Glaucoma Pathophysiology and Vascular Factor


Glaucoma is among the major causes of blindness globally. Glaucoma is a persistent neurodegenerative condition that affects the optic nerve (Casson et al. 2012). The condition results from a progressive deterioration of cell fibers of the retinal ganglion and visual area abnormalities. Excess intraocular pressure has been identified as the most critical risk factor for the start, gradual development and chronic condition of glaucoma. Since its discovery as a medical condition, any interventions for glaucoma have focused on lessening the pressure on the intraocular to inhibit the progression of the condition. In some instances, however, the condition of the glaucomatous optic nerve may worsen even with effective control of the pressure. Moreover, in normal tension glaucoma, there are noticeable changes in optic disc and visual field abnormality when the intraocular pressure is classified as normal (McKinnon et al. 2008). Recent studies in glaucoma have introduced new techniques to the pathophysiology of glaucoma. In this case, such studies have focused on understanding pathologic changes associated with cells, tissues and genetics among others.

The purpose of this research paper is to review the most likely role of vascular factors in pathophysiology of glaucoma.


Ophthalmologists and optometrists normally conduct diagnosis for glaucoma as a component of eye examination. In this case, the points of concerns are the intraocular pressure, angle assessment, evaluation of the optic nerve for possible degeneration or damages, rim appearance and alterations in the vascular. It is also imperative to conduct a visual field test. The retinal nerve fiber materials also require assessment.

Diagnosis for glaucoma is an extremely sensitive process and some techniques require extreme caution to avoid misdiagnosis, particularly when measuring the central corneal thickness (CCT). A larger cornea could lead to slightly higher pressure than normal while narrow cornea may result in low pressure than the actual pressure.

The role of the vascular factors

Disorders associated with glaucoma can be classified into two major areas, including open and closure angles. Open-angle is chronic but a painless type of glaucoma. The condition is progressive, develops slowly over time, and usually has no clear symptoms until it has reached advanced stages. Open-angle glaucoma can be managed by glaucoma medication or surgeries to reduce pressure on the optic fibers. On the other hand, closed-angle glaucoma takes place suddenly and is associated with ocular pain, redness, queasiness and vomiting and other related symptoms that may originate from the abrupt reactions in intraocular pressure. Closed-angle glaucoma requires ocular emergency intervention.

Both medications and surgeries can restore the normalcy intraocular pressure.

Glaucoma is a serious condition that can permanently destroy one’s vision in the affect eyes through reducing the normal marginal vision area and may significantly lead to blindness if no interventions are offered (McKinnon et al. 2008).

There are several small divisions of the condition, which can be classified under the optic neuropathy. In this case, the fundamental consideration is given to damages noted in retinal ganglion cells. High intraocular pressure (more than 21 mmHg) is the major vital and single adaptable risk factor for glaucoma. In some instances, individuals however may have high intraocular pressure for several years but fail to develop damages to the eye. This situation is referred to as ocular hypertension. Low or normal tension glaucoma, on the other hand, only occur in people with optic nerve injuries and could result in the loss of visual field. The condition may also present low or normal intraocular pressure.

Glaucoma causes a gradual loss of sight for a considerably long period. In addition, the related symptoms may only be identified when the condition is in advanced stages. Once the sight is lost, it is normally difficult to recover it but any further treatment is meant to control further loss.

Relative to cataract, this condition is the next major cause of sight loss in the world (Bonomi et al. 2000). Glaucoma affects people of all ages, but the condition is generally common among individuals aged over 80 years old. Earlier detection of the condition however can lead to medical or surgical interventions that can slow down or stop the progress.

A study by Costa et al. (2009) noted that there were notable relations between glaucoma and ocular perfusion pressure. Moreover, it was found that the condition could develop even in low intraocular pressure. The study was imperative for understanding the importance of automatically controlling and maintaining enough perfusion of the optic nerve (Costa et al. 2009). It further showed that it was imperative to measure ocular perfusion pressure and related changes in individuals with glaucoma to understand its dimensions (Costa et al. 2009). In the condition of normal tension glaucoma, the condition’s progression results in defective function of control systems of ocular circulation. It is imperative to note that a decline in the blood flow was also identified in some folded capillaries found in individuals with glaucoma to show that such a decline in the flow of blood do not necessarily results from elevated intraocular pressure or because of glaucoma. Instead, vascular dysregulation is the major cause of the progression of the condition especially in the case of normal tension glaucoma. New patterns have emerged from Doppler imaging of the ophthalmic artery in individuals with low tension glaucoma relative to normal people. The condition exhibits enhanced resistance to blood flow and advancement in systolic velocity. Research has indicated that certain prolonged changes in the retinal circulation could result in glaucoma-like conditions on the optic disc, which do not relate to intraocular pressure (Costa et al. 2009).

