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Introduction to Physiological Regulators and Control Systems
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
Clearly, in the steady state, the AH must exit the eye at the same volume flow rate at which it enters. Outflow of AH is through the canal of Schlemm, into the episcleral veins, then into the main venous circulation, etc. The eyeball is slightly elastic, with most of its compliance coming from the thin, clear cornea. Normal intraocular pressure (IOP) is about 16 mmHg. If there is an increase in the outflow resistance, the normal IOP rises, and if the IOP exceeds its normal high range (about 30 mmHg), the condition known as glaucoma exists. In extreme situations, the IOP can exceed 60 to 80 mmHg. Such acute glaucoma sharply reduces normal arterial blood flow to the retina, causing poor oxygenation and impaired nutrition of retinal neurons and glial cells. If prolonged, glaucoma can lead to the death of retinal neurons, including the loss of retinal ganglion cells which comprise the optic nerve. Such neuron loss is irreversible, and it causes loss of visual acuity and even total blindness.
The Biological Bases of Photoreception in the Process of Image Vision
Published in Agnieszka Wolska, Dariusz Sawicki, Małgorzata Tafil-Klawe, Visual and Non-Visual Effects of Light, 2020
Agnieszka Wolska, Dariusz Sawicki, Małgorzata Tafil-Klawe
Retinal ganglion cells represent the last stage of retinal processing and the first stage in providing responses in the form of action potentials along the visual pathways. They share properties with cortical neurons, such as anatomical structure, functions, and neurotransmitters (dopamine, serotonin, glutamate, and GABA) [Schwitzer et al. 2017a; Bernardin et al. 2019]. Retinal ganglion cell function has been studied in various psychiatric disorders (using electroretinogram recordings): major depressive disorder [Bubl et al. 2010], autism [Tebartz-van Elst et al. 2015], attention deficit hyperactivity disorder [Bubl et al. 2015], cannabis use disorder [Schwitzer et al. 2017b; Schwitzer et al. 2018], and in schizophrenia [Demmin 2018]. Recently, Bernardin et al. [2019] demonstrated a slowing of retinal ganglion cells signaling in schizophrenia patients with visual hallucinations, which could affect the quality of visual information reaching the visual cortex. The data collected suggest that changes of the physiological function of the ganglion cells might be involved in the pathogenesis of psychiatric disorders. Wostyn [2020] in a study from this year suggests that retinal nerve fiber layer (RNFL) thinning may occur in patients with Chronic Fatigue Syndrome (CFS) and may serve as “an ocular biomarker of underlying glymphatic system dysfunction” in CFS and in neurodegenerative diseases that result from protein toxicity [Wostyn 2020].
Neurophotonic Vision Restoration
Published in Francesco S. Pavone, Shy Shoham, Handbook of Neurophotonics, 2020
Adi Schejter Bar-Noam, Shy Shoham
Finally, an additional attractive approach is to target the retinal ganglion cell layer (Bi et al., 2006; Zhang et al., 2009; Greenberg et al., 2011) (Figure 20.2c). These cells are also known to have a high survival rate in late-stage outer retinal degeneration diseases (30% in patients with severe RP (Santos et al., 1997) and 70% in GA-stage AMD patients (Kim et al., 2002)), and since they directly project to the thalamus, they provide an important alternative at advanced stages of retinal diseases when severe retinal remodeling hinders the ability to restore vision via stimulation of cells in the inner nuclear layer. The challenge of targeting this layer, however, is that it requires pre-processing of the projected image, as these cells naturally receive input following retinal processing. These cells are typically divided into ON, OFF, or ON–OFF cells according to the type of response to projected light onto their center-surround receptive field (Hubel and Wiesel, 1962, 1959, 1968). Moreover, there are over 20 different ganglion cell subtypes, each encoding distinct features of the visual scene (Huberman and Niell, 2011). Therefore, this raises the question whether it is necessary to individually target different cell types, or even subtypes, according to their natural encoding characteristics, or whether it would suffice to simply mimic natural responses in a majority of the RGCs.
