EMPOWERING TIPS FOR PATIENTS

 

1. Everyone should undergo glaucoma screening after 40 years of age. This can be done earlier and is a must if there is a close relative having glaucoma.

2. Follow your health center's appointment schedule. Not all patients have the same follow-up pattern. Stick to what the doctor ordered.

3. Tests are sometimes required to get a baseline even if you do not have glaucoma.

4. Intraocular pressure (IOP) is the most important factor in glaucoma and must be monitored. Try checking the IOP at different times of the day. The air puff or non-contact tonometer, which uses a burst of air to check IOP, is sensitive to your eyes. Do not squeeze your eyes during the test. Loosen the necktie before the test. If there is any doubt, get the IOP checked with a different machine.

5. Structural-functional tests are required for diagnosis. They need to be repeated at regular intervals to provide an idea about the trend in the changes.

6. Maintain a healthy lifestyle. Have a balanced diet, exercise regularly, and avoid stress and smoking. Avoid any supplements like body-building products without consulting a doctor first. Some of them have steroids which can cause/worsen glaucoma.

7. Seek support. Join a support group or keep in touch with individuals/relatives having glaucoma. This will give moral support and also information regarding any new treatment options.

8. Stay informed yourself. Educate yourself about glaucoma.

9. Avoid anxiety and depression regarding the condition. Glaucoma damage occurs very slowly in most cases. Use the medications regularly.

10. Compliance with treatment is the foundation of glaucoma management. It is seen that individuals who adhere to treatment in the first 2 years have long-term compliance. Therefore, the patient and treating healthcare worker should be very diligent in enforcing compliance in the first few years.

OPTIC NERVE REGENERATION

 

The optic nerve is regarded as an extension of the brain. It is usually recognized that once damaged, the optic nerve does not regenerate, leading to visual loss lasting the lifetime of the individual. The degeneration of the optic nerve follows a timeline of events, starting milliseconds to hours after the initiating event, such as trauma or ischemia.

A few days after axonal injury, the associated retinal ganglion cells (RGCs) begin to degenerate. This is especially so if the injury is close to the eye.

The mature optic nerve contains many molecules that suppress axon growth, including the myelin-associated inhibitors Nogo-A, myelin-associated glycoprotein, and oligodendrocyte-myelin glycoprotein; proteoglycans that accumulate in the scar at the injury site; and additional axon repellants (eg, semaphorins).

The death of RGCs can be prevented almost completely by overexpression of the antiapoptotic Bcl family proteins, such as, Bcl-2 and Bcl-xL.

However, the regeneration and survival of axons is also dependent on numerous intracellular signaling pathways. This is seen when RGCs overexpressing Bcl-2 or Bcl-xL fail to regenerate axons, unless provided with additional growth factors.

A number of trophic factors can slow, but not completely stop, the death of RGCs. These factors include ciliary neurotrophic factor (CNTF), brain-derived neurotrophic factor (BDNF), neurotrophin 4/5 nerve growth factor, Fibroblast growth factor-2 (FGF-2), insulin-like growth factor-1, granulocyte colony-stimulating factor, glial-derived neurotrophic factor, and neurturin. 

The death of axotomized RGCs is also slowed by preventing caspase cleavage, blocking the nuclear enzyme poly (adenosine diphosphate–ribose) polymerase (a substrate for caspases), blocking nitric oxide synthase, introducing reducing agents, or inhibiting cell death via caspase-independent pathways. Long-term prevention of RGC death after axotomy may require the development of long-term delivery systems or a combination of treatments.

Two molecules present in the eye were found to stimulate mature RGCs to regenerate their axons. One is mannose, a simple sugar that is abundant in the vitreous. Mannose stimulates RGCs to extend moderately long axons if cells have sufficiently high levels of intracellular cyclic adenosine monophosphate (cAMP). The second growth factor is oncomodulin (Ocm), a 12-kDa, calcium-binding protein secreted by macrophages. 

The death of axotomized RGCs can be slowed by preventing caspase cleavage, blocking the nuclear enzyme poly(adenosine diphosphate–ribose) polymerase (a substrate for caspases), blocking nitric oxide synthase, introducing reducing agents, or inhibiting cell death via caspase-independent pathways. 

The advances during the past few years give hope for the possibility that at least some RGCs will be able to regenerate their axons all the way to their central targets. The future challenges will include finding ways to optimize this regeneration and testing whether they restore functionally meaningful levels of vision.

REFERENCES:

Li HJ, Sun ZL, Yang XT, Zhu L, Feng DF. Exploring Optic Nerve Axon Regeneration. Curr Neuropharmacol. 2017;15(6):861-873.

Benowitz LI, Yin Y. Optic Nerve Regeneration. Arch Ophthalmol. 2010;128(8):1059–1064. doi:10.1001/archophthalmol.2010.152.

 

INITIAL ADHERENCE IS ASSOCIATED WITH LONG-TERM COMPLIANCE

 

Studies have shown that patients on anti-glaucoma treatment can be identified for their specific characteristics, regarding long-term adherence and compliance to treatment.

According to a study by Kolko et al, individuals who have high adherence in the first 2 years of treatment have long-term compliance with the medications.

The study also found that adherence is less likely among men (OR first year: 0.78, 95%CI: 0.75 to 0.82), younger individuals, and those with a positive Charlson Comorbidity Index (CCI) score (OR first year/CCI≥3: 0.71, 95%CI: 0.63 to 0.80).

Adherence in the first one and two years of treatment was associated with better adherence in the 5^th and also in the 10^th year of treatment, to some extent.

It was also found that patients with poor adherence prove to be more expensive for hospital contacts in the long run.

