Visual Anatomy Free Download For Pc
Tyler Janicke
To grow is to teach. In that spirit this article aims to teach best practice for visualizations and at the same time to highlight some of the harvest we could reap in our lab. Following figures recently published in one of our manuscripts, we demonstrate how creativity in figure making goes hand in hand with storytelling, a deepened understanding of the scientific work and an increase in lateral thinking inside the research avenue. We hope it will help to promote scientific visualizations as a useful, even if sometimes harsh, mirror to give new angles to the laboratory work.
Visual stimuli from our surroundings are processed by an intricate system of interconnecting neurons, which begins with the optic nerve in the eye up to the visual processing center in our forebrain called the visual cortex. All the information travels in the form of nerve impulses that are triggered by photosensitive chemical reactions occurring in the retina. Several separate and parallel pathways code its processing at multiple sites in the nervous system.
The ganglion cell layer and nerve fiber layer serve as the foundation of the optic nerve; the former contains the cell bodies, and the latter contains the axons as they stream across the retina. It consists of two types of fibers, namely temporal and nasal fibers, which control the nasal and temporal parts of the visual field, respectively. These fibers join together at the optic disc and are redirected posteriorly out of the eye to form the orbital part of the optic nerve. The nerve is surrounded by the dura, which is in continuation of that of the brain, allowing free movement of CSF between the eye and the intracranial vault.
It then enters the optic canal, a bone-encased tunnel intended to protect the nerve. It exits into the middle cranial fossa to form the intracranial part of the optic nerve. This continues till the two optic nerves join together to form the optic chiasm directly behind and above the pituitary stalk. Here, more than half of the nasal fibers from the left eye decussate to join the temporal fibers of the right eye and form the right optic tract and vice versa. This anomaly helps eye healthcare professionals in the assessment of the site of the lesion along the visual pathway, which produces well-described visual field defects, also known as hemianopias, posterior, or at the chiasm.
The majority of the fibers pass posteriorly to become the genico-calcarine tracts, which have both parietal and temporal loops in the form of the dorsal optic radiation and Meyer's loop and terminate into the cuneus gyrus and lingual gyrus of the primary visual cortex, respectively (Broadmann area number 17).
In the blind population, various determinants could influence post-chiasmal visual anatomy. These include differences in the method of braille reading, involvement of the retinal ganglionic cells, and, most importantly, light sensitivity and visual fields.[6]
The ipsilateral monocular visual loss can be permanent or transient. In the latter case, we speak of "amaurosis fugax" or "transient monocular blindness." Amaurosis fugax is generally due to interruption of blood flow (ischemia) at the level of the optical pathways, for example, caused by retinal embolism or by severe homolateral carotid atheroma stenosis (usually near the common carotid artery bifurcation) or other causes of ischemia in the visual cortex or optic nerve. Possible causes are:
The term hemianopia or hemianopsia refers to a visual impairment characterized by the inability to perceive half of the visual field. The disorder can affect one eye or both; we can speak of lateral or vertical hemianopsia and superior or inferior hemianopsia (altitudinal or horizontal hemianopsia). The disorder can affect one eye or both. There is lateral or vertical hemianopsia and superior or inferior hemianopsia (altitudinal or horizontal hemianopsia). Other definitions include heteronymous bitemporal (loss of the temporal visual field of each eye due to a median lesion of the optic chiasma), binasal heteronymous hemianopsia (the left half of the visual field of the right eye and the right half of the visual field of the left eye is negatively affected due to bilateral lesions affecting both edges of the optic chiasm, which is rare; hemianopia homonymous (loss of the right/left visual field due to an injury to the left/right optic tract); and quadrantanopia (the loss of a single quadrant of the visual field).
