Effectiveness of Tai Chi vs Cognitive Behavioural Therapy for Insomnia in Middle-Aged and Older Adults
November 27, 2025
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Background
Ocular hypertension (OHT) is a phenomenon when intraocular pressure (IOP) is above a certain level, typically 21 mm Hg and above in the general population. The term does not indicate whether or not there is glaucomatous nerve damage present, nor does it say how long these elevated pressures have been noticed. The term ‘ocular hypertension’ was first formally coined much later in the twentieth century. Even though Drance used the term in his paper in 1962, Perkins and others provided an official definition of this term in 1966 for the English literature.
Ocular hypertension is characterized by the following criteria:
Periocular inflammation accompanied by observation of intraocular pressure above 21 mm Hg in one or both eyes with the use of applanation tonometer, on two different occasions at least.
According to visual-field tests, no pathologic changes related to glaucoma are identified.
Open angles with no physical changes in the structure of the drainage as seen through gonioscopy.
No other associated ocular complications like angle closure, neovascularization or uveitis to add to the raised intraocular pressure.
Epidemiology
Based on the population-based epidemiological data available, it has been established that about 4 to 10% of people older than 40 years have IOP of 21 mm Hg or more without signs of glaucomatous damage, while OH is 10 to 15 times more frequent than POAG.
In the Barbados Eye Study, Black people demonstrated higher frequencies of increased IOP than other populations, although the Baltimore Eye Survey showed that the average IOP was not significantly different for Black and White groups of people. It is also panel from this study, Latinos being at greater likelihood of ocular hypertension than non-Latino Whites but lower than Blacks.
Some population-based surveys showed that women have higher incidence of Ocular hypertension according to Barbados Eye study. It is evident that mean IOP rises with increasing age and thus, being over forty years of age is considered a risk factor for both ocular hypertension and the development of POAG.
Anatomy
Pathophysiology
The clinically diagnosed pathophysiology of ocular hypertension and the specific reasons for the increased IOP remain not fully clarified. To date, mutations have been found in primary open-angle glaucoma, which affect protein folding in MYOC, and thus the function of trabecular meshwork and IOP. Elevated IOP has been reported as a contributing factor to glaucoma in patients by either inducing vascular dysfunctions and embodying ischemia of the optic nerve or by exerting mechanical pressure on neuronal axons. The participation of IOP in these factors regarding glaucomatous damage has not fully been established.
Etiology
Reduced Outflow Facility: Abnormality or obstruction of trabecular mesh work or the out-flow chamber such as Schlemm’s canal hampers aqueous humor out flow hence raising the IOP.
Genetic Factors: Molecular changes involving the gene known as MYOC can result in structural alterations of the trabecular meshwork cell, and thus reduce the outflow and elevate the IOP.
Structural Anomalies: Several factors that affect IOP would include anatomical abnormalities involving the eye where these can include a narrow angle and trabecular mesh work too.
Age: Ocular hypertension is particularly prevalent in elderly patients and could be attributed to modifications in the drainage apparatus of the eye and other factors associated with aging.
Steroid Use: Steroids whether topical or systemic when used for a long time affect the regulation of aqueous humor and thus raising the IOP.
Genetics
Prognostic Factors
Ocular hypertension has a favorable outcome depending on certain factors such as IOP and risk factors involved as well as overall health of the eyes. This means that if not managed, ocular hypertension may result in glaucoma especially if the IOP is high and prolonged, coupled with other factors. But if the condition is detected early enough and treated with close monitoring and the necessary care, the possibility of acquiring glaucoma is low. It is essential to prevent or manage glaucomatous damage through proper IOP management depending on the cause such as early intervention through adjusting one’s lifestyle.
Clinical History
Age Group
Ocular hypertension does not have a specific age of onset, but it is more prevalent in patients above 40 years. It becomes common with age because both alteration in the eyes’ drainage mechanism and other age-associated factors cause high IOP.
Physical Examination
Intraocular Pressure (IOP) Measurement: Perform tonometry to assess IOP; any increase beyond 21 mm Hg characterizes ocular hypertension.
Visual Field Testing: Perform screening tests to determine is there is any indication of glaucomatous damage to the nerve fiber.
Optic Nerve Head Examination: Use fundoscopy to observe the optic nerve shaft for signs of cupping or nerve damage.
Gonioscopy: Measures the drainage angle of the eyeball to check the pathological outflow of liquids.
Corneal Pachymetry: Assess corneal thickness since thin corneas are associated with a higher tendency of glaucoma development.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Asymptomatic: Most times, ocular hypertension does not present any symptoms, and it is only diagnosed during routine eye tests.
Progressive Changes: If the intraocular pressure stays high in the long run, glaucomatous damage may occur, which may manifest as peripheral vision loss or visual field defect. It is important to diagnose the disease in the early stages to check its progression to glaucoma.
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Regular Monitoring: The patients should have their IOP checked frequently as well as performing the necessary visual field tests to monitor the steady movement towards glaucoma. Control risk factors that are linked to CKD such as high blood pressure and elevated levels of blood sugar.
Lifestyle Modifications: The patient may need modifications on any drugs that causes increased IOP including corticosteroids. Some dietary habits and activities such as balanced diet and exercise may be useful in the prevention of high IOP.
