Related Experiment Video
Updated: Jun 22, 2026
08:55
Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
Published on: April 24, 2020
[Autonomic nervous system and primary open angle glaucoma--pathogenetic and clinical correlations]
Joanna Wierzbowska1, Robert Wierzbowski, Andrzej Stankiewicz
1Z Kliniki Okulistycznej Wojskowego Instytutu Medycznego w Warszawie. joanna.wierzbowska@gmail.com
Klinika Oczna
|June 13, 2009
Summary
Primary open angle glaucoma is associated with autonomic nervous system dysfunction. This review highlights the autonomic nervous system's role in regulating heart rate and blood pressure, and its connection to the human circadian clock.
Area of Science:
- Ophthalmology
- Cardiology
- Neuroscience
Context:
- Primary open-angle glaucoma (POAG) is a leading cause of irreversible blindness.
- Autonomic nervous system (ANS) dysfunction is increasingly recognized as a contributing factor in various systemic diseases.
- Understanding the interplay between POAG, ANS, and circadian rhythms is crucial for comprehensive patient care.
Purpose:
- To review the established links between primary open-angle glaucoma and autonomic nervous system dysfunction.
- To elucidate the role of the ANS in modulating systemic hemodynamic parameters, including heart rate and blood pressure.
- To emphasize the influence of the human circadian clock on ANS activity and its relevance to glaucoma.
Summary:
- The review presents evidence connecting primary open-angle glaucoma with autonomic nervous system dysfunction.
- It details the ANS's critical role in determining systemic hemodynamic parameters like heart rate and blood pressure.
- The impact of the human circadian clock on ANS function is highlighted, alongside a description of autonomic function tests and therapeutic implications.
Impact:
- This review provides a comprehensive overview of the autonomic nervous system's involvement in primary open-angle glaucoma.
- It underscores the importance of considering ANS function and circadian rhythms in glaucoma diagnosis and management.
- Potential therapeutic strategies targeting the ANS may offer novel treatment avenues for glaucoma patients.
Related Concept Videos
01:25Glaucoma: Overview
Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
01:27Open Angle Glaucoma: Treatment
In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Drugs such as carbonic anhydrase inhibitors, α2- and...
01:28Angle Closure Glaucoma: Treatment
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
01:29Increased Intracranial Pressure ll: Pathophysiology
Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
01:22Myasthenia Gravis ll: Pathophysiology
The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
01:25Secondary Spinal Cord Injury llI: Pathophysiology
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...