The scotoma can be relative or absolute; in the first case, the alteration is related to a decrease in the sensitivity of the retina (one is no longer able to perceive some or all colors except for white), while in the second case, this sensitivity, in some areas, is of the all absent (the image is no longer perceived or in any case, perceived minimally). The disorder can affect one or both eyes. The term derives from the Greek ("skotos," darkness, dark). The scotoma can also be negative or positive; in the first case, it is a non-vision area within the visual field (the subject perceives a dark spot on the fixed objects). In the second case, there is the perception of an intermittent bright spot of variable color. A scotoma is generally referred to as a pathological alteration of vision, but it should be specified that there is also a physiological scotoma, the so-called blind spot or blind area of Mariotte; it is a point of the eye where vision is absent, the so-called optical papilla, an area where photoreceptors are absent. Examination of the visual field (campimetry), the scotoma is graphically represented as a black area located centrally or peripherally). Scotoma is one of the symptoms of various diseases affecting the functionality of the eye, and the ocular structures involved may be different; the main causes include:
Vigabatrin: Vigabatrin is an anti-epileptic drug used to treat refractory, complex partial seizures in adults who have failed. Vigabatrin has been shown to cause permanent peripheral visual field loss. Although the mechanism for how this happens is not fully understood, it most likely involves the toxicity of both retinal photoreceptors and ganglion cells.[9][10]
Diabetic retinopathy (DR) is the most common cause of moderate and severe vision loss in working-age adults1. Diabetic macular edema (DME) is a major cause of vision loss in DR patients and is characterized by an accumulation of extracellular fluid in the macula due to increased vascular permeability2. With intravitreal anti-vascular endothelial growth factor (VEGF) and intravitreal dexamethasone implant treatment, the visual/anatomical prognosis of DME has improved3,4,5,6,7,8,9,10,11,12,13,14,15,16. However, the visual outcomes of DME patients in real-world clinical practice were relatively poorer than those in clinical trials17,18. Loss to follow-up (LTFU) during treatment might be one of the contributing factors that could lead to the poorer visual outcomes of DME patients in real-world practice, compared to those in clinical trials.
In the treatment of diabetic retinopathy, poor treatment adherence could lead to LTFU during treatment26. Recently, the prognosis of LTFU in proliferative diabetic retinopathy (PDR) patients following pan-retinal photocoagulation or intravitreal anti-VEGF injections has been reported27,28. In that study, the best-corrected visual acuity (BCVA) of PDR patients became significantly worse after the return visit from LTFU, regardless of the treatment method27.
Regarding treatment adherence in DME patients, about 28.8% of DME patients showed LTFU during anti-VEGF treatment in a previous report29. Among these LTFU patients, some returned and received re-treatment for DME. However, there is limited understanding of the visual/anatomical outcomes of re-treatment in LTFU DME patients. Therefore, we aimed to investigate the clinical outcome of DME patients who were lost to follow-up for more than 1 year during the anti-VEGF injection. We also tried to find characteristics of the LTFU patients during treatment.
A retrospective review was conducted on treatment-naïve DME patients who had received bevacizumab injection at the Chungbuk National University Hospital, Cheongju, South Korea, between January 1, 2013, and December 31, 2017. The primary objective of this study was to analyze the visual/anatomical outcome of LTFU DME patients. The secondary objectives were to (1) know the rate of LTFU during anti-VEGF treatment and (2) determine the characteristics of those LTFU during treatment. All study participants provided informed consent for study participation and the publication of their data. This study was approved by the Institutional Review Board of the Chungbuk National University Hospital and followed the tenets of the Declaration of Helsinki.
Bevacizumab was used as initial treatment in the treatment-naïve DME patients. All patients were treated with 3-monthly consecutive intravitreal bevacizumab injections (IVBI). Subsequently, bevacizumab was injected every 4 weeks until treatment responsiveness was achieved. Treatment response was defined as an increase in visual acuity of one or more Snellen lines (5 letter score) or a BCVA of 20/20, or a decrease in the CST by 10% or more, after three consecutive IVBIs32. If DME eyes achieved treatment response, IVBI was deferred to the next 4 weeks. After two consecutive treatment deferrals, the treatment interval was gradually extended. Then, we extended the treatment deferral interval up to 12 weeks. Subsequently, if there was no further worsening, we observed the DME patients at 12-week intervals.
In our study, we found that 33% of DME patients were LTFU for more than 1 year during anti-VEGF treatment. When the return group received re-treatment with anti-VEGF, they achieved a significant CST improvement. However, even after re-treatment, the percentage of ellipsoid zone defect was significantly increased, and visual acuity did not recover to the previous level before LTFU.
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