The therapeutic effect of nano-zinc on the optic nerve of offspring rats and their mothers treated with lipopolysaccharides
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Eman Mohammed Emara, Hassan Ih El-Sayyad, Amr M Mowafy, Heba a El-Ghaweet
The optic nerve (cranial nerve II) is a central nervous system (CNS) tract that passes through the optic canal to leave the orbit. It is made up of the retinal ganglion cells (RGCs) axons. It allows vision by transmitting neural impulses from the retina to the brain. It is divided into four sections: the intraocular nerve head, the intraorbital, the intracanalicular and the intracranial [6]. The types of glial cells in the optic nerve are oligodendrocytes, astrocytes and microglia. Oligodendrocytes are responsible for producing the myelin sheaths that protect the CNS axons and contact nodes of Ranvier as well as they are the locations where action potentials are propagated and axonal integrity. Astrocytes are responsible for numerous physiological and pathological activities such as potassium homeostasis and metabolism as well as reactive astrogliosis in response to CNS trauma. Microglia are immune cells in CNS and have a significant impact on inflammation and infections [7].
Influence of the breathing pattern during resistance training on intraocular pressure
Published in European Journal of Sport Science, 2020
Jesús Vera, Alejandro Perez-Castilla, Beatríz Redondo, Juan Carlos De La Cruz, Raimundo Jiménez, Amador García-Ramos
Glaucoma is characterized by a progressive optic neuropathy that causes the death of retinal ganglion cells and, subsequently, visual loss (Weinreb, Aung, & Medeiros, 2014). Nowadays, glaucoma affects more than 70 million people worldwide and it is estimated to increase to approximately 110 million by 2040 (Tham et al., 2014). Reduction of intraocular pressure (IOP) is the only proven method to treat glaucoma, and pressure-lowering medications are the mainstay treatment for this disease (Heijl et al., 2002). However, IOP values should be reduced using as little medication as possible to minimize side effects (Yee, 2007). In this regard, daily life activities such as food intake (Giaconi et al., 2012; Kang et al., 2016), sleeping position (Prata, De Moraes, Kanadani, Ritch, & Paranhos, 2010), caffeine intake (Li, Wang, Guo, Wang, & Sun, 2011; Vera, Redondo, Molina, Bermúdez, & Jiménez, 2019), smoking (Chan et al., 2016) or the practice of physical exercise (Zhu et al., 2018) have also demonstrated to affect IOP values.
Glaucoma Detection Using Optical Coherence Tomography Images: A Systematic Review of Clinical and Automated Studies
Published in IETE Journal of Research, 2022
Hina Raja, Muhammad Usman Akram, Taimur Hassan, Aneeqa Ramzan, Amtual Aziz, Hira Raja
Glaucoma is a group of ocular diseases with several causes that ultimately result in progressive and degenerative optic neuropathy leading to visual field defects [2]. Glaucoma is an eye condition, caused usually by an increase in intraocular pressure leading to optical nerve damages [3]. The ciliary body produces aqueous humor which passes through the pupil and goes into the trabecular mesh. The rate of aqueous humor production and drainage through the trabecular mesh should be the same. In normal eyes, the pressure should be ≤20 mmHg and they show the symptoms of glaucoma if it ranges from 20 to 24 mmHg. However, once intraocular pressure exceeds 24 mmHg, it is diagnosed as glaucoma. If the pressure in the anterior chamber of the eye increases, thus raising the pressure in the posterior chamber that further damages the optic nerve head fibers [9]. Glaucoma is a slow progressive neuropathy; the early stages of the disease do not often show any symptoms. The axon of ganglion cells dies due to glaucoma and results in irreversible vision loss. A normal optic nerve consists of 1.2–1.5 million nerve fibers, approximately. Loss of the axon layer results in the thinning of the nerve fiber layer, thus increasing the cup size this phenomenon is known as cupping. However, the most threatening issue is that a significant nerve fiber layer damage occurs before the visual field defect, which leads to permanent blindness. It was observed that 60% of the patients have significant RNFL loss, approximately six years prior to any detectable defects in the visual field [10,11]. In the early stages of glaucoma, peripheral vision loss occurs, which is difficult to diagnose even by the patient. Figure 1 shows the visual field of normal and different stages of glaucoma patients. An analysis of the RNFL loss is of significant importance for the diagnosis, especially in the early stages of glaucoma. Some individuals are more prone to develop glaucoma than others. These include people who are severely myopic or nearsighted; people who crossed the age of forty; individuals who have diabetes, narrow angles; people diagnosed with low systemic blood pressure, hypertension, long term steroid or cortisone users; people who have high intra ocular pressure and with enlarged optic nerves.