Synergistic approach to achieve better clinical outcomes in APMPPE
Reducing ocular inflammation, improving ocular blood flow and neuroretinal repair in a synergistic manner is key to achieving better clinical outcomes in APMPPE.
Reducing ocular inflammation, improving ocular blood flow and neuroretinal repair in a synergistic manner is key to achieving better clinical outcomes in APMPPE.
Corticosteroids Treat Inflammation — But APMPPE Is Not Just Inflammatory
Corticosteroids suppress inflammation in APMPPE, but inflammation is only part of the disease. APMPPE is largely driven by choriocapillaris hypoperfusion and ischemic injury, which steroids do not correct. As a result, inflammation may resolve while underlying vascular and neuroretinal damage persists, leading to incomplete visual recovery.
Primary Disease Driver: Choriocapillaris Ischemia
Current evidence strongly favors primary choriocapillaris ischemia as the initiating event in APMPPE, with secondary inflammatory choriocapillaritis amplifying and sustaining the damage. APMPPE is primarily initiated by choriocapillaris ischemia, leading to inadequate blood supply to the outer retina and RPE. This vascular non-perfusion precedes retinal inflammation and results in secondary photoreceptor and RPE injury. Because restoring microvascular blood flow is essential for tissue survival and recovery, treatments that address inflammation alone are insufficient to fully halt disease progression or optimize visual outcomes.
Steroids Do Not Prevent Ischemia-Induced Oxidative Stress
In APMPPE, reduced choriocapillaris blood flow leads to ischemia and subsequent oxidative stress within the retina. This process generates reactive oxygen species that damage photoreceptors and retinal pigment epithelial cells. While corticosteroids suppress inflammation, they do not neutralize oxidative stress or protect retinal cells from ischemia-related metabolic injury, allowing tissue damage to continue even after inflammation is controlled.
Neuroretinal Recovery Requires Active Support — Steroids Are Passive
APMPPE causes direct injury to photoreceptors and retinal neurons, and meaningful visual recovery depends on restoring blood flow, metabolic function, and neurotrophic support. Corticosteroids act passively by suppressing inflammation but do not promote neuronal repair, synaptic recovery, or retinal regeneration. Without targeted support for neuroretinal healing, visual improvement may remain incomplete despite resolution of inflammatory signs.
Steroids May Mask Progression Without Fixing the Cause
Corticosteroids can reduce visible inflammation and improve imaging findings in APMPPE, creating the appearance of disease resolution. However, they do not correct the underlying vascular ischemia or metabolic injury driving retinal damage. As a result, structural improvement may occur while functional deficits such as persistent scotomas or reduced contrast sensitivity continue, masking ongoing disease impact rather than addressing its root cause.
Reducing ocular inflammation, improving ocular blood flow, and supporting neuroretinal repair together is essential for better clinical outcomes in APMPPE. Inflammation control alone may calm the disease, but restoring choriocapillaris blood flow helps prevent ongoing ischemic damage, while active neuroretinal support promotes functional recovery of the retina. When these processes are addressed simultaneously, patients are more likely to achieve more complete and sustained visual improvement rather than partial recovery.
Reduced ocular blood flow—specifically hypoperfusion of the choriocapillaris—is considered a central mechanism in Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE). The choriocapillaris supplies oxygen and nutrients to the retinal pigment epithelium (RPE) and outer retina; when this circulation is patchily reduced or transiently occluded, localized ischemia develops. This ischemic insult leads to dysfunction and injury of the RPE and adjacent photoreceptors, producing the characteristic placoid lesions and acute visual disturbances. Modern imaging (ICGA and OCTA) consistently demonstrates areas of choriocapillaris non-perfusion that spatially correlate with active lesions, supporting hypoperfusion as a key driver of tissue damage in APMPPE.