Pharmacological Management:
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-a-non-pharmacological-approach-for-treating-ocular-hypertension
Dietary Changes: Diets containing antioxidants should be taken to support the eyes since fruits and vegetables are rich in these nutrients. Recent medical research also shows that omega-3 fatty acids and green vegetables might aid in the prevention of high IOP.
Regular Exercise: Conducting aerobic exercises and other physical activity at a moderate level also help to reduce IOP in some cases. For instance, walking, jogging, swimming, are some of the advisable exercises among others.
Weight Management: The glaucoma and high IOP risk amongst the obesity population should ensure that one keeps to a healthy weight.
Mindfulness and Relaxation Techniques: Activities like yoga, meditation, and deep breathing therefore appear to be useful in managing stress, which might be of advantage in controlling IOP.
Adequate Sleep: Minimize sleep disorders and other conditions such as sleep apnea because they often cause an increase in IOP.
Role of Antiglaucoma, Prostaglandin Agonists
Latanoprost (Xalatan 0. 005%): Reduce the intraocular pressure within the eye through the promotion of aqueous humor drainage. May affect the outward appearance of the eye and eyelashes and is more noticeable in clients who have undergone one-eye treatment.
Bimatoprost Ophthalmic Implant (Durysta): A device that is inserted to achieve long-term IOP control in patients with POAG or other forms of glaucoma or OHT.
Travoprost Ophthalmic Solution (Travatan Z): It is a prostaglandin analogue that work through increasing the uveoscleral outflow thus reducing IOP. There exists controversy when used in African Americans, and it can result in conjunctival hyperemia.
Bimatoprost Ophthalmic Solution (Lumigan): Hydroxyprostaglandin that reduces IOP but often leads to the appearance of eye redness (conjunctival hyperemia).
Travoprost Intracameral Implant: A device employed to manage IOP in the disorder in the grown-ups with open angle glaucoma or the heightened ocular pressure.
Tafluprost: An option that is a preservative free prostaglandin analogue that reduces IOP probably through augmenting on uveoscleral pathway.
Latanoprostene Bunod Ophthalmic: Reduces IOP through enhancing the facility of outflow through the trabecular meshwork, together with the uveoscleral pathway and therefore helps to lessen the risk of glaucoma related perceptive visual field loss.
Omidenepag Isopropyl Ophthalmic: Reduces IOP in patients with open angle glaucoma by encouraging uveoscleral drainage. This form of prostaglandin is less likely to result in the cosmetic problems that have been associated with other prostaglandin analogs.
Latanoprost (Xalatan 0. 005%): Reduce the intraocular pressure within the eye through the promotion of aqueous humor drainage. May affect the outward appearance of the eye and eyelashes and is more noticeable in clients who have undergone one-eye treatment. Bimatoprost Ophthalmic Implant (Durysta): A device that is inserted to achieve long-term IOP control in patients with POAG or other forms of glaucoma or OHT. Travoprost Ophthalmic Solution (Travatan Z): It is a prostaglandin analogue that work through increasing the uveoscleral outflow thus reducing IOP. There exists controversy when used in African Americans, and it can result in conjunctival hyperemia. Bimatoprost Ophthalmic Solution (Lumigan): Hydroxyprostaglandin that reduces IOP but often leads to the appearance of eye redness (conjunctival hyperemia). Travoprost Intracameral Implant: A device employed to manage IOP in the disorder in the grown-ups with open angle glaucoma or the heightened ocular pressure. Tafluprost: An option that is a preservative free prostaglandin analogue that reduces IOP probably through augmenting on uveoscleral pathway. Latanoprostene Bunod Ophthalmic: Reduces IOP through enhancing the facility of outflow through the trabecular meshwork, together with the uveoscleral pathway and therefore helps to lessen the risk of glaucoma related perceptive visual field loss. Omidenepag Isopropyl Ophthalmic: Reduces IOP in patients with open angle glaucoma by encouraging uveoscleral drainage. This form of prostaglandin is less likely to result in the cosmetic problems that have been associated with other prostaglandin analogs.
Betaxolol Ophthalmic: It is a nonselective agent that competitively antagonizes beta1 receptors and causes minimal antagonism of beta2 receptors. It inhibits the production of aqueous humor in the eye thus reducing IOP and this means that it has less effect on the respiratory system compared to nonselective beta-blockers. It may reduce IOP to a lesser degree, promote optic nerve blood flow, and afford neuroprotection.
Carteolol 1%: Carteolol belongs to the group of drugs having intrinsic agonist activity and may have less deleterious effects involving the heart and lipid profiles.
Timolol 0.25%, 0.5%: Conventional timolol therapy reduces IOP including normal IOP through its ability to suppress production of aqueous humour and suitable for use in glaucoma patients including primary open angle glaucoma patients. The active compound in the gel-forming solution (Timoptic XE) is administered at night, but not when used together with latanoprost. Both Timoptic XE and Istalol are used in the form of eye drops and are administered in the day. Timolol is also available as fixed-combination formulations with dorzolamide (as Cosopt) and brimonidine (as Combigan).
Levobunolol 0.25%, 0.5%: It is a beta-adrenergic blocker, which does not have selectivity for beta subtypes, that can reduce IOP by influencing the formation of aqueous humor and the outflow.
Metipranolol 0. 3%: The drug is a beta-blocker classified under second generation with low ISA and MSAA plus minimal local anaesthetic activity. It works by decreasing IOP due to a decrease in the production of the aqueous humour.
