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Fascicular Specialization Does Not Prove the Existence of Pulleys
Author Response: Fascicular Specialization Does Not Prove the Existence of Pulleys
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Robert S. Jampel, ophthalmologist Wayne State University, Kresge Eye Institute
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rjampel{at}comcast.net Robert S. Jampel
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In previous work Demer and Miller used MRI scans and histological sections to derive the active pulley hypothesis (APH) of ocular motor kinematics.1,2 The aim of this current paper by Lim, Poukens, and Demer3 is to provide additional histological evidence for the APH by showing that there are more collagen fibers in the orbital layers than in the global layers of the extraocular muscles (EOMs) and that the collagen fibers of the orbital layer are inserted into a pulley that surrounds and controls the origin of the global layer. It is difficult to deduce tissue connections and function from chemically fixed histological sections. The EOMs are ensheathed in connective tissue and they insert by tendons of varying lengths into the sclera. The histological sections reveal muscle fibers adjacent to collagen fibers, but there is no evidence that the collagen fibers constitute a mobile pulley or that they are attached to muscle fibers along the length of the muscle. In the sections the muscle fibers appear parallel to the collagen fibers and they do not interdigitate or fuse with them (Figs. 1-8 in Lim, Poukens, and Demer3). Furthermore, the authors did not stain the nerve connections to the motor units. They ignored the physiological and pharmacological research performed on the innervations of the EOM motor units. The nerves to the motor units have at least two types of endings: one is multinucleated and produces tonic contractions and the other mono-nucleated and produces twitch contractions. This work is evidence that the brain controls eye movements without the need for an independent orbital mechanical system.4-6 Also, I reviewed my own7 and Demer's1 published MRI scans. The medial and lateral recti, in the contracted state, showed a straight-line connection between the annulus of Zinn and the globe. There were no mid-orbit fascial connections between the sheaths of the recti and the periosteum of the orbital walls. The muscles showed no inflections. There were no dense fibro-elastic smooth muscle bands (pulley bars), looping around the so-called global layers of the recti muscles. No demarcation lines or membranes were seen splitting the recti into orbital and global layers. The so-called check ligaments were attached to anterior third of the muscle sheaths and horizontal gaze movements did not retract them. Miller2 explains the fact that the pulleys are not seen on MRI because pulleys are not discrete, sharply delineated structures. They are "distributed structures, characterized only by relative condensations of SM [smooth muscle], elastin, and collagen, arrayed over the three-dimensional orbital volume." In my scans there were no relative condensations. Is it reasonable to believe that precise angulations take place around relative condensations? In conclusion there is no histological or MRI evidence that the orbit has an independent mechanical system consisting of mobile pulleys that control the origins of the eye muscles. No system exists in the orbit that the brain does not control. Moreover, there is no physiological or clinical evidence for pulleys.7 Ideas have consequences and the effects of the APH may inhibit progress. Robert S. Jampel References 1. Demer JL. Pivotal role of orbital connective tissues in binocular alignment and strabismus. The Friedenwald Lecture. Invest Ophthalmol Vis Sci. 2004;45:729-738. |
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Joseph L. Demer
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jld{at}ucla.edu Joseph L. Demer
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Paradigms and Evidence This is a reply to the latest in a series of Letters to the Editor1-3 and a polemic4 by Robert S. Jampel against the active pulley hypothesis (APH). Jampel inaccurately characterizes the aim of our most recent paper5 as to show that there are more collagen fibers in the orbital layers than in the global layers of the extraocular muscles (EOMs). In fact, it was one of the several findings of our recent paper that the orbital layers contain more collagen than the global layers. Furthermore, by tracing individual bundles of fibers as well as individual EOM fibers through serial sections, we demonstrated that orbital layer fibers insert on connective tissues, but do not insert on the scleral tendons, while global layer fibers uniformly pass through these connective tissues and presumably act on the scleral insertion of tendons. This finding was consistent in all four rectus muscles, as well as in both monkeys and humans. Jampel went on in his letter to make perplexing assertions, implying, for example, that it is difficult to study anatomy from histological sections. Certainly, quantitative microanatomy in serial sections was tedious work for us, but it is doubtful that there is any better technique available to address the questions at issue. Obviously, all techniques have their limitations, but it seems that Dr. Jampel questions techniques only when they produce results inconsistent with his opinions. Jampel criticized our recent paper for not staining myoneural junctions. While myoneural connections are interesting, their structures and locations would have no direct relevance to the issue of terminations of the ends of EOM fibers. This criticism is irrelevant. In the conclusion of his letter, Jampel repeated a broad range of statements about the absence of EOM connective tissue pulleys. These statements repeat his assertions published elsewhere,1-4 have elsewhere received detailed replies,6,7 and continue to ignore detailed evidence that we have published.8-13 The reader may be perplexed by Dr. Jampel's denial of the voluminous evidence that many other serious scientists find compelling. The noted philosopher of science, Thomas Kuhn,14 has provided a lucid explanation of Dr. Jampel's behavior. Dr. Jampel is an adherent of a traditional paradigm of EOM function. This paradigm is a self-contained approach to thinking about the EOMs and to studying them, but the traditional paradigm is beset by internal and external inconsistencies. Over the last decade or so, my collaborators and I have advanced a fundamentally different paradigm of the EOMs and connective tissues that is consistent with a wide range of external evidence. Thomas Kuhn has explained that the development of a fundamentally different paradigm represents a scientific revolution. So many things change in a scientific revolution that adherents to the old and the new paradigms find it impossible to communicate with one another, and impossible to convince one another by mutually acceptable evidence. Kuhn has explained that this communication arises because paradigms constrain the sort of observations that might be considered "evidence" in the first place. Thomas Kuhn has provided historical examples illustrating times of revolution in the sciences, and times in which competing paradigms have briefly coexisted.14 History shows that competing scientific paradigms cannot coexist indefinitely. Eventually, the newer paradigm prevails because it offers advantages to practitioners of science. Such advantages of the new paradigm include a better and more elegant ability to explain existing observations, internal consistency, and the ability to predict new observations. Ultimately, a new paradigm succeeds because it is more practical and useful than the older paradigm. Kuhn has observed, "There is nothing more practical than a good theory." Ultimately, students of orbital and EOM anatomy, ocular motility and the neurosciences, as well as clinicians interested in the correction of strabismus, will find the APH useful to them. These scientists and practitioners are likely to embrace the APH, or at least some parts of it, until better ideas come along. Dr. Jampel is unlikely to be persuaded to embrace the APH by any observations that are contrary to his way of thinking. Joseph L. Demer References 1. Jampel RS. Pulley and global stability (E-letter). Invest Ophthalmol Vis Sci. Available at http://www.iovs.org/cgi/eletters/47/1/188#316. Published April 19, 2006. |
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