• Demer JL (2008). Through a Scanner Darkly.
• Klier EM & Angelaki DM (2008). Misrepresentations and Confusion in the Oculomotor Plant.
• Miller JM (2008). False Differential Predictions in Lee, Lai, Brodale & Jampolsky (2007).
• Lee K-M & Jampolsky A (2008). Reply to the Letters on "Sideslip of the Medial Rectus Muscle during Vertical Eye Rotation".

Lee & Jampolsky begin their letter of reply by warmly thanking Klier & Angelaki for their "many thoughtful comments, expressed with expected civility", although Klier & Angelaki actually make very sharp accusations. They express "dismay" over Lee & Jampolsky's "erroneous summary and critique of [K&A's] recent work", their "misquoting of [K&A's] papers", their "misrepresentation of [K&A's] experiments", their "mistaken claims" belied by "even a simple scan" of published work, and their "blatant misquotes and condemnations of correct experiments". Klier & Angelaki quite properly conclude by urging that recent "progress should not be undone" by reports such as Lee & Jampolsky's.

Lee & Jampolsky are much less generous toward Demer and me, berating us for "accusative impugning of motives ... unbefitting space in a reputable journal". Actually, as you can see, Demer takes an entirely scholarly approach in his discussion of their "four errors". Presumably, then, it is Demer's final section to which Lee & Jampolsky take umbrage, in which he characterizes the pulley controversy as a paradigm shift in the Kuhnian sense, and Lee & Jampolsky as adherents to the old paradigm. Kuhn's theory is a standard and completely respectable way to understand such a disconcerting scientific controversy as this.

Finally, my own letter is highly critical of the evidence and arguments in Lee & Jampolsky's paper, but devoid of the ad-hominem attacks they nonetheless accuse me of making. I challenge Lee & Jampolsky to substantiate their allegation. My letter speaks only to their scientific work, and shows that it collapses due to its intrinsic lack of merit. How did such muddled, retrograde work enter the primary scientific literature?

Considering the many fundamental scientific problems raised in the 3 critical letters, Lee & Jampolsky might have given some attention in their letter of reply to the following issues:

• Incoherent Argument. Ghasia & Angelaki (2005) and Klier, Meng & Angelaki (2006) proved that ocular plant mechanics can maintain Listing torsion across gaze shifts without brainstem involvement. Now that Lee & Jampolsky accept, rather than completely reject, the work of Angelaki's lab, they must explain how orbital tissues accomplish this feat. The explanation they offer us is that the "whole ensemble of muscles ... resists yet allows the evoked eye movement to follow the half-angle rule" as a result of the "passive mechanical reaction of other muscles that are actively maintaining the eye position". Is this a clear alternative to pulley theory?
• Flawed MRI Data Collection. Lee & Jampolsky offer no defense of their unusual measurements of horizontal muscle paths in sagittal view, in which muscles were viewed against poorly contrasting globe and optic nerve as they drifted in and out of image planes with eye rotation and head movement, and and no explanation of their image segmentation methods. Instead, they simply assert that their post-processing was "more important to spatial resolution". The old GIGO adage would suggest instead that competent data collection is paramount.
• Fabricated Models & Abandoned Theories. Lee, Lai, Brodale & Jampolsky (2007) make differential predictions based on a "pulley model" and a "non-pulley model", claiming to disprove the former and support the later. Demer and I show very clearly that the pulley model they tested was a "straw man" of their own creation, unlike anything elsewhere proposed, and that their non-pulley model had already been abandoned as implausible by DA Robinson and others a quarter of a century ago. Their letter of reply makes no attempt to defend the models upon which their conclusions rest.
• Wrong Experiment. Their study was essentially the one I reported in 1989, with changes in methodology. I explained in my letter why such a study could not then, and cannot now, in principle, distinguish plausible pulley from non-pulley models. Lee & Jampolsky offer no counterarguments.
• Conceptual Confusion. The most bizarre aspect of Lee, et al (2007) is that they explain their own results by explicitly proposing that orbit-relative muscle paths are determined by "distributed resistance from the surrounding tissue," which is exactly the pulley theory I proposed in 1989, and which they claim to have disproved! Lee & Jampolsky's letter of reply does not explain how their research can refute the notion of pulleys in name, while supporting it in substance, or why they would seek to do so.

Miller JM (2006). Understanding & Misunderstanding EOM Pulleys – Grand Rounds at the Department of Ophthalmology & Visual Sciences, University of Iowa (Presentation PDF, 7.2MB.

As evidence has mounted for the critical role of extraocular muscle (EOM) pulleys in normal ocular motility and disease, opposition to the notion has grown more strident. We review the stages through which pulley theory has developed, distinguishing passive, coordinated, weak differential, and strong differential pulley theories and focusing on points of controversy. There is overwhelming evidence that much of the eye's kinematics, once thought to require brainstem coordination of EOM innervations, is determined by orbital biomechanics. The main criticisms of pulley theory only apply to the strong differential theory, abandoned in 2002. Critiques of the notion of dual EOM insertions are shown to be mistaken. The role of smooth muscle and the issue of rotational noncommutativity are clarified. We discuss how pulley sleeves can be stabilized as required by the theory, noting that more work needs to be done in specifying the tissues involved.

Miller JM, Rossi EA, Wiesmair M, Alexander DE & Gallo O (2006). Stability of gold bead tissue markers. Journal of Vision, vol 6, num 5, art 6, pgs 616-624, http://journalofvision.org/6/5/6/, doi:10.1167/6.5.6.

A new soft tissue imaging method that uses tiny (~0.1 mm dia) gold beads as markers to visualize tissue movements with high spatial (~100 m) and moderate temporal (~100 ms) resolution.

Neural Control of a Complex Oculomotor Plant – Invited Lecture by JM Miller at the Vision Sciences Research Center at the Univ of Alabama at Birmingham, 10 Sep 2004 (Presentation PDF, 2.7MB).

EOM Co-Contraction: Theories & Data - Journal Club at S-K 13 Jul 2004 & Talk at UAB Vision Science Research Center 10 Sep 2004 by JM Miller (Presentation PDF, 1.5MB). InfoIcon illustrates dubious claim of horizontal rectus co-contraction in convergence.

Bupivacaine Injection Treatment of Strabismus (PI: Alan B Scott)

Existing treatments for strabismus rely on compensatory impairment of EOMs; we are harnessing the hypertrophic consequences of bupivacaine myotoxicity to directly strengthen them. Development of bupivacaine for controlled muscle strengthening would provide a unique and powerful tool for strabismus management, and would likely have value for treatment of muscle disorders beyond ophthalmology (Paper PDF, 0.3MB).

EOM Forces & Neural Control of a Complex Oculomotor Plant

Motor control issues raised by conflicts between classical motoneuron studies and physiologic EOM force measurements • Forces in convergence (Paper • Sample Data)

Extraocular Biomechanics

Biomechanics of the eye, surrounding tissues and innervations • Computer model for researchers and clinicians

Extraocular Tissue Architecture

3-D architecture of the extraocular space, distinguishing striated muscle, smooth muscle, collagen, elastin, and other tissues. Techniques include MRI, histochemistry and 3D reconstruction from distorted slices using hierarchical warping and intrinsic fiducials