Role of Carbonic Anhydrase Inhibitors
Dorzolamide (Trusopt): Reduces the formation of aqueous humour by blocking carbonic anhydrase; decreases intraocular pressure (IOP). It may also cause dysfunction of the kidneys thus increasing sodium, potassium bicarbonate and water output.
Brinzolamide (Azopt): Also, a carbonic anhydrase inhibitor, it lowers IOP and is classified as eye drop preparations and may be used with other eye preparations. It has a buffered pH and as such does not feel as stinging when applied.
Acetazolamide (Diamox): Commonly used in chronic POAG, various secondary glaucoma, but not for primary HT because of its side effects.
Methazolamide: Competitively antagonises carbonic anhydrase to decrease formation of aqueous humour and subsequently IOP.
Role of Alpha agonists
Brimonidine: It is a selective alpha-2 adrenergic receptor agonist that lowers intraocular pressure (IOP) through two mechanisms: it affects the antiblockage by decreasing the formation of aqueous humor and increasing the uveoscleral drainage. It has limited effects on cardiac and pulmonary disorders, but oral dose may produce moderate to severe allergic reactions in patients with known hypersensitivity to Iopidine.
Alphagan-P: It does not include a preservative known as Purite and in general is not well tolerated as Alphagan.
Role of Rho Kinase/Norepinephrine Transporter Inhibitor
Netarsudil Ophthalmic: It is employed in the management of increased IOP in patients with open angle glaucomatous disease or ocular hypertension.
Role of Antiglaucoma Combos
Brimonidine/Timolol: This eye drop contains a selective alpha two adrenergic receptor stimulant along with a non-selective beta-adrenergic receptor inhibitor. Both components help to reduce raised intraocular pressure (IOP), regardless of whether this is the case with glaucoma.
Timolol/Dorzolamide: Timolol a nonselective beta-adrenergic receptor antagonist is known to reduce the secretion of aqueous humor as well as has a small influence on the increase in the outflow of aqueous humor. Combined use of timolol and dorzolamide twice daily results in significantly more IOP lowering than either agent given individually, but slightly less than if dorzolamide is given three times daily with timolol in the morning and evening.
Brinzolamide/Brimonidine: This is a fixed combination product consisting of the carbonic anhydrase inhibitor, brinzolamide and the alpha2 adrenergic receptor agonist brimonidine. It is approved to lower’s IOP in patients with ocular hypertension.
use-of-intervention-with-a-procedure-in-treating-ocular-hypertension
Laser Iridotomy: This procedure involves making a small opening in the peripheral section of the iris to facilitate the drainage of the aqueous humour and thereby lowering IOP. It is mainly indicated in angle closure glaucoma or secondary glaucoma depending on specific eye conditions.
Laser Trabeculoplasty: This method applies laser energy to increase drainage in the trabecular mesh work and may help reduce IOP. It is commonly employed when pharmacological management of the disease is insufficient.
Selective Laser Trabeculoplasty (SLT): SLT aims at certain cells in the trabecular meshwork to increase the availability of aqueous humor and consequently, to decrease IOP without causing much harm to neighbouring tissues. The drug is mainly employed in managing open angle glaucoma though can be effective in ocular hypertension also.
Trabeculectomy: The aim of this surgical operation is to form a new, alternative route that allows the aqueous humor to drain out without passing through the trabecular meshwork, thus reducing IOP. This is often employed when less invasive therapies have not produced the desired outcomes.
Tube Shunt Surgery: In this procedure, a tube is inserted in the eye to act as a shunt to remove balance of the aqueous humor and, therefore, IOP. It is reserved for use in those with advanced or treatment-resistant glaucoma and high intraocular pressure.
use-of-phases-in-managing-ocular-hypertension
The management of the ocular hypertension is systematic bearing in mind there are the different phases. First, in the assessment phase, IOP measurements are done again to clarify the diagnosis and risk factors. During the Initial Treatment Phase, treatments that are given may include prostaglandin analogues or betablockers and few adjustments in the patient’s lifestyle. More precisely, in the Monitoring Phase, follow up visits are made to check IOP and make further alteration if necessary. The Advanced Treatment Phase might contain additional measures or mechanical procedures if main treatments are ineffective. Finally, the Long-Term Management Phase is needed to confirm the absence of the disease worsening and to underline the importance of the regular adherence to the prescribed therapy.
Medication
Instill one drop on the affected eye
Instill 1 drop in the affected eye every day in the evening
Indicated for Elevated intraocular pressure with Glaucoma:
Instil 1 drop in each affected eye twice a day,12 hours apart approximately
Indicated to lower intraocular pressure:
Administer one drop into each affected eye daily twice
Put one drop in affected eye(s) every 3 times a day
One drop in affected eye(s) every 2 times a day 0.25%, if ineffective, may increase to 0.5% one drops every 2 times a day following
Decrease to one drop daily if intraocular pressure is controlled
Formulation of XE (0.5% or 0.25%): one drop daily
brinzolamide and timolol maleate
Administer one drop of ophthalmic suspension in the affected eye twice daily
Instill one drop in the affected eye three times a day
In patients suffering with ocular hypertension, it is indicated for the reduction of raised intra ocular pressure (IOP)
Note: If >1 drop is administered, the medication is recommended to wait at least 5 min between instilling different ophthalmic drops.