Ocular inflammation plays a secondary pathogenic role in APMPPE, with most evidence supporting an immune-mediated inflammatory process targeting the inner choroid and choriocapillaris. Inflammatory cell activation and cytokine release increase vascular permeability, promote endothelial dysfunction, and can precipitate inflammatory occlusion of the choriocapillaris. This inflammatory cascade disrupts the RPE–photoreceptor complex and amplifies ischemic injury, explaining the acute onset, multifocal distribution, and self-limited inflammatory course typical of the disease. The frequent association of APMPPE with recent viral illness or systemic inflammatory symptoms further supports inflammation as a core initiating factor rather than a secondary phenomenon.
APMPPE results in direct injury to the outer retina, including photoreceptors and retinal neurons, largely due to ischemia and secondary inflammatory damage. Corticosteroids are effective in controlling inflammation, but they function as a passive therapy that does not restore retinal metabolism, support neuronal survival, or promote repair of damaged photoreceptor–RPE interactions. Meaningful visual recovery depends on re-establishing adequate blood supply, reducing oxidative injury, and actively supporting neuroretinal repair processes such as cellular resilience and synaptic function. Without addressing these factors, patients may experience persistent scotomas or reduced visual quality despite apparent resolution of inflammation.
Reducing ocular inflammation and improving ocular blood flow in a synergistic manner is key to achieving better clinical outcomes in APMPPE. Reducing inflammation stabilizes the vascular endothelium and removes the primary trigger for capillary occlusion, while improving perfusion limits secondary ischemic injury, oxidative stress, and photoreceptor loss. Together, this dual approach addresses both the cause (inflammatory choriocapillaritis) and the consequence (ischemic retinal damage) of APMPPE. This integrated strategy explains why patients with faster and more complete recovery of choriocapillaris flow tend to experience better visual outcomes than those in whom inflammation resolves but perfusion remains compromised.
Our signature Netra Restoration Therapy is a unique treatment method available exclusively at Netra Eye Institute, which has shown to halt AMD progression, improve visual acuity, reduce foggy/hazy vision, improve contrast sensitivity and reduce glare.
The Mechanism of Action (MOA) of Netra Restoration Therapy works by enhancing ocular blood flow through the regulation of vascular function, reducing oxidative stress and ocular inflammation, increasing neurotrophin levels and neuroprotection, and reducing ferroptosis.
The potential for visual improvement depends on the severity of retinal damage present at the time of treatment for Wet AMD. Taking these factors into account, our therapeutic approach has been shown to result in:
Stops vision loss progression by reducing the ocular inflammation, regulating ocular blood flow and nourshing the retinal cells.
Improvement in visual field by restoring
dormant and unhealthy retinal cells.
An improvement of at least one line on the distance and near vision eye chart.
Improved contrast vision, making it easier to distinguish shapes, edges, and details.
Improvement in color, brightness perception and clarity making it easier to see in low-light or nighttime conditions, thereby supporting safer mobility and daily activities.
Reduced glare, less light sensitivity, and improved comfort in bright environments, such as sunlight, headlights, or digital screens.
Patients experience considerable reduction
in eye pain and eye strains.
Patients often report feeling “healthier overall,” not just in their eyes.
I recently completed my three weeks of Netra Restoration Therapy and I am already seeing major improvements with the reduction in my eye prescription correction numbers. Netra Eye Institute is not just a well equipped clinic with modern ophthalmic instruments but is also backed up by professional and patient-caring staff. Thank you Dr. Gandapodi for your services and care.
– Sarang - Grateful Netra Patient
Netra Restoration Therapy is grounded in contemporary biomedical research demonstrating that many eye diseases are driven by reduced ocular blood flow, ongoing neurodegeneration, and cellular stress. Scientific studies show that improving vascular regulation enhances oxygen and nutrient delivery to the retina and optic nerve, while supporting neurotrophin activity and neuroprotection helps preserve vulnerable nerve cells. At the same time, controlling oxidative stress, ferroptosis, and chronic inflammation is critical to slowing tissue damage and disease progression. Netra Restoration integrates these evidence-based principles into a comprehensive approach designed to support long-term eye health and visual function.
Want to learn more about Netra Restoration Therapy and holistic eye treatments or need help to schedule an appointment for a consultation?
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