Towards understanding the etiology of high myopic strabismus using mechanical analysis and finite element modeling

It has been widely accepted that the pathology of high myopic esotropia, a special form of strabismus, is still not fully understood. In this study, the mechanical analysis and finite element analysis (FEA) of the oculomotor system was based on clinical MRI data and applied to examine the physiological hypotheses of extraocular muscle obliquity and deformation respectively. Our mechanical analysis indicated that the muscular obliquity is not the dominated cause of high myopic strabismus. Next, by simulating the effect of different forces applied to the cross section of each extraocular rectus muscles, the corresponding eyeball rotations were quantified on normal eyes, and high myopic eyes with and without strabismus. The model suggests that the limitation of rotation in high myopic strabismic eyes is mainly caused by the extraocular muscle deformation instead of, but related with ,its obliquity, providing a better understanding of the etiology of high myopic strabismus. To the best of our knowledge, this is the first mechanical and FEA model developed from clinical data to investigate the etiology of high myopic strabismus, providing important tools for future studies

Optic Nerve Deformation by Eye Movements

Ocular rotation can cause mechanical deformation of the optic nerve head and surrounding tissues. During extreme angles of gaze, the optic nerve can become stretched and impose strain on other ocular tissues. Over a lifetime, the ill effects of repetitive mechanical injury from large adduction can compound, resulting in progressive optic neuropathy in some glaucoma patients.We investigated the etiology of this form of glaucoma through a series of papers focusing on anatomical analysis of the human optic nerve from donated tissue and clinical studies utilizing optical coherence tomography (OCT) and confocal scanning laser ophthalmoscopy (cSLO). The optic nerve is surrounded and protected by a bi-layered dural sheath that bears the bulk of exerted mechanical force. Elastin fibers embedded within the sheath and peripapillary tissues around the nerve head form a three-dimensional meshwork that reinforces the tissue against mechanical strain. While the tissue at the globe optic nerve junction is heavily fortified with organized layers of collagen and elastin fibers, irregularities in the elastin fiber arrangement resulting in large dense elastin deposits were observed to correlate with older age. These elastin deposits could be a pathologic byproduct of optic nerve injury from mechanical strain, or serve as a protective mechanism to further reinforce the ocular tissues.In OCT studies, adduction of angles beyond 26� caused marked deformation of the peripapillary tissues around the optic nerve head, and choroidal volume change. cSLO imaging showed similar deformations of the retina surface during large angle adduction. Ocular tissue of younger subjects appears more compliant, while those of glaucoma patients were stiffer and thus experienced less deformation.We explored possible therapies for optic nerve traction during eye movement. Using collagen crosslinking to fortify ocular tissue, we observed that exposure to riboflavin and UV light can stiffen scleral tissue. In addition, we investigated whether prostaglandin agonists could be used to reduce ocular fat and found that topical administration of these agonists had insignificant effects on the retrobulbar fat