Many degenerative tissues have been found in the choroid, retrobulnar and retinal systems of individuals with progressive, chronic open angle conditions (Bonomi et al. 2000). Changes in technologies such as Retina Flowmeter have led to new discoveries, particularly in getting actual situation of the retinal circulation. In addition, studies have shown that there is relationship between damages in the glaucomatous and changes in the noted in the patterns of retinal flow (Logan et al. 2004). As a result, such changes in the retinal flow could depict early signs of the progressing glaucoma (Logan et al. 2004). The study concurs with the idea that old age, reduced blood circulation and inflammation (atherosclerosis and endothelial lesions) could lead degeneration of the nerve fibers of the retina and other core joining tissues. The flow of the blood however differs in various ocular tissues. The retina’s vascular control system is the same as that of the brain, but it only lacks automatic nervous systems for unconscious responses.

In the reviewed vascular risk factors, some studies have pointed to pathogenic factor of endothelial malfunction (McKinnon et al. 2008). A major endothelial failure to work properly could impair blood vessels and cause high blood flow repression. Molecules released from endothelial cells, vasodilator and vasoconstrictor are responsible for blood flow in the retina.

Generally, endothelial cell controls the flow of blood of the retina through its compounds referred to as endothelium derived vasoactive compounds (EDVCs) (Grieshaber and Flammer 2007). Individuals with the main vascular dysregulation usually have elevated levels of endothelin – 1. Endothelin – 1 has vasoconstriction capabilities and can negatively affect vascular permeability. In this case, endothelin -1 can enhance permeability of the vascular and cause retinal bleeding. This condition has been noted individuals with normal tension glaucoma cases. A leakage in the vascular system could result in increased movement of injurious elements to pass the deficient blood brain obstruction in the retina. Endothelin – 1 is also associated with the control of the blood brain barrier through the control of the prostaglandin E2 and in turn lowers the endothelial firm junction system. It affects both vasoconstriction and changes processes of adenosine triphosphatase dependent sodium and potassium pump.

Nitric Oxide (NO) is a critical element in the transportation system, both inside and outside molecular and is generally associated with vasodilatation, inflammation and neurotransmission among others. NO has been linked with several activities in degenerative conditions such as glaucoma, cardiovascular diseases and Alzheimer disease among others. Nitric oxide plays several roles in starting glaucoma. It can break up in tissues and move within cell because of its microscopic feature. In addition, some researchers have suggested that nitric oxide is responsible for providing balance when the vessel tone elevates (Grieshaber and Flammer, 2007). At the same time, nitric oxide is also a critical element in neuronal physiology, acts carrier and can alter the movement of sodium in the cell. By depending on these processes, nitric oxide facilitates the release of glutamate and other messengers in the cellular, which in turn result in long modification of activities of the ATP dependent elements like sodium and potassium. This situation is linked to several degenerative conditions, including glaucoma (Grieshaber and Flammer 2007).

Various types of NO-Synthetase can provide clue to explain several roles associated with nitric oxide in inducing glaucoma. Endothelial nitric oxide synthase generates nitric oxide, which has diverse metabolic functions from nitric oxide generated by nitric oxide synthase found in the trabeculuym. In this case, nitric oxide from nitric oxide synthase is not responsible for generation of free radicals, which are possibly hazardous for ocular components. The distribution of nitric oxide synthase can assist in understanding how nitric oxide increase chances of glaucoma and may assist in developing effective interventions. When nitric oxide increases, vasodilatation takes place and it enhances contractility within the trabecular elements. This finally causes a decline in intraocular pressure and a subsequent contra-apoptotic effect for the protection of neuron.

Overall, the review of studies on glaucoma strives to identify the role of vascular factors in the pathophysiology of the condition. There are notable vascular risk factors for glaucoma. They include low systolic blood pressure and decrease systolic and poor intraocular perfusion pressure, which can increase the progression of open-angle glaucoma (Leske et al. 2008). Distinctively, low intraocular perfusion pressure increases the risk of glaucoma for a given group of individuals (Leske et al. 2008). For early signs of glaucoma, the primary indicators of the condition’s progression of open-angle glaucoma may include low intraocular systolic perfusion pressure, conditions or history of cardiovascular diseases and reduced blood flow or pressure. Further, a low blood pressure of less than 90 mmHg associated with hypersensitive interventions could result in high optic nerve restriction and reduce the rim field of the optic disk in individuals without glaucoma.


