A stroke is a disruption of blood flow to the brain, commonly leading to neurological deficits affecting motor skills, speech, and sensation. Glaucoma is a progressive condition that damages the optic nerve, frequently associated with elevated intraocular pressure (IOP). The relationship between stroke and glaucoma is complex, involving shared vascular risk factors and secondary complications rather than simple cause-and-effect. This article explores the indirect ways a stroke or its underlying causes can lead to optic nerve damage or a form of glaucoma.
The Relationship Between Stroke and Ocular Health
A stroke does not typically trigger primary open-angle glaucoma, the most common form of the disease. The connection is rooted in systemic health issues that predispose a person to both conditions, primarily severe vascular disease. Conditions such as high blood pressure, atherosclerosis, and diabetes compromise blood vessel health throughout the body, affecting both cerebral and ocular circulations. This shared vascular pathology means the medical history leading to a stroke often creates a high-risk environment for developing secondary, severe forms of glaucoma.
The risk of developing an ischemic stroke is higher in patients with Neovascular Glaucoma (NVG). This suggests that the severe vascular compromise necessary to cause NVG is closely linked to the mechanisms that cause blockages in the brain. The underlying circulatory problems, rather than the stroke event itself, are the common denominator linking these two diseases.
Circulatory Changes Leading to Optic Nerve Damage
The most direct link between stroke-related pathology and glaucoma involves severe restriction of blood flow in the carotid arteries. These large vessels supply blood to both the brain and the eye via the ophthalmic artery. Advanced carotid artery obstructive disease (CAOD), a major precursor to ischemic stroke, can lead to Ocular Ischemic Syndrome (OIS).
OIS occurs when the blood supply to the eye is severely reduced, causing chronic oxygen deprivation (ischemia) in the ocular tissues. This prolonged lack of oxygen triggers the retina to release high levels of pro-angiogenic factors, primarily Vascular Endothelial Growth Factor (VEGF). VEGF stimulates the growth of new, abnormal, and fragile blood vessels on the iris and in the drainage angle of the eye, a process called neovascularization.
These new vessels block the eye’s natural drainage system, the trabecular meshwork, leading to a rapid and severe increase in intraocular pressure. This secondary condition is Neovascular Glaucoma, a blinding form of glaucoma resulting directly from the systemic vascular failure that can cause a stroke. In atypical OIS cases, the ciliary body’s perfusion is so low that aqueous humor production decreases, resulting in normal or low eye pressure despite neovascularization.
Central Nervous System Influence on Eye Pressure
Beyond the direct vascular connection, the brain regulates eye pressure through the autonomic nervous system (ANS). The ANS, with centers in the brainstem and hypothalamus, controls involuntary functions like heart rate and blood pressure, and influences aqueous humor production and outflow. Sympathetic and parasympathetic nerve fibers innervate ocular structures, including the ciliary body and the trabecular meshwork, which maintain stable IOP.
A stroke, particularly one affecting the brainstem or deep brain structures like the thalamus or hypothalamus, can disrupt these autonomic pathways. Damage to these central networks can lead to an imbalance between sympathetic and parasympathetic signals reaching the eye. This neurological disruption could cause secondary fluctuations or a sustained elevation in IOP by altering the rate of aqueous humor production or resistance in the outflow pathways.
Damage to the central nervous system following a stroke is associated with a disruption of the blood-ocular barrier, similar to the blood-brain barrier. This illustrates a direct neurological connection between acute cerebral injury and ocular health. While the clinical significance of stroke-induced ANS dysfunction on developing chronic glaucoma remains an area of research, the anatomical and physiological links are established.
Screening and Treating Post-Stroke Ocular Conditions
Given the vascular and neurological risks, comprehensive eye assessment is an important part of post-stroke care. The standard recommendation is for all stroke survivors to receive an assessment of their visual acuity, visual fields, and eye movement. Screening for conditions like Ocular Ischemic Syndrome and Neovascular Glaucoma is particularly important, as they are often silent until vision loss is severe.
Management of these secondary ocular conditions must address both the eye disease and the underlying systemic vascular problem. Treating Neovascular Glaucoma often involves pressure-lowering eye drops and anti-VEGF injections directly into the eye to reverse abnormal vessel growth. Laser treatment, specifically panretinal photocoagulation (PRP), is also used to destroy the ischemic retinal tissue producing the VEGF. Concurrently, the patient’s underlying conditions, such as carotid artery stenosis, hypertension, and diabetes, must be aggressively managed to prevent further ischemic events in the eye and brain.