Why does iop lead to blindness

Along with other things, high IOP is considered an important risk factor for the disease. Other risk factors include:.

The more risk factors you have, the more concerned you and your doctor will be that your high IOP should be treated even though your optic nerves may show no signs of glaucoma. Another important measurement is the thickness of the cornea. If the cornea is thick CCT , then your pressure may actually be lower when measured.

If the cornea is thin, then the pressure may be higher than detected by our measuring techniques. Beside the fact that not everyone with high IOP will go on to develop glaucoma, lowering IOP is an important decision. The medication used to lower IOP can be costly, and it can be difficult for patients who lack dexterity or the ability to follow schedules to administer.

Patients using these medications must be monitored closely by their eye doctors, which requires regular office visits. Some patients experience significant side effects from their medications, and there can be interactions with other medicines they take for different chronic health conditions.

In this case, eye drops may be prescribed to lower and control IOP. Another cause is the side effects of certain medications such as steroids.

If you have been prescribed steroid medications for any reason, consult with your eye doctor to see how frequently you should have your IOP checked. An injury or trauma to the eye can also cause high eye pressure that may be temporary or long term. Make sure to tell your eye doctor about any such incidence, past or present, to help in monitoring your eye health.

Inadequate aqueous drainage. High eye pressure also can occur If the aqueous is produced at a normal rate, but drains too slowly from the eye. Certain medications can have the side effect of causing ocular hypertension. Steroid medicines used to treat asthma and other conditions have been shown to increase the risk for high eye pressure.

Be sure to tell your eye doctor if you are using steroid eye drops for any reason. Eye trauma. An injury to the eye is another thing that can affect the balance of aqueous production and drainage, possibly leading to ocular hypertension.

Sometimes this can occur months or years after the injury. During your routine eye exams, be sure to mention to your doctor if you have experienced any recent or past eyew injuries. Also, race, age and family history play a role in your risk for ocular hypertension and glaucoma. Though anyone can develop high eye pressure, the following groups are generally at greater risk:.

If you have ocular hypertension, your eye doctor may prescribe eye drops to reduce your eye pressure. Fluctuations of ocular blood flow are particularly damaging and may be a more significant measurement for progression than baseline OBF measurements. The intrinsic capability of vascular autoregulation serves to continuously provide oxygen and nutrients despite any metabolic or pressure irregularities. The importance of autoregulation lies in the ability to maintain constant ocular blood flow despite OBF inconsistent ocular perfusion pressure OPP.

Though elevated IOP results in decreased OPP, normal autoregulation enables microvascular consistency thus preventing ischemic damage. However, the ONH becomes vulnerable to OPP fluctuations if autoregulation is compromised or its regulatory range is surpassed. Such autoregulation impairment is one potential vasculopathic mechanism for the risk and progression of GON despite relatively normal IOP and BP fluctuations.

When either the range of autoregulation is exceeded or autoregulation function is impaired, the ONH is at risk for ischemic injury. Studies also indicate dysregulation or even non-regulation of ocular vasculature in glaucoma patients. Some researchers believe systemic primary vascular dysregulation PVD is the source of ocular vascular dysfunction triggering GON. While some optic neuropathies are caused by hypoxia, the fluctuations in OBF triggering oxidative stress may contribute to glaucoma risk and progression.

PVD commonly results in stiff and irregular retinal vessels, increased retinal venous pressure, impaired neuro-coupling, and decreased autoregulation capacity, all of which increase glaucoma risk and progression.

For this reason, primary vascular dysregulation is a substantial risk factor for GON as it is associated with impaired autoregulation, low nocturnal BP, and increased retinal venous pressure — each of which can cause GON independently.

It is reasonable to assume that reduced OBF from dysfunctional autoregulation may play a significant role in GON risk and progression. Furthermore, research findings suggest proper autoregulatory responses are altered or missing with glaucoma. These daily and repetitive ischemic events suggest a potential vascular mechanism in glaucoma, especially NTG. Despite this, vascular etiology in glaucoma is rarely considered amongst eye care professionals, even in NTG eyes with vasculopathic risk factors.

This may explain why cardiovascular disease, hypertension, and diabetes are risk factors for glaucoma progression. Such evidence is biologically plausible and suggestive of a vasculopathic mechanism for progression. As research continues to support the concept of multiple pressure types having roles in GON, new findings suggest a previously overlooked intracranial pressure that may contribute to GON. Interestingly, initial studies in cats indicate an association between low cerebrospinal fluid CSF pressure and glaucoma development.

Though research is ongoing, these initial results suggest that pressure behind the eyes can be as significant as pressure inside the eyes, especially in NTG patients. As previously mentioned, though elevated IOP is certainly a risk factor for glaucoma progression, vision deterioration often still occurs despite successfully lowering IOP using medicinal and surgical treatments.

Such instances suggest an IOP independent mechanism triggering this progression. Neuroimaging technology can potentially shed light on another side of glaucoma. For decades, glaucoma has been classified as a neurodegenerative disease by many researchers and clinicians. Recent neuroimaging findings demonstrate that glaucoma patients have focal brain damage in other brain areas besides the retina and optic nerve. Brain tomography reveals structural changes of the lateral geniculate nucleus LGN , optic radiations, and visual cortex associated with glaucoma.

Remarkably, structural changes have even been observed in non-visual areas of the brain. New fascinating evidence is emerging showing that glaucoma patients undergo atrophy of the amygdala potentially resulting in emotional and memory related complications. Such abnormalities of the amygdala may explain why those afflicted with glaucoma often experience mood instability, increased anxiety, heightened fear, and feelings of anger.

Given these new discoveries, glaucoma may be either a primary neurodegenerative disease or a primary optic neuropathy with secondary CNS damage. Provided that VF defects in glaucoma are related more to nerve bundle fiber patterns rather than LGN injuries, glaucoma is likely a primary optic neuropathy with secondary neurodegenerative involvement. Nonetheless, glaucoma is not a disease limited to the eye, but is now also recognized as a brain disease.

Currently all glaucoma treatment models are centered on lowering IOP, which can potentially lead to the misinformation of glaucoma being caused by high IOP only. Topical medications, oral medications, laser surgeries, and implants all attempt to limit glaucoma progression through IOP reduction.

It's well known that some patients continue to progress despite a low or normal IOP which further suggests an IOP-independent mechanism at play. Research suggests vascular dysfunction being a primary component in glaucoma, rather than occurring secondarily.

In cases of systemic vascular disease blood vessels are stiffer, more irregular, demonstrate reduced neuro-coupling, and have diminished autoregulation function. Such abnormalities are not isolated systemically, but affect the eyes as well. Due to the vascular nature of glaucoma, it is reasonable to conclude that what is healthy for the vascular system is healthy for ocular blood supply.