This lecture has sought to provide a broadly unifying paradigm for conceptualizing the role of the orbital connective tissues in ocular motility. Some of the material presented, such as the structure of the connective tissues and EOMs, represents a set of readily verifiable observations that can be incorporated into any favorite way of thinking about eye movements. The functional anatomic descriptions of EOM paths and their changes with gaze area are also verifiable observations whose kinematic consequences seem unavoidable as long as classic mechanics are accepted. Beyond these issues lie matters of interpretation and speculation. This is particularly true of teleological arguments, which by nature can only be subjective. This risky business has been undertaken to encourage a novel paradigm for studying ocular motility. Novel paradigms are not accepted because they are more “correct” or because older paradigms are in “error.”
93 Among the reasons for acceptance of novel paradigms is a kind of “intellectual neatness” that leads to the feeling that loose ends have been tied up better than with older paradigms. The broad theoretical presentation has been aimed at tying up many loose ends. More concrete, if no less compelling, reasons to adopt a novel paradigm include the ability to explain previously mysterious phenomena, the ability to predict correctly entirely new observations, and the accurate ability to practical outcomes from measurements.
93 Examples of these sorts have been included in this presentation.
The task of understanding ocular motility is far from complete, however. Even within the general paradigm of ocular motility stated herein, there remain numerous unanswered questions and related topics that are not addressed. Vastly more must be learned about the organization of the brain stem motor nuclei involved in eye movement. For example, what are the roles of oculomotor subnuclei, and how, for example, might they be involved in proprioception?
94 How are the precise properties and locations of the EOMs and pulleys specified by genes, regulated during development, and repaired during a lifetime of accumulated wear and tear? What are the relative contributions of mechanical, muscular, and neural factors to the development of strabismus? In the process of answering such important questions through specifically designed experiments it may well emerge that some of the “loose ends” tied up in this broad scheme have been tied up incorrectly. The important thing is that progress will nonetheless have occurred.
Douglas D. Tweed, PhD, and Lance M. Optican, PhD, provided valuable theoretical discussions of these concepts; Joel M. Miller and Lance M. Optican provided helpful comments on the manuscript; and the following have provided invaluable assistance and collaboration in this work: Tin Chan, MD; Robert A. Clark, MD; Mark Cohen, PhD; Benjamin T. Crane, MD, PhD; Nicolasa De Salles, BS; Estafonous Detorakis, MD; Elizabeth Engle, MD; Paul Foeller; Ben Glasgow, MD; Robert A. Goldberg, MD; Nathan Kim, BS; Jan Koniarek, PhD; Reika Kono, MD, PhD; Helene Lam, MD; Ashish Mehta, MD; Paul Micevych, PhD; Joel M. Miller, PhD; James Lynch, PhD; Christopher Murphy, DVM, PhD; Sei Yeul Oh, MD; Carolina Ortube, MD; Carl Park, MD; Amir Pirouzian, MD; John D. Porter, PhD; Vadims Poukens, MD; Arthur L. Rosenbaum, MD; Mark Silverberg, MD; Bradley R. Straatsma, MD; Neepa Thacker, MD; Jun-Ru Tian, MD, PhD; Lawrence Tychsen, MD; Gerald Underdahl, MD; Federico Velez, MD; Harry Vinters, MD; and Weldon Wright, MD.