Indicated for Elevated IOP in Patients with Glaucoma :
>2 years: Instil 1 drop in each affected eye twice a day,12 hours apart approximately
<2 years: Contraindicated
Same as adults; Put one drop in affected eye(s) every 3 times a day
Below 2 yrs
Safety & efficacy were not established
Above 2 yrs
One drop in affected eye(s) every 2 times a day 0.25%, if ineffective, may increase to 0.5% one drops every 2 times a day following
Decrease to one drop daily if intraocular pressure is controlled
Age > 2 years Instill one drop in the affected eye three times a day
In patients suffering with ocular hypertension, it is indicated for the reduction of raised intra ocular pressure (IOP)
Note:
If >1 drop is administered, the medication is recommended to wait at least 5 min between instilling different ophthalmic drops
Future Trends
Ocular hypertension (OHT) is a phenomenon when intraocular pressure (IOP) is above a certain level, typically 21 mm Hg and above in the general population. The term does not indicate whether or not there is glaucomatous nerve damage present, nor does it say how long these elevated pressures have been noticed. The term ‘ocular hypertension’ was first formally coined much later in the twentieth century. Even though Drance used the term in his paper in 1962, Perkins and others provided an official definition of this term in 1966 for the English literature.
Ocular hypertension is characterized by the following criteria:
Periocular inflammation accompanied by observation of intraocular pressure above 21 mm Hg in one or both eyes with the use of applanation tonometer, on two different occasions at least.
According to visual-field tests, no pathologic changes related to glaucoma are identified.
Open angles with no physical changes in the structure of the drainage as seen through gonioscopy.
No other associated ocular complications like angle closure, neovascularization or uveitis to add to the raised intraocular pressure.
Based on the population-based epidemiological data available, it has been established that about 4 to 10% of people older than 40 years have IOP of 21 mm Hg or more without signs of glaucomatous damage, while OH is 10 to 15 times more frequent than POAG.
In the Barbados Eye Study, Black people demonstrated higher frequencies of increased IOP than other populations, although the Baltimore Eye Survey showed that the average IOP was not significantly different for Black and White groups of people. It is also panel from this study, Latinos being at greater likelihood of ocular hypertension than non-Latino Whites but lower than Blacks.
Some population-based surveys showed that women have higher incidence of Ocular hypertension according to Barbados Eye study. It is evident that mean IOP rises with increasing age and thus, being over forty years of age is considered a risk factor for both ocular hypertension and the development of POAG.
The clinically diagnosed pathophysiology of ocular hypertension and the specific reasons for the increased IOP remain not fully clarified. To date, mutations have been found in primary open-angle glaucoma, which affect protein folding in MYOC, and thus the function of trabecular meshwork and IOP. Elevated IOP has been reported as a contributing factor to glaucoma in patients by either inducing vascular dysfunctions and embodying ischemia of the optic nerve or by exerting mechanical pressure on neuronal axons. The participation of IOP in these factors regarding glaucomatous damage has not fully been established.
Reduced Outflow Facility: Abnormality or obstruction of trabecular mesh work or the out-flow chamber such as Schlemm’s canal hampers aqueous humor out flow hence raising the IOP.
Genetic Factors: Molecular changes involving the gene known as MYOC can result in structural alterations of the trabecular meshwork cell, and thus reduce the outflow and elevate the IOP.
Structural Anomalies: Several factors that affect IOP would include anatomical abnormalities involving the eye where these can include a narrow angle and trabecular mesh work too.
Age: Ocular hypertension is particularly prevalent in elderly patients and could be attributed to modifications in the drainage apparatus of the eye and other factors associated with aging.
Steroid Use: Steroids whether topical or systemic when used for a long time affect the regulation of aqueous humor and thus raising the IOP.
Ocular hypertension has a favorable outcome depending on certain factors such as IOP and risk factors involved as well as overall health of the eyes. This means that if not managed, ocular hypertension may result in glaucoma especially if the IOP is high and prolonged, coupled with other factors. But if the condition is detected early enough and treated with close monitoring and the necessary care, the possibility of acquiring glaucoma is low. It is essential to prevent or manage glaucomatous damage through proper IOP management depending on the cause such as early intervention through adjusting one’s lifestyle.
Age Group
Ocular hypertension does not have a specific age of onset, but it is more prevalent in patients above 40 years. It becomes common with age because both alteration in the eyes’ drainage mechanism and other age-associated factors cause high IOP.
Intraocular Pressure (IOP) Measurement: Perform tonometry to assess IOP; any increase beyond 21 mm Hg characterizes ocular hypertension.
Visual Field Testing: Perform screening tests to determine is there is any indication of glaucomatous damage to the nerve fiber.
Optic Nerve Head Examination: Use fundoscopy to observe the optic nerve shaft for signs of cupping or nerve damage.
Gonioscopy: Measures the drainage angle of the eyeball to check the pathological outflow of liquids.
Corneal Pachymetry: Assess corneal thickness since thin corneas are associated with a higher tendency of glaucoma development.
Asymptomatic: Most times, ocular hypertension does not present any symptoms, and it is only diagnosed during routine eye tests.
Progressive Changes: If the intraocular pressure stays high in the long run, glaucomatous damage may occur, which may manifest as peripheral vision loss or visual field defect. It is important to diagnose the disease in the early stages to check its progression to glaucoma.
