Evoked potentials in clinical medicine , Evoked potentials in clinical medicine , کتابخانه مرکزی دانشگاه علوم پزشکی ایران

Evoked Potentials in Clinical Medicine

Binocular vision and ocular motility , Binocular vision and ocular motility , کتابخانه دیجیتال جندی شاپور اهواز

Binocular Vision and Ocular Motility

I. PHYSIOLOGY OF THE SENSORIMOTOR COORDINATION OF THE EYES 1.General Introduction 2. Binocular Vision and Space Perception 3. Summary of the Gross Anatomy of the Extraocular Muscles 4. Physiology of the Ocular Movements 5. The Near Vision Complex 6. Histology and Physiology of the Extraocular Muscles 7. Visual Acuity, Geometric Optical Effects of Spectacles, Aniseikonia II. INTRODUCTION TO NEUROMUSCULAR ANOMALIES OF THE EYES 8. Classification of Neuromuscular Anomalies of the Eyes 9. Etiology of Heterophoria and Heterotropia 10. Symptoms in Heterophoria and Heterotropia and Psychological Effects of Strabismus 11. Examination of Patient I - Preliminaries 12. Examination of Patient II - Motor Signs in Heterophoria and Heterotropia 13. Examination of Patient III - Sensory Signs, Symptoms, and Binocular Adaptations in Strabismus 14. Examination of Patient IV - Amblyopia 15. Examination of Patient V - Depth Perception III. CLINICAL CHARACTERISTICS OF NEUROMUSCULAR ANOMALIES OF THE EYES 16. Esodeviations 17. Exodeviations 18. Cyclovertical Deviations 19. A and V Patterns 20. Paralytic Strabismus 21. Special Forms of Strabismus 22. Anomalies of Convergence and Divergence 23. Nystagmus IV. PRINCIPLES OF THERAPY 24. Principles of Nonsurgical Treatment 25. Chemodenervation of Extraocular Muscles Botulinum Toxin 26. Principles of Surgical Treatment

Burian-von Noorden's Binocular vision and ocular motility: Theory and management of strabismus

Diabetic retinopathy (DR) causes significant visual loss on a global scale. Treatments for the vision-threatening complications of diabetic macular edema (DME) and proliferative diabetic retinopathy (PDR) have greatly improved over the past decade. However, additional therapeutic options are needed that take into account pathology associated with vascular, glial, and neuronal components of the diabetic retina. Recent work indicates that diabetes markedly impacts the retinal neurovascular unit and its interdependent vascular, neuronal, glial, and immune cells. This knowledge is leading to identification of new targets and therapeutic strategies for preventing or reversing retinal neuronal dysfunction, vascular leakage, ischemia, and pathologic angiogenesis. These advances, together with approaches embracing the potential of preventative or regenerative medicine, could provide the means to better manage DR, including treatment at earlier stages and more precise tailoring of treatments based on individual patient variations.

/pdf/diabetic-retinopathy-current-understanding-mechanisms-and-2mleh6waux.pdf

Diabetic retinopathy: current understanding, mechanisms, and treatment strategies

Diabetic retinopathy (DR) is a common complication of diabetes and a leading cause of legal blindness in working-age adults. The clinical hallmarks of DR include increased vascular permeability, leading to edema, and endothelial cell proliferation. Much of the research effort has been focused on vascular changes, but it is becoming apparent that other degenerative changes occur beyond the vascular cells of the retina. These include increased apoptosis, glial cell reactivity, microglial activation, and altered glutamate metabolism. When occurring together, these changes may be considered as neurodegenerative and could explain some of the functional deficits in vision that begin soon after the onset of diabetes. This review will present the current evidence that neurodegeneration of the retina is a critical component of DR. There are two basic hypotheses that account for loss of cells in the neural retina. First, the loss of blood-retinal barrier integrity, which initially manifests as an increase in vascular permeability, causes a failure to control the composition of the extracellular fluid in the retina, which in turn leads to edema and neuronal cell loss. Alternatively, diabetes has a direct effect on metabolism within the neural retina, leading to an increase in apoptosis, which in turn causes breakdown of the blood-retinal barrier. It is not clear which hypothesis will be found to be correct, and, in fact, it is likely that vascular permeability and neuronal apoptosis are closely linked components of DR. However, the gradual loss of neurons suggests that progress of the disease is ultimately irreversible, since these cells cannot usually be replaced. In light of this possibility, new treatments for DR should be preventive in nature, being implemented before overt clinical symptoms develop. While vascular permeability is the target that is primarily considered for new treatments of DR, evidence presented here suggests that apoptosis of neurons is also an essential target for pharmacological studies. The vision of people with diabetes will be protected only when we have discovered a means to prevent the gradual but constant loss of neurons within the inner retina.

A new view of diabetic retinopathy: a neurodegenerative disease of the eye

• Contrast sensitivity measurements were obtained from 64 patients with insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus who had normal Snellen acuity and minimal or no visible diabetic retinopathy. Contrast thresholds were determined for stationary gratings at six spatial frequencies, ranging from 0.5 to 22.8 cycles/degree (c/deg), and for 1.0-c/deg gratings phase-alternated at 15 Hz. Data from each group of diabetic patients were compared with data from age-matched normal subjects. We found that (1) patients with IDDM and no retinopathy had normal contrast sensitivity, (2) patients with NIDDM and no retinopathy had abnormal contrast sensitivity at only one spatial frequency (22.8 c/deg), and (3) patients with NIDDM and background retinopathy had abnormal contrast sensitivity at all spatial frequencies tested. We also found a dissociation of Snellen acuity and contrast sensitivity, indicating that contrast sensitivity can be used as an early index of changes in the retina not demonstrated by measurements of visual acuity.

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=OPHTH&articleId=635359&pdfFileName=archopht_103_1_018.pdf

Samuel Sokol

Papers

Contrast Sensitivity in Diabetics with and Without Background Retinopathy

Measurement of infant visual acuity from pattern reversal evoked potentials

Visually evoked potentials: Theory, techniques and clinical applications☆

Age-related changes in the latency of the visual evoked potential: Influences of check size ☆

Developmental changes in the human visual system as reflected by the latency of the pattern reversal VEP