Yes, the Unfinished, I. Allegro moderato in B minor and II. Andante con moto in E major, and then, "That's all, folks."
Eye research will always remain unfinished, albeit in a much different sense. Schubert is long gone (1797-1828); luckily, there will always be dedicated people who try very hard to understand the eye and figure out the cure for eye diseases. So whatever is unfinished is actually an opportunity and a challenge for the newcomers.
In the US, the ongoing areas of research are defined and sponsored by the National Eye Institute/NIH, including retina, cornea, lens and cataracts, glaucoma, strabismus (plus myopia), and low vision. Each of the areas is also supported by non-profit private organizations and the instrumentation/pharmaceutical industries.
A very good example of the translation of NEI-supported research into treatment success is the anti-VGEF therapy. Because of the demonstrated efficacy in the treatment of neovascular AMD, clinical trials have now extended into other neovascular eye diseases, e.g., RAVE (rubeosis anti-VGEF trial for ischemic central retinal vein occlusion) and VISION (VGEF inhibition study in ocular neovascularization). Others are being examined as well that include diabetic macular edema, cystoid macular edema, and proliferative diabetic retinopathy.
On the other hand, we have noticed a gap between neurophysiology and impaired vision. A very versatile yet under-utilized imaging tool has been available since 1993, i.e., fMRI.
Functional magnetic resonance imaging (fMRI) permits visualization and quantitation of blood flow, volume, and oxygenation in the brain during sensory and motor stimulation. There are two variations of this technique, one detects the susceptibility effect from intravenously administered contrast agents, e.g., GdDTPA, and the other oxygen-induced susceptibility and changes in tissue diffusion but without the use of contrast agents. The non-contrast method is preferred because of its total non-invasiveness. Its applicability to brain function research, especially the photically stimulated primary visual cortex has been verified with a number of studies. Indeed, fMRI has been designed to test various visual stimuli, the studies also pave the groundwork for testing higher functions such as color vision, eye tracking and movement, retinal rivalry, suppression, and stereopsis.
An example is correlating cerebral activation with eye blinking.
Notice the upper leftmost image is activation of the orbitofrontal lobe during normal blinking of once per 4 sec. The rest of the cerebral cortex remains quiet until when the blinking is inhibited, then even the visual cortex is activated.
Much more on ocular malfunctions and the brain's plasticity can be learned by using fMRI. For example, correlating fMRI results and retinal lesions can be done with point-to-point projection between fMRI and the patient's visual field defects from, e.g., open-angle glaucoma, hemifield defects, optic neuritis/atrophy, diabetic retinopathy, and AMD. Indeed, it is not even known, for example, how the primary visual cortex responds to central scotoma, let alone the understanding of brain plasticity in association with preferred retinal loci.
What about lazy eye, treatment (L-DOPA?), plasticity...
Indeed, this field is still wide open.
Eye research will always remain unfinished, albeit in a much different sense. Schubert is long gone (1797-1828); luckily, there will always be dedicated people who try very hard to understand the eye and figure out the cure for eye diseases. So whatever is unfinished is actually an opportunity and a challenge for the newcomers.
In the US, the ongoing areas of research are defined and sponsored by the National Eye Institute/NIH, including retina, cornea, lens and cataracts, glaucoma, strabismus (plus myopia), and low vision. Each of the areas is also supported by non-profit private organizations and the instrumentation/pharmaceutical industries.
A very good example of the translation of NEI-supported research into treatment success is the anti-VGEF therapy. Because of the demonstrated efficacy in the treatment of neovascular AMD, clinical trials have now extended into other neovascular eye diseases, e.g., RAVE (rubeosis anti-VGEF trial for ischemic central retinal vein occlusion) and VISION (VGEF inhibition study in ocular neovascularization). Others are being examined as well that include diabetic macular edema, cystoid macular edema, and proliferative diabetic retinopathy.
On the other hand, we have noticed a gap between neurophysiology and impaired vision. A very versatile yet under-utilized imaging tool has been available since 1993, i.e., fMRI.
Functional magnetic resonance imaging (fMRI) permits visualization and quantitation of blood flow, volume, and oxygenation in the brain during sensory and motor stimulation. There are two variations of this technique, one detects the susceptibility effect from intravenously administered contrast agents, e.g., GdDTPA, and the other oxygen-induced susceptibility and changes in tissue diffusion but without the use of contrast agents. The non-contrast method is preferred because of its total non-invasiveness. Its applicability to brain function research, especially the photically stimulated primary visual cortex has been verified with a number of studies. Indeed, fMRI has been designed to test various visual stimuli, the studies also pave the groundwork for testing higher functions such as color vision, eye tracking and movement, retinal rivalry, suppression, and stereopsis.
An example is correlating cerebral activation with eye blinking.
Notice the upper leftmost image is activation of the orbitofrontal lobe during normal blinking of once per 4 sec. The rest of the cerebral cortex remains quiet until when the blinking is inhibited, then even the visual cortex is activated.
Much more on ocular malfunctions and the brain's plasticity can be learned by using fMRI. For example, correlating fMRI results and retinal lesions can be done with point-to-point projection between fMRI and the patient's visual field defects from, e.g., open-angle glaucoma, hemifield defects, optic neuritis/atrophy, diabetic retinopathy, and AMD. Indeed, it is not even known, for example, how the primary visual cortex responds to central scotoma, let alone the understanding of brain plasticity in association with preferred retinal loci.
What about lazy eye, treatment (L-DOPA?), plasticity...
Indeed, this field is still wide open.
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