Regular Monitoring: The patients should have their IOP checked frequently as well as performing the necessary visual field tests to monitor the steady movement towards glaucoma. Control risk factors that are linked to CKD such as high blood pressure and elevated levels of blood sugar.
Lifestyle Modifications: The patient may need modifications on any drugs that causes increased IOP including corticosteroids. Some dietary habits and activities such as balanced diet and exercise may be useful in the prevention of high IOP.
Pharmacological Management:
Ophthalmology
Dietary Changes: Diets containing antioxidants should be taken to support the eyes since fruits and vegetables are rich in these nutrients. Recent medical research also shows that omega-3 fatty acids and green vegetables might aid in the prevention of high IOP.
Regular Exercise: Conducting aerobic exercises and other physical activity at a moderate level also help to reduce IOP in some cases. For instance, walking, jogging, swimming, are some of the advisable exercises among others.
Weight Management: The glaucoma and high IOP risk amongst the obesity population should ensure that one keeps to a healthy weight.
Mindfulness and Relaxation Techniques: Activities like yoga, meditation, and deep breathing therefore appear to be useful in managing stress, which might be of advantage in controlling IOP.
Adequate Sleep: Minimize sleep disorders and other conditions such as sleep apnea because they often cause an increase in IOP.
Ophthalmology
Latanoprost (Xalatan 0. 005%): Reduce the intraocular pressure within the eye through the promotion of aqueous humor drainage. May affect the outward appearance of the eye and eyelashes and is more noticeable in clients who have undergone one-eye treatment.
Bimatoprost Ophthalmic Implant (Durysta): A device that is inserted to achieve long-term IOP control in patients with POAG or other forms of glaucoma or OHT.
Travoprost Ophthalmic Solution (Travatan Z): It is a prostaglandin analogue that work through increasing the uveoscleral outflow thus reducing IOP. There exists controversy when used in African Americans, and it can result in conjunctival hyperemia.
Bimatoprost Ophthalmic Solution (Lumigan): Hydroxyprostaglandin that reduces IOP but often leads to the appearance of eye redness (conjunctival hyperemia).
Travoprost Intracameral Implant: A device employed to manage IOP in the disorder in the grown-ups with open angle glaucoma or the heightened ocular pressure.
Tafluprost: An option that is a preservative free prostaglandin analogue that reduces IOP probably through augmenting on uveoscleral pathway.
Latanoprostene Bunod Ophthalmic: Reduces IOP through enhancing the facility of outflow through the trabecular meshwork, together with the uveoscleral pathway and therefore helps to lessen the risk of glaucoma related perceptive visual field loss.
Omidenepag Isopropyl Ophthalmic: Reduces IOP in patients with open angle glaucoma by encouraging uveoscleral drainage. This form of prostaglandin is less likely to result in the cosmetic problems that have been associated with other prostaglandin analogs.
Ophthalmology
Betaxolol Ophthalmic: It is a nonselective agent that competitively antagonizes beta1 receptors and causes minimal antagonism of beta2 receptors. It inhibits the production of aqueous humor in the eye thus reducing IOP and this means that it has less effect on the respiratory system compared to nonselective beta-blockers. It may reduce IOP to a lesser degree, promote optic nerve blood flow, and afford neuroprotection.
Carteolol 1%: Carteolol belongs to the group of drugs having intrinsic agonist activity and may have less deleterious effects involving the heart and lipid profiles.
Timolol 0.25%, 0.5%: Conventional timolol therapy reduces IOP including normal IOP through its ability to suppress production of aqueous humour and suitable for use in glaucoma patients including primary open angle glaucoma patients. The active compound in the gel-forming solution (Timoptic XE) is administered at night, but not when used together with latanoprost. Both Timoptic XE and Istalol are used in the form of eye drops and are administered in the day. Timolol is also available as fixed-combination formulations with dorzolamide (as Cosopt) and brimonidine (as Combigan).
Levobunolol 0.25%, 0.5%: It is a beta-adrenergic blocker, which does not have selectivity for beta subtypes, that can reduce IOP by influencing the formation of aqueous humor and the outflow.
Metipranolol 0. 3%: The drug is a beta-blocker classified under second generation with low ISA and MSAA plus minimal local anaesthetic activity. It works by decreasing IOP due to a decrease in the production of the aqueous humour.
Ophthalmology
Dorzolamide (Trusopt): Reduces the formation of aqueous humour by blocking carbonic anhydrase; decreases intraocular pressure (IOP). It may also cause dysfunction of the kidneys thus increasing sodium, potassium bicarbonate and water output.
Brinzolamide (Azopt): Also, a carbonic anhydrase inhibitor, it lowers IOP and is classified as eye drop preparations and may be used with other eye preparations. It has a buffered pH and as such does not feel as stinging when applied.
Acetazolamide (Diamox): Commonly used in chronic POAG, various secondary glaucoma, but not for primary HT because of its side effects.
Methazolamide: Competitively antagonises carbonic anhydrase to decrease formation of aqueous humour and subsequently IOP.
Ophthalmology
Brimonidine: It is a selective alpha-2 adrenergic receptor agonist that lowers intraocular pressure (IOP) through two mechanisms: it affects the antiblockage by decreasing the formation of aqueous humor and increasing the uveoscleral drainage. It has limited effects on cardiac and pulmonary disorders, but oral dose may produce moderate to severe allergic reactions in patients with known hypersensitivity to Iopidine.
