Glaucoma is the second leading cause of blindness globally. It is a wide spectrum of chronic ocular diseases that have in common a chronic and progressive optic neuropathy, which is characterized by the dysfunction and death of retinal ganglion cells (RGC), a population of CNS neurons with their soma in the inner retina and whose axons constitute the electrically active component of the optic nerve. Glaucomatous neurodegeneration is most commonly identified through detection of typical morphological alterations of the optic nerve head (ONH) and functional alterations of the visual field. Even though the pathophysiology of glaucoma has been studied extensively via animal models, it hasn’t been completely elucidated yet, due to its complexity and multifactoriality. The main risk factor is an elevated intra-ocular pressure (IOP) and the main therapeutic tools at our disposal are aimed at reducing the IOP through medical and surgical approaches; nonetheless, several studies have demonstrated that even with a substantial reduction of the IOP, the disease continues its progression in some patients, suggesting the presence of other factors playing an important neurodegenerative role in glaucoma. RGC axons, somata and synapses are the main target of glaucomatous degeneration but glial cells, among which are astrocytes and microglia, respond in a different way: they exert both supportive and potentially harmful actions, playing a fundamental role in RGC survival or death. Induction of ocular hypertension (OHT) in animal studies has shown that glial cells are involved in the immune response and activation of the complement, giving rise to neuroinflammation and secondary lesions. It has been demonstrated that cytokines and antibodies are increased in the aqueous humor of glaucomatous patients: chronic glial activation is associated to increased production of TNF-alpha, a pro-inflammatory cytokine synthesized by activated glial cells in glaucoma. In the literature, the activation of glial cells has been associated to an increase in the number of hyperreflective retinal spots (HRS) seen at the optical coherence tomography (OCT), as a sign of inflammation. An increase in the HRS count has been observed in several ocular pathologies, such as diabetic retinopathy and retinal vascular occlusions, but the existence of a correlation between increased HRS and glaucoma had yet to be studied. We evaluated and compared the number of HRS on Heidelberg OCT scans (macula and RNFL) of glaucomatous versus healthy patients. The scans were analyzed by 3 blinded experimenters who independently counted the HRS. Our purpose was to investigate the presence of HRS in glaucomatous patients as a sign of glial reactivity in this pathology.
Confronto della numerosità di spot iperriflettenti alla tomografia a coerenza ottica in pazienti glaucomatosi e sani
COMPARISON OF HYPERREFLECTIVE RETINAL SPOT COUNT AT OPTICAL COHERENCE TOMOGRAPHY IN GLAUCOMATOUS AND HEALTHY SUBJECTS
FOLCO, GIANLUCA
2018/2019
Abstract
Glaucoma is the second leading cause of blindness globally. It is a wide spectrum of chronic ocular diseases that have in common a chronic and progressive optic neuropathy, which is characterized by the dysfunction and death of retinal ganglion cells (RGC), a population of CNS neurons with their soma in the inner retina and whose axons constitute the electrically active component of the optic nerve. Glaucomatous neurodegeneration is most commonly identified through detection of typical morphological alterations of the optic nerve head (ONH) and functional alterations of the visual field. Even though the pathophysiology of glaucoma has been studied extensively via animal models, it hasn’t been completely elucidated yet, due to its complexity and multifactoriality. The main risk factor is an elevated intra-ocular pressure (IOP) and the main therapeutic tools at our disposal are aimed at reducing the IOP through medical and surgical approaches; nonetheless, several studies have demonstrated that even with a substantial reduction of the IOP, the disease continues its progression in some patients, suggesting the presence of other factors playing an important neurodegenerative role in glaucoma. RGC axons, somata and synapses are the main target of glaucomatous degeneration but glial cells, among which are astrocytes and microglia, respond in a different way: they exert both supportive and potentially harmful actions, playing a fundamental role in RGC survival or death. Induction of ocular hypertension (OHT) in animal studies has shown that glial cells are involved in the immune response and activation of the complement, giving rise to neuroinflammation and secondary lesions. It has been demonstrated that cytokines and antibodies are increased in the aqueous humor of glaucomatous patients: chronic glial activation is associated to increased production of TNF-alpha, a pro-inflammatory cytokine synthesized by activated glial cells in glaucoma. In the literature, the activation of glial cells has been associated to an increase in the number of hyperreflective retinal spots (HRS) seen at the optical coherence tomography (OCT), as a sign of inflammation. An increase in the HRS count has been observed in several ocular pathologies, such as diabetic retinopathy and retinal vascular occlusions, but the existence of a correlation between increased HRS and glaucoma had yet to be studied. We evaluated and compared the number of HRS on Heidelberg OCT scans (macula and RNFL) of glaucomatous versus healthy patients. The scans were analyzed by 3 blinded experimenters who independently counted the HRS. Our purpose was to investigate the presence of HRS in glaucomatous patients as a sign of glial reactivity in this pathology.È consentito all'utente scaricare e condividere i documenti disponibili a testo pieno in UNITESI UNIPV nel rispetto della licenza Creative Commons del tipo CC BY NC ND.
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https://hdl.handle.net/20.500.14239/21815