Optic Disc Edema in Raised Intracranial Pressure

The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension

“…It may be speculated that the compression of the optic nerve as such and its microstructural consequences could add to the functional visual deficit induced by the papilledema, which is induced by a pressure-induced decrease in axoplasmic flow, but the answering of this question was beyond the scope of our study. The fact that we did not observe an alteration in the MD value of the ON supports the current pathophysiological concept that the pressure-induced edema is limited to the prelaminar part of the ON head [37, 59], which is located in front of the lamina cribrosa, and the adjacent retina [37], without affecting the postlaminar myelinated section of the ON [60].…”

The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension

“…It may be speculated that the compression of the optic nerve as such and its microstructural consequences could add to the functional visual deficit induced by the papilledema, which is induced by a pressure-induced decrease in axoplasmic flow, but the answering of this question was beyond the scope of our study. The fact that we did not observe an alteration in the MD value of the ON supports the current pathophysiological concept that the pressure-induced edema is limited to the prelaminar part of the ON head [37, 59], which is located in front of the lamina cribrosa, and the adjacent retina [37], without affecting the postlaminar myelinated section of the ON [60].…”

Protective Effects of Minocycline and Acetazolamide on Visual Function in Simulated Microgravity Rats

“…As theorized earlier, perturbations to pressure homeostasis may manifest in three potential scenarios: (1) Directional TLCPD reversal with stable magnitude; (2) Magnitude alteration without directional shift; (3) Baseline pressure modifications (IOP/ICP) without TLCPD alteration[33] [34]. Our study primarily observed Scenario 1 (increased TLCPD magnitude), whereas AZE intervention induced Scenario 2 (direction reversal with elevated magnitude).…”

“…As theorized earlier, perturbations to pressure homeostasis may manifest in three potential scenarios: (1) Directional TLCPD reversal with stable magnitude; (2) Magnitude alteration without directional shift; (3) Baseline pressure modifications (IOP/ICP) without TLCPD alteration [33] [34].…”

“…This mechanism shares commonality across glaucoma, idiopathic intracranial hypertension (IIH), and spaceflight-associated neuro-ocular syndrome (SANS). For instance, elevated ICP in IIH patients impedes neurotrophic signaling across the LC, while optic nerve damage in glaucoma and irreversible visual dysfunction in SANS are closely linked to abnormal translaminar pressure gradients (IOP-ICP differentials) [34] Microgravity-induced cephalad fluid redistribution drives multisystem adaptations, including cardiovascular dysregulation and intracranial hemodynamic abnormalities [35]. Our study revealed that simulated microgravity provoked a mild elevation in intraocular pressure (IOP) at 2 weeks, with further amplification observed at 4 weeks, consistent with prior reports attributing acute IOP spikes to choroidal congestion during short-term microgravity exposure [36].…”

Optical Coherence Tomography Findings in the Optic Disc Before and After Removal of Brain Tumor in a Case of Foster Kennedy Syndrome

“…Papilledema occurs as a result of the axonal expansion of the prelaminar and peripapillary nerve fibers. After acute axonal blood flow stagnation, vascular congestion, leakage, and ischemia occur, accompanied by interstitial edema, which is thought to lead to RNFL thickening [ 10 ]. After tumor removal, a reduction in OD edema was observed.…”

The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension

“…It may be speculated that the compression of the optic nerve as such and its microstructural consequences could add to the functional visual deficit induced by the papilledema, which is induced by a pressure-induced decrease in axoplasmic flow, but the answering of this question was beyond the scope of our study. The fact that we did not observe an alteration in the MD value of the ON supports the current pathophysiological concept that the pressure-induced edema is limited to the prelaminar part of the ON head [37, 59], which is located in front of the lamina cribrosa, and the adjacent retina [37], without affecting the postlaminar myelinated section of the ON [60].…”

Protective Effects of Minocycline and Acetazolamide on Visual Function in Simulated Microgravity Rats

“…As theorized earlier, perturbations to pressure homeostasis may manifest in three potential scenarios: (1) Directional TLCPD reversal with stable magnitude; (2) Magnitude alteration without directional shift; (3) Baseline pressure modifications (IOP/ICP) without TLCPD alteration[33] [34]. Our study primarily observed Scenario 1 (increased TLCPD magnitude), whereas AZE intervention induced Scenario 2 (direction reversal with elevated magnitude).…”