The dependence of binocular contrast sensitivity on binocular single vision

This study involved the determination of the effects of binocular viewing on contrast sensitivities in 11 normal subjects and in different categories of amblyopes. These were simple anisometropic amblyopes (n=9), micro-esotropic amblyopes with anomalous BSV (n=6), esotropic amblyopes with anomalous BSV (n=3) esotropic without BSV 9n=5), exotropic amblyopes without BSV (n=2) and a group of non-amblyopic strabismics (non-amblyopic esotropes without BSV (n=4); non-amblyopic exotropes without BSV (n=2).An ophthalmic examination was carried out on all individuals. The examination procedures undertaken comprised determination of the visual acuity, subjective refraction, the results of which were confirmed by retinoscopy, and assessment of uniocular fixation patterns. The state of BSV, the direction and magnitude of the angle of deviation, the amplitude of accommodation and pupillary diameter were also determined. The subjects were accordingly placed into the appropriate groups on the basis of the basis of the results of the ophthalmic examination.Measurement of uniocular and binocular contrast sensitivities in response to stationary vertical sinusoidal grating patterns were undertaken. The stimulus display consisted of a Tektronix 5103 cathode ray tube (CRT) with a screen subtense of 2 degrees. Mean contrast threshold values were measured for monocular and binocular viewing over the range of spatial frequencies studied which varied between 8c/deg to 40c/deg depending on the group being examined.The conclusions reached were, first, in individuals with BSV (normal or anomalous), binocular enhancement of contrast sensitivities occurred. However, strabismic amblyopes without BSV and non-amblyopic strabismics without BSV did not exhibit enhanced binocular contrast sensitivities; on the contrary, binocular contrast sensitivities were reduced compared to those obtained through the better eye. Furthermore, when bifoveal stimulation was effected, a further reduction in binocular contrast sensitivity occurred.This study has thus shown that binocular contrast sensitivities are augmented compared with monocular contrast sensitivities when BSV is present, but are decreased when BSV is absent. Furthermore, correction of the angle of squint in strabismics, whether BSV is present or not, further reduces the binocular contrast sensitivities

Updates on Myopia

This book is open access under a CC BY 4.0 license. This open access book discusses basic clinical concepts of myopia, prevention of progression and surgical treatments for myopia and pathological myopia. It also summarises the latest evidence and best practices for managing myopia, high myopia and its complications. Written by leading experts, the book addresses clinical diagnosis and interpretation of imaging modalities, and various complications of myopia such as glaucoma, choroidal neovascularization, retinal degeneration and cataracts. It is a valuable comprehensive resource for general and sub-specialist ophthalmologists as well as residents and ophthalmologists in training.

Guidelines for conducting birth defects surveillance

"In January of 1999, the National Birth Defects Prevention Network (NBDPN) established a Surveillance Guidelines and Standards Committee (SGSC) in order to develop and promote the use of standards and guidelines for birth defects surveillance programs in the United States. This set of guidelines is designed to serve as an important first step in the documentation of this process and as the vehicle for dissemination of the committee's findings. The Guidelines for Conducting Birth Defects Surveillance (henceforth referred to as The Surveillance Guidelines) were developed with three major long-term objectives in mind: To improve the quality of state birth defects surveillance data, including accuracy, comparability, completeness, and timeliness; To enhance the utility of state birth defects surveillance data for research on the distribution and etiology of birth defects; To encourage and promote the use of state birth defects surveillance data for the purposes of linking affected children with services and evaluation of those services. The technical guidelines that make up this document provide a way of improving the quality of birth defects surveillance data, which in turn enhances their use in support of the latter two objectives. Fundamental to quality is ensuring that procedures for all aspects of data definition, collection, management, and analysis are established and followed. Because state-based surveillance systems operate with different objectives and data needs, it is clear that, with respect to procedures and standards, 'one size does not fit all.' It is also clear, however, that common guidelines can provide a basis for the development of system-specific operating procedures and supporting manuals." - p. iIntroduction -- -- Chapter 1. The Whys and Hows of Birth Defects Surveillance - Using Data -- -- Chapter 2. Legislation -- Appendix 2.1. Sample State Legislation -- Appendix 2.2. Table of Birth Defects Legislation -- Appendix 2.3. Definitions Used to Determine Covered Entity Status Under the Privacy Rule -- Appendix 2.4. Office of Civil Rights (OCR) HIPAA Privacy Regulation Text -- -- Chapter 3.Case Definition -- Appendix 3.1. Birth Defects Included in the Case Definition of the National Birth Defects Prevention Network -- Appendix 3.2. NBDPN Abstractor's Instructions -- Appendix 3.3. Examples of Conditions Considered to Be Minor Anomalies -- Appendix 3.4. Conditions Related to Prematurity in Infants Born at Less Than 36 Weeks Gestation -- -- Chapter 4. Data Variables -- Appendix 4.1. Descriptions of Minimum (Core) Data Variables -- Appendix 4.2. Descriptions of Recommended Data Variables -- -- Chapter 5. Classification and Coding -- Appendix 5.1. Texas Disease Index -- Appendix 5.2. 6-Digit CDC Codes (updated 8/2007) -- -- Chapter 6. Case Ascertainment Methods -- Appendix 6.1. Data Source Described in Detail - Vital Records -- Appendix 6.2. Data Source Described in Detail - Hospital Data Sets -- Appendix 6.3. Data Source Described in Detail - Hospital and Patient Services Logs -- Appendix 6.4. Data Source Described in Detail - Genetic Services -- -- Chapter 7. Data Quality Management -- Appendix 7.1. Data Sources Descriptive Assessment Tool -- -- Chapter 8. Statistical Methods -- -- Chapter 9. Data Management and Security -- -- Chapter 10. Data Collaboration and Dissemination through the NBDPN -- -- Chapter 11. Data Presentation -- Appendix 11.1. Data Suppression -- Appendix 11.2. Use of Geographic Information Systems (GIS) to Map Data -- Appendix 11.3. Data Users Matrix -- Appendix 11.4. What Type of Chart or Graph Should I Use?edited by Lowell E. Sever."June 2004."Support for development, production, and distribution of these guidelines was provided by the Birth Defects State Research Partnerships Team, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention.Title from title caption (viewed on Jan. 6, 2012).Mode of access: Internet from the CDC web site as an Acrobat .pdf file ((7.6 MB, 627 p.).System requirements: Adobe Acrobat Reader.Includes bibliographical references.Text in PDF format.National Birth Defects Prevention Network (NBDPN). Guidelines for Conducting Birth Defects Surveillance. Sever, LE, ed. Atlanta, GA: National Birth Defects Prevention Network, Inc., June 2004