Alphagan-P: It does not include a preservative known as Purite and in general is not well tolerated as Alphagan.
Ophthalmology
Netarsudil Ophthalmic: It is employed in the management of increased IOP in patients with open angle glaucomatous disease or ocular hypertension.
Ophthalmology
Brimonidine/Timolol: This eye drop contains a selective alpha two adrenergic receptor stimulant along with a non-selective beta-adrenergic receptor inhibitor. Both components help to reduce raised intraocular pressure (IOP), regardless of whether this is the case with glaucoma.
Timolol/Dorzolamide: Timolol a nonselective beta-adrenergic receptor antagonist is known to reduce the secretion of aqueous humor as well as has a small influence on the increase in the outflow of aqueous humor. Combined use of timolol and dorzolamide twice daily results in significantly more IOP lowering than either agent given individually, but slightly less than if dorzolamide is given three times daily with timolol in the morning and evening.
Brinzolamide/Brimonidine: This is a fixed combination product consisting of the carbonic anhydrase inhibitor, brinzolamide and the alpha2 adrenergic receptor agonist brimonidine. It is approved to lower’s IOP in patients with ocular hypertension.
Ophthalmology
Laser Iridotomy: This procedure involves making a small opening in the peripheral section of the iris to facilitate the drainage of the aqueous humour and thereby lowering IOP. It is mainly indicated in angle closure glaucoma or secondary glaucoma depending on specific eye conditions.
Laser Trabeculoplasty: This method applies laser energy to increase drainage in the trabecular mesh work and may help reduce IOP. It is commonly employed when pharmacological management of the disease is insufficient.
Selective Laser Trabeculoplasty (SLT): SLT aims at certain cells in the trabecular meshwork to increase the availability of aqueous humor and consequently, to decrease IOP without causing much harm to neighbouring tissues. The drug is mainly employed in managing open angle glaucoma though can be effective in ocular hypertension also.
Trabeculectomy: The aim of this surgical operation is to form a new, alternative route that allows the aqueous humor to drain out without passing through the trabecular meshwork, thus reducing IOP. This is often employed when less invasive therapies have not produced the desired outcomes.
Tube Shunt Surgery: In this procedure, a tube is inserted in the eye to act as a shunt to remove balance of the aqueous humor and, therefore, IOP. It is reserved for use in those with advanced or treatment-resistant glaucoma and high intraocular pressure.
Ophthalmology
The management of the ocular hypertension is systematic bearing in mind there are the different phases. First, in the assessment phase, IOP measurements are done again to clarify the diagnosis and risk factors. During the Initial Treatment Phase, treatments that are given may include prostaglandin analogues or betablockers and few adjustments in the patient’s lifestyle. More precisely, in the Monitoring Phase, follow up visits are made to check IOP and make further alteration if necessary. The Advanced Treatment Phase might contain additional measures or mechanical procedures if main treatments are ineffective. Finally, the Long-Term Management Phase is needed to confirm the absence of the disease worsening and to underline the importance of the regular adherence to the prescribed therapy.
Ocular hypertension (OHT) is a phenomenon when intraocular pressure (IOP) is above a certain level, typically 21 mm Hg and above in the general population. The term does not indicate whether or not there is glaucomatous nerve damage present, nor does it say how long these elevated pressures have been noticed. The term ‘ocular hypertension’ was first formally coined much later in the twentieth century. Even though Drance used the term in his paper in 1962, Perkins and others provided an official definition of this term in 1966 for the English literature.
Ocular hypertension is characterized by the following criteria:
Periocular inflammation accompanied by observation of intraocular pressure above 21 mm Hg in one or both eyes with the use of applanation tonometer, on two different occasions at least.
According to visual-field tests, no pathologic changes related to glaucoma are identified.
Open angles with no physical changes in the structure of the drainage as seen through gonioscopy.
No other associated ocular complications like angle closure, neovascularization or uveitis to add to the raised intraocular pressure.
Based on the population-based epidemiological data available, it has been established that about 4 to 10% of people older than 40 years have IOP of 21 mm Hg or more without signs of glaucomatous damage, while OH is 10 to 15 times more frequent than POAG.
In the Barbados Eye Study, Black people demonstrated higher frequencies of increased IOP than other populations, although the Baltimore Eye Survey showed that the average IOP was not significantly different for Black and White groups of people. It is also panel from this study, Latinos being at greater likelihood of ocular hypertension than non-Latino Whites but lower than Blacks.
Some population-based surveys showed that women have higher incidence of Ocular hypertension according to Barbados Eye study. It is evident that mean IOP rises with increasing age and thus, being over forty years of age is considered a risk factor for both ocular hypertension and the development of POAG.
The clinically diagnosed pathophysiology of ocular hypertension and the specific reasons for the increased IOP remain not fully clarified. To date, mutations have been found in primary open-angle glaucoma, which affect protein folding in MYOC, and thus the function of trabecular meshwork and IOP. Elevated IOP has been reported as a contributing factor to glaucoma in patients by either inducing vascular dysfunctions and embodying ischemia of the optic nerve or by exerting mechanical pressure on neuronal axons. The participation of IOP in these factors regarding glaucomatous damage has not fully been established.
Reduced Outflow Facility: Abnormality or obstruction of trabecular mesh work or the out-flow chamber such as Schlemm’s canal hampers aqueous humor out flow hence raising the IOP.