“…As theorized earlier, perturbations to pressure homeostasis may manifest in three potential scenarios: (1) Directional TLCPD reversal with stable magnitude; (2) Magnitude alteration without directional shift; (3) Baseline pressure modifications (IOP/ICP) without TLCPD alteration [33] [34].…”

“…This mechanism shares commonality across glaucoma, idiopathic intracranial hypertension (IIH), and spaceflight-associated neuro-ocular syndrome (SANS). For instance, elevated ICP in IIH patients impedes neurotrophic signaling across the LC, while optic nerve damage in glaucoma and irreversible visual dysfunction in SANS are closely linked to abnormal translaminar pressure gradients (IOP-ICP differentials) [34] Microgravity-induced cephalad fluid redistribution drives multisystem adaptations, including cardiovascular dysregulation and intracranial hemodynamic abnormalities [35]. Our study revealed that simulated microgravity provoked a mild elevation in intraocular pressure (IOP) at 2 weeks, with further amplification observed at 4 weeks, consistent with prior reports attributing acute IOP spikes to choroidal congestion during short-term microgravity exposure [36].…”

Optical Coherence Tomography Findings in the Optic Disc Before and After Removal of Brain Tumor in a Case of Foster Kennedy Syndrome

“…Papilledema occurs as a result of the axonal expansion of the prelaminar and peripapillary nerve fibers. After acute axonal blood flow stagnation, vascular congestion, leakage, and ischemia occur, accompanied by interstitial edema, which is thought to lead to RNFL thickening [ 10 ]. After tumor removal, a reduction in OD edema was observed.…”

The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension

“…It may be speculated that the compression of the optic nerve as such and its microstructural consequences could add to the functional visual deficit induced by the papilledema, which is induced by a pressure-induced decrease in axoplasmic flow, but the answering of this question was beyond the scope of our study. The fact that we did not observe an alteration in the MD value of the ON supports the current pathophysiological concept that the pressure-induced edema is limited to the prelaminar part of the ON head [37, 59], which is located in front of the lamina cribrosa, and the adjacent retina [37], without affecting the postlaminar myelinated section of the ON [60].…”

Protective Effects of Minocycline and Acetazolamide on Visual Function in Simulated Microgravity Rats

“…As theorized earlier, perturbations to pressure homeostasis may manifest in three potential scenarios: (1) Directional TLCPD reversal with stable magnitude; (2) Magnitude alteration without directional shift; (3) Baseline pressure modifications (IOP/ICP) without TLCPD alteration[33] [34]. Our study primarily observed Scenario 1 (increased TLCPD magnitude), whereas AZE intervention induced Scenario 2 (direction reversal with elevated magnitude).…”

“…As theorized earlier, perturbations to pressure homeostasis may manifest in three potential scenarios: (1) Directional TLCPD reversal with stable magnitude; (2) Magnitude alteration without directional shift; (3) Baseline pressure modifications (IOP/ICP) without TLCPD alteration [33] [34].…”

“…This mechanism shares commonality across glaucoma, idiopathic intracranial hypertension (IIH), and spaceflight-associated neuro-ocular syndrome (SANS). For instance, elevated ICP in IIH patients impedes neurotrophic signaling across the LC, while optic nerve damage in glaucoma and irreversible visual dysfunction in SANS are closely linked to abnormal translaminar pressure gradients (IOP-ICP differentials) [34] Microgravity-induced cephalad fluid redistribution drives multisystem adaptations, including cardiovascular dysregulation and intracranial hemodynamic abnormalities [35]. Our study revealed that simulated microgravity provoked a mild elevation in intraocular pressure (IOP) at 2 weeks, with further amplification observed at 4 weeks, consistent with prior reports attributing acute IOP spikes to choroidal congestion during short-term microgravity exposure [36].…”

Optical Coherence Tomography Findings in the Optic Disc Before and After Removal of Brain Tumor in a Case of Foster Kennedy Syndrome

“…Papilledema occurs as a result of the axonal expansion of the prelaminar and peripapillary nerve fibers. After acute axonal blood flow stagnation, vascular congestion, leakage, and ischemia occur, accompanied by interstitial edema, which is thought to lead to RNFL thickening [ 10 ]. After tumor removal, a reduction in OD edema was observed.…”