Glaucoma

This book addresses the basic and clinical science of glaucomas, a group of diseases that affect the optic nerve and visual fields and is usually accompanied by increased intraocular pressure. The book incorporates the latest development as well as future perspectives in glaucoma, since it has expedited publication. It is aimed for specialists in glaucoma, researchers, general ophthalmologists and trainees to increase knowledge and encourage further progress in understanding and managing these complicated diseases

Treatise on Hearing: The Temporal Auditory Imaging Theory Inspired by Optics and Communication

A new theory of mammalian hearing is presented, which accounts for the auditory image in the midbrain (inferior colliculus) of objects in the acoustical environment of the listener. It is shown that the ear is a temporal imaging system that comprises three transformations of the envelope functions: cochlear group-delay dispersion, cochlear time lensing, and neural group-delay dispersion. These elements are analogous to the optical transformations in vision of diffraction between the object and the eye, spatial lensing by the lens, and second diffraction between the lens and the retina. Unlike the eye, it is established that the human auditory system is naturally defocused, so that coherent stimuli do not react to the defocus, whereas completely incoherent stimuli are impacted by it and may be blurred by design. It is argued that the auditory system can use this differential focusing to enhance or degrade the images of real-world acoustical objects that are partially coherent. The theory is founded on coherence and temporal imaging theories that were adopted from optics. In addition to the imaging transformations, the corresponding inverse-domain modulation transfer functions are derived and interpreted with consideration to the nonuniform neural sampling operation of the auditory nerve. These ideas are used to rigorously initiate the concepts of sharpness and blur in auditory imaging, auditory aberrations, and auditory depth of field. In parallel, ideas from communication theory are used to show that the organ of Corti functions as a multichannel phase-locked loop (PLL) that constitutes the point of entry for auditory phase locking and hence conserves the signal coherence. It provides an anchor for a dual coherent and noncoherent auditory detection in the auditory brain that culminates in auditory accommodation. Implications on hearing impairments are discussed as well.Comment: 603 pages, 131 figures, 13 tables, 1570 reference

Health Sciences handbook

2006 handbook for the faculty of Health Science