Genetic Factors: Molecular changes involving the gene known as MYOC can result in structural alterations of the trabecular meshwork cell, and thus reduce the outflow and elevate the IOP.
Structural Anomalies: Several factors that affect IOP would include anatomical abnormalities involving the eye where these can include a narrow angle and trabecular mesh work too.
Age: Ocular hypertension is particularly prevalent in elderly patients and could be attributed to modifications in the drainage apparatus of the eye and other factors associated with aging.
Steroid Use: Steroids whether topical or systemic when used for a long time affect the regulation of aqueous humor and thus raising the IOP.
Ocular hypertension has a favorable outcome depending on certain factors such as IOP and risk factors involved as well as overall health of the eyes. This means that if not managed, ocular hypertension may result in glaucoma especially if the IOP is high and prolonged, coupled with other factors. But if the condition is detected early enough and treated with close monitoring and the necessary care, the possibility of acquiring glaucoma is low. It is essential to prevent or manage glaucomatous damage through proper IOP management depending on the cause such as early intervention through adjusting one’s lifestyle.
Age Group
Ocular hypertension does not have a specific age of onset, but it is more prevalent in patients above 40 years. It becomes common with age because both alteration in the eyes’ drainage mechanism and other age-associated factors cause high IOP.
Intraocular Pressure (IOP) Measurement: Perform tonometry to assess IOP; any increase beyond 21 mm Hg characterizes ocular hypertension.
Visual Field Testing: Perform screening tests to determine is there is any indication of glaucomatous damage to the nerve fiber.
Optic Nerve Head Examination: Use fundoscopy to observe the optic nerve shaft for signs of cupping or nerve damage.
Gonioscopy: Measures the drainage angle of the eyeball to check the pathological outflow of liquids.
Corneal Pachymetry: Assess corneal thickness since thin corneas are associated with a higher tendency of glaucoma development.
Asymptomatic: Most times, ocular hypertension does not present any symptoms, and it is only diagnosed during routine eye tests.
Progressive Changes: If the intraocular pressure stays high in the long run, glaucomatous damage may occur, which may manifest as peripheral vision loss or visual field defect. It is important to diagnose the disease in the early stages to check its progression to glaucoma.
Regular Monitoring: The patients should have their IOP checked frequently as well as performing the necessary visual field tests to monitor the steady movement towards glaucoma. Control risk factors that are linked to CKD such as high blood pressure and elevated levels of blood sugar.
Lifestyle Modifications: The patient may need modifications on any drugs that causes increased IOP including corticosteroids. Some dietary habits and activities such as balanced diet and exercise may be useful in the prevention of high IOP.
Pharmacological Management:
Ophthalmology
Dietary Changes: Diets containing antioxidants should be taken to support the eyes since fruits and vegetables are rich in these nutrients. Recent medical research also shows that omega-3 fatty acids and green vegetables might aid in the prevention of high IOP.
Regular Exercise: Conducting aerobic exercises and other physical activity at a moderate level also help to reduce IOP in some cases. For instance, walking, jogging, swimming, are some of the advisable exercises among others.
Weight Management: The glaucoma and high IOP risk amongst the obesity population should ensure that one keeps to a healthy weight.
Mindfulness and Relaxation Techniques: Activities like yoga, meditation, and deep breathing therefore appear to be useful in managing stress, which might be of advantage in controlling IOP.
Adequate Sleep: Minimize sleep disorders and other conditions such as sleep apnea because they often cause an increase in IOP.
Ophthalmology
Latanoprost (Xalatan 0. 005%): Reduce the intraocular pressure within the eye through the promotion of aqueous humor drainage. May affect the outward appearance of the eye and eyelashes and is more noticeable in clients who have undergone one-eye treatment.
Bimatoprost Ophthalmic Implant (Durysta): A device that is inserted to achieve long-term IOP control in patients with POAG or other forms of glaucoma or OHT.
Travoprost Ophthalmic Solution (Travatan Z): It is a prostaglandin analogue that work through increasing the uveoscleral outflow thus reducing IOP. There exists controversy when used in African Americans, and it can result in conjunctival hyperemia.
Bimatoprost Ophthalmic Solution (Lumigan): Hydroxyprostaglandin that reduces IOP but often leads to the appearance of eye redness (conjunctival hyperemia).
Travoprost Intracameral Implant: A device employed to manage IOP in the disorder in the grown-ups with open angle glaucoma or the heightened ocular pressure.
Tafluprost: An option that is a preservative free prostaglandin analogue that reduces IOP probably through augmenting on uveoscleral pathway.
Latanoprostene Bunod Ophthalmic: Reduces IOP through enhancing the facility of outflow through the trabecular meshwork, together with the uveoscleral pathway and therefore helps to lessen the risk of glaucoma related perceptive visual field loss.
Omidenepag Isopropyl Ophthalmic: Reduces IOP in patients with open angle glaucoma by encouraging uveoscleral drainage. This form of prostaglandin is less likely to result in the cosmetic problems that have been associated with other prostaglandin analogs.
Ophthalmology
Betaxolol Ophthalmic: It is a nonselective agent that competitively antagonizes beta1 receptors and causes minimal antagonism of beta2 receptors. It inhibits the production of aqueous humor in the eye thus reducing IOP and this means that it has less effect on the respiratory system compared to nonselective beta-blockers. It may reduce IOP to a lesser degree, promote optic nerve blood flow, and afford neuroprotection.