The primary aims of any management of glaucoma are to prevent damages to glaucomatous and nerves, and protect the visual field and an individual’s health without serious side effects. Glaucoma interventions require effective diagnostic approaches and follow-up evaluation, careful selection of intervention options for every patient. While intraocular pressure is one of the major risk factors for the condition, reducing it through different medications or surgical methods is the current best options available for patients.

Currently, researchers are interested in blood flow and neurodegenerative aspects of the glaucomatous optic neuropath. As a result, ongoing studies focus on different neuroprotective therapeutic strategies. There are medications to reduce intraocular pressure and control glaucoma. These medications are usually eye drops. However, these medications differ and are in various categories based on the subtypes of glaucoma.

Medications for glaucoma may have different side effects on patients. It is however important for patients to adhere to ophthalmologists’ recommendations or seek advice when side effects take place. Generally, failure to comply with medications and follow-up recommendations could be responsible for subsequent loss of sight in patients with glaucoma. In fact, patients who fail to fill the medications consecutively have contributed to large numbers of failed treatment. Patient education and communication are therefore necessary to ensure that interventions are successful and continuous because treatments for glaucoma are long-term initiatives.

Glaucoma can also be managed through conventional surgeries and laser treatment. Surgery is the most preferred option for individuals with inveterate glaucoma. It is imperative to note that glaucoma has no permanent cure and therefore any interventions are temporary measures to curb its spread.

Trabeculectomy is the most common and it involves punching of the sclera to relieve intraocular pressure. Other forms of surgeries such as canaloplasty, Argon laser trabeculoplasty and glaucoma drainage implant are available. In addition, there is a laser-assisted non-penetrating treatment for glaucoma. Consequently, recent studies have focused on improving nonpenetrating deep sclerectomy (NPDS) surgery. This surgery is changed and requires another deep scleral flap is created carefully without penetrating the eye. This intervention has been noted as safe and lead to few cases of side effects. The intervention however is manual and needs higher levels of expertise to conduct safely. It is also necessary to inhibit any wound adhesion after the process and ensure effective filtering outcomes. The procedure may also need different types of biocompatible devices like ologen Collagen Matrix (Aptel et al. 2009).


Glaucoma is a complex condition in terms of physiopathogenic mechanisms, causes blindness, and therefore requires a critical evaluation of the role of vascular factors and any other risk factors. Intraocular pressure has been identified as the major cause and management of the condition focuses on reducing the pressure (McKinnon et al. 2008). Poor vascular activities require critical evaluation and management. New studies focus on improving treatment, understanding how the retinal ganglion cells work and striving to prevent progression. Further studies and new findings might offer the best solutions for protecting retinal nerve cells and inhibiting physiopathologic processes that lead to glaucoma.


Aptel F, S Dumas, and P Denis (2009) Ultrasound biomicroscopy and optical coherence tomography imaging of filtering blebs after deep sclerectomy with new collagen implant. European Journal of Ophthalmology 19(2): 223–30.

Bonomi L, G Marchini and M Marraffa (2000) Vascular risk factors for primary open angle glaucoma: the Egna–Neumarkt Study. Ophthalmology 107: 1287–1293.

Casson RJ, G Chidlow, JP Wood, JG Crowston and I Goldberg (2012) Definition of glaucoma: Clinical and experimental concepts. Clinical & Experimental Ophthalmology 40(4): 341–9.

Costa V, E Arcieri and A Harris (2009) Blood pressure and glaucoma. British Journal of Ophthalmology 93: 1276-1282.

Grieshaber M and J Flammer (2007) Does the blood-brain barrier play a role in Glaucoma? Survey of Ophthalmology 52(Suppl 2): S115–S121.

Leske M, S Wu, A Hennis, R Honkanen and B Nemesure (2008) Risk factors for incident open-angle glaucoma: the Barbados eye studies. Ophthalmology 115(1): 85-93.

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McKinnon S, LP Goldberg, J Walt, and T Bramley (2008) Current management of glaucoma and the need for complete therapy. American Journal of Managed Care 14(1 Suppl): S20-7.

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