes the divide between truth and fiction ever larger.
While I do not in general blame parents for wanting something positive to anticipate for their child, I find it beyond bizarre how, once faced with this new information, there remains a desperate desire to remain ignorant of the truth. However, it is their problem to deal with, not mine. I will continue to shake the trees of the medical profession until at least one reasonable professional emerges to start facing the realities we clubbies face, and who is willing to begin grappling with the true nature of club feet.
As for those who feel insulted by the use of the term "clubby": I will continue to use it, as a reclamation of the truth of what I endure. Those who object to this term are free to not use it. It is basically that simple.
The following is an excerpt from a publication in the © 1981 British Editorial Society of Bone and Joint Surgery 0301 -620X181/30S6-0417
A HISTOCHEMICAL STUDY OF MUSCLE IN CLUB FOOT
D. H. GRAY, JUNE M. KATZ
From the Departments of Orthopaedic Surgery, Middlemore and Auckland Hospitals, and the Department of Surgery, University of Auckland, New Zealand
Abstract
A histochemical analysis was made of 103 muscle biopsies taken from 62 patients with idiopathic club feet. Any reduction in the diameter of the muscle fibres associated with wasting of the calf muscle was recorded. Histochemical abnormalities existing in these biopsies were revealed by comparison with normal biopsies obtained from the normal legs of 13 children with unilateral deformities. No significant difference was found between the diameter of the muscle fibres taken from normal and affected legs aged under six months. This indicates that wasting ofthe calfmuscle is due to a reduction in the number of fibres rather than their size. The muscle structure was normal excluding denervation and reinnervation. The soleus muscle in patients aged under six months contained 61 per cent Type 1 fibres in the affected legs, compared to 44.3 per cent in normal legs. Similar values were found in the normal and abnormal tibialis posterior muscles, long flexors of the toe and peroneal muscles. The change in composition of the soleus
muscle and the reduction in the number of fibres may be caused by a defective neural influence on the development of the limb in club foot.
The next is the last paragraph of the Discussion:
The development of a full complement of fibres is under neural control in all types of muscle. Therefore defective neural influences on the development of the limb could account for the wasting of the calf and the maturation peculiar to the soleus. It is unknown whether this latter abnormality is an aetiological factor in the generation of the club foot, or merely concomitant with the primary genesis of the deformity in the bones of the feet. Isaacs et a!. (1 977) have also suggested that idiopathic club foot may have a neurogenic basis. There appears to be increasing evidence that the nervous system is involved in the genesis of club foot, and we suggest that the result of such involvement is defective myogenesis.
It should be noted that this is merely one of 11 such studies I have located so far. There is nearly always a speculation as to the role played in the etiology of talipes, yet there is no parallel response from the same medical community as to how these factors might actually shift thinking, how they might cause some reconsideration of treatment, and most importantly, how they might re-shape how and what doctors tell parents about the true nature of talipes as it may affect their child. The silence, one might be pressed to say, is deafening.
I'm curious as to the ages of the patients in the study and when their initial treatment may have been done? Also, this study is from 1981. Surely there must be more recent data?
ReplyDeleteThere are more recent studies, but sadly, they merely provide the same information, and roughly similar conclusions/discussions. The ages are for most of these studies from still-born cadavers to four years of age. There does not appear to be any study that seeks to learn if these same distortions of the muscle fibers remain the same in older clubbies, so we have no idea if what many of us experience as we get older may be related to this element of CF syndrome, as I prefer to call it now.
ReplyDeleteAdditionally, what might this say about cases of so-called recurrent CF, where there is a second, and sometimes third tendo-achilles lengthening? Since the tendon is attached to the muscle, perhaps it is this muscle fiber distortion that is causing the tendon to tighten. If so, might there be alternatives to further surgery? The problem is, no one knows, because no one has asked the question and done the research.
I will eventually put all the abstracts up here with links to the papers so that anyone who wants to can read them. It just takes me some time to get to things lately, this not being mmy day job right now. Stay tuned...