Carteolol 1%: Carteolol belongs to the group of drugs having intrinsic agonist activity and may have less deleterious effects involving the heart and lipid profiles.
Timolol 0.25%, 0.5%: Conventional timolol therapy reduces IOP including normal IOP through its ability to suppress production of aqueous humour and suitable for use in glaucoma patients including primary open angle glaucoma patients. The active compound in the gel-forming solution (Timoptic XE) is administered at night, but not when used together with latanoprost. Both Timoptic XE and Istalol are used in the form of eye drops and are administered in the day. Timolol is also available as fixed-combination formulations with dorzolamide (as Cosopt) and brimonidine (as Combigan).
Levobunolol 0.25%, 0.5%: It is a beta-adrenergic blocker, which does not have selectivity for beta subtypes, that can reduce IOP by influencing the formation of aqueous humor and the outflow.
Metipranolol 0. 3%: The drug is a beta-blocker classified under second generation with low ISA and MSAA plus minimal local anaesthetic activity. It works by decreasing IOP due to a decrease in the production of the aqueous humour.
Ophthalmology
Dorzolamide (Trusopt): Reduces the formation of aqueous humour by blocking carbonic anhydrase; decreases intraocular pressure (IOP). It may also cause dysfunction of the kidneys thus increasing sodium, potassium bicarbonate and water output.
Brinzolamide (Azopt): Also, a carbonic anhydrase inhibitor, it lowers IOP and is classified as eye drop preparations and may be used with other eye preparations. It has a buffered pH and as such does not feel as stinging when applied.
Acetazolamide (Diamox): Commonly used in chronic POAG, various secondary glaucoma, but not for primary HT because of its side effects.
Methazolamide: Competitively antagonises carbonic anhydrase to decrease formation of aqueous humour and subsequently IOP.
Ophthalmology
Brimonidine: It is a selective alpha-2 adrenergic receptor agonist that lowers intraocular pressure (IOP) through two mechanisms: it affects the antiblockage by decreasing the formation of aqueous humor and increasing the uveoscleral drainage. It has limited effects on cardiac and pulmonary disorders, but oral dose may produce moderate to severe allergic reactions in patients with known hypersensitivity to Iopidine.
Alphagan-P: It does not include a preservative known as Purite and in general is not well tolerated as Alphagan.
Ophthalmology
Netarsudil Ophthalmic: It is employed in the management of increased IOP in patients with open angle glaucomatous disease or ocular hypertension.
Ophthalmology
Brimonidine/Timolol: This eye drop contains a selective alpha two adrenergic receptor stimulant along with a non-selective beta-adrenergic receptor inhibitor. Both components help to reduce raised intraocular pressure (IOP), regardless of whether this is the case with glaucoma.
Timolol/Dorzolamide: Timolol a nonselective beta-adrenergic receptor antagonist is known to reduce the secretion of aqueous humor as well as has a small influence on the increase in the outflow of aqueous humor. Combined use of timolol and dorzolamide twice daily results in significantly more IOP lowering than either agent given individually, but slightly less than if dorzolamide is given three times daily with timolol in the morning and evening.
Brinzolamide/Brimonidine: This is a fixed combination product consisting of the carbonic anhydrase inhibitor, brinzolamide and the alpha2 adrenergic receptor agonist brimonidine. It is approved to lower’s IOP in patients with ocular hypertension.
Ophthalmology
Laser Iridotomy: This procedure involves making a small opening in the peripheral section of the iris to facilitate the drainage of the aqueous humour and thereby lowering IOP. It is mainly indicated in angle closure glaucoma or secondary glaucoma depending on specific eye conditions.
Laser Trabeculoplasty: This method applies laser energy to increase drainage in the trabecular mesh work and may help reduce IOP. It is commonly employed when pharmacological management of the disease is insufficient.
Selective Laser Trabeculoplasty (SLT): SLT aims at certain cells in the trabecular meshwork to increase the availability of aqueous humor and consequently, to decrease IOP without causing much harm to neighbouring tissues. The drug is mainly employed in managing open angle glaucoma though can be effective in ocular hypertension also.
Trabeculectomy: The aim of this surgical operation is to form a new, alternative route that allows the aqueous humor to drain out without passing through the trabecular meshwork, thus reducing IOP. This is often employed when less invasive therapies have not produced the desired outcomes.
Tube Shunt Surgery: In this procedure, a tube is inserted in the eye to act as a shunt to remove balance of the aqueous humor and, therefore, IOP. It is reserved for use in those with advanced or treatment-resistant glaucoma and high intraocular pressure.
Ophthalmology
The management of the ocular hypertension is systematic bearing in mind there are the different phases. First, in the assessment phase, IOP measurements are done again to clarify the diagnosis and risk factors. During the Initial Treatment Phase, treatments that are given may include prostaglandin analogues or betablockers and few adjustments in the patient’s lifestyle. More precisely, in the Monitoring Phase, follow up visits are made to check IOP and make further alteration if necessary. The Advanced Treatment Phase might contain additional measures or mechanical procedures if main treatments are ineffective. Finally, the Long-Term Management Phase is needed to confirm the absence of the disease worsening and to underline the importance of the regular adherence to the prescribed therapy.
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