Glaucoma patients with diseases of the eye and adnexa, diseases of the musculoskeletal system and connective tissue, and ischemic heart diseases were less likely to be adherent to glaucoma treatment compared with glaucoma patients without the presence of these comorbidities.

A study by Newman-Casey has classified glaucoma patients into 5 groups, based on their adherence to therapy.

These groups were:

1) Never adherent after their index prescription fill (7.5%,15.6% of persons in the one and four-year models, respectively)

2) Persistently very poor adherence (14.9%, 23.4%)

3) Declining adherence (9.5%, 9.1%)

4) Persistently moderate adherence (48.1%, 37.0%)

5) Persistently good adherence (20.0%, 15.0%)

Persons with the best adherence over 4 years were more likely to be white, older age, earn >

$60,000/year, and have more eye care visits (p<0.05 for all comparisons).

CONCLUSION:

These studies indicate that improving adherence in the first two years of treatment has long-term benefits regarding compliance. This can translate into better clinical outcomes.

REFERENCES:

Kolko M, Faergemann Hansen R, G Dal L, Sabelström E, Brandel M, Hoiberg Bentsen A, Falch-Joergensen AC. Predictors and long-term patterns of medication adherence to glaucoma treatment in Denmark-an observational registry study of 30 100 Danish patients with glaucoma. BMJ Open Ophthalmol. 2024 Apr 15;9(1):e001607. doi: 10.1136/bmjophth-2023-001607. PMID: 38626933; PMCID: PMC11029215.

Newman-Casey PA, Blachley T, Lee PP, Heisler M, Farris KB, Stein JD. Patterns of Glaucoma Medication Adherence over Four Years of Follow-Up. Ophthalmology. 2015 Oct;122(10):2010-21. doi: 10.1016/j.ophtha.2015.06.039. Epub 2015 Aug 25. PMID: 26319441; PMCID: PMC4581955.

 

BITTER KOLA EYEDROPS

 

Bitter Kola is a nut widely grown in African countries. It has many systemic health benefits, which have been reported elsewhere.

Bitter Kola fruit

Professor Adefule Ositelu, a retired ophthalmologist from the University of Lagos, Nigeria has reported the effect of Bitter Kola eye drops in glaucoma patients. According to her study, 0.5% Bitter Kola eye drops are as effective as Timolol eye drops in controlling intraocular pressure (IOP).

To assess the effectiveness of Bitter Kola eyedrops, a double-blind case-control study was performed by Professor Bernice Adegbehingbe, head of the department of ophthalmology and head of glaucoma services at the Obafemi Awolowo University Teaching Hospital Complex, Ile-Ife, Osun State, Nigeria. In the study conducted in four centers, half of the patients received Timolol 0.5% eye drops, while the other half were given Bitter Kola 0.5% eye drops. The patients were followed up for 6 months. At the end of the study period, the two medications were found to be equally effective in reducing IOP.

Although the study was conducted on open-angle glaucoma patients and ocular hypertensives, the authors believe that the agent can be effective for closed-angle patients as well. The agent acts by constricting the pupil/iris and thus overcoming the angle crowding seen in closed-angle patients.

WHAT IS BITTER KOLA?

Garcinia kola (bitter kola, a name sometimes also used for G. afzelii) is a species of flowering plant belonging to the Mangosteen genus Garcinia of the family Clusiaceae (a.k.a. Guttiferae). It is found in Benin, Cameroon, The Gambia, Democratic Republic of the Congo, Ivory Coast, Guinea, Mali, Gabon, Ghana, Liberia, Nigeria, Senegal and Sierra Leone. Its natural habitat is subtropical or tropical moist lowland forests.

Garcinia kola is traditionally used by African folk healers who believe that it has purgative, antiparasitic, and antimicrobial properties. The seeds are used for liver disorders, bronchitis, throat infections, colic, head or chest colds, and cough. It is also used as a chewing stick.

REFERENCE:

Adefule-Ositelu AO, Adegbehingbe BO, Adefule AK, Adegbehingbe OO, Samaila E, Oladigbolu K. Efficacy of Garcinia kola 0.5% Aqueous Eye Drops in Patients with Primary Open-Angle Glaucoma or Ocular Hypertension. Middle East Afr J Ophthalmol. 2010 Jan;17(1):88-93. doi: 10.4103/0974-9233.61224. PMID: 20543944; PMCID: PMC2880381.

VIOLENCE IN INDIA SHOULD STOP

VIOLENCE SHOULD STOP !!!!!

 

THE IMPACT OF OBESITY ON EYE HEALTH: A GROWING CONCERN

 

DR. SAMREEN FARHA

P.G. SCHOLAR

DEPT OF ILAJ BIT TADBEER,

AJMAL KHAN TIBBIYA HOSPITAL

ALIGARH MUSLIM UNIVERSITY

ALIGARH, INDIA

 

1. INTRODUCTION:

Obesity is a global health concern affecting millions of individuals throughout the world. Obesity's influence on general health is widely known, but its consequences on eye health are sometimes underestimated. Obesity, on the other hand, can have major effects on eyesight and eye health, increasing the chances of developing chronic eye illnesses and losing sight.

This article will examine the complex link between obesity and eye health, specifically how extra weight can damage our eyes and vision. We will also cover the need to keep a healthy weight and lifestyle to safeguard our eyes.

2. EPIDEMIOLOGICAL EVIDENCE:

(i). Glaucoma:

The JMDC Claims Database (JMDC Inc., Tokyo, Japan) between 2005 and 2020 reported that one of the factors associated with increased risk of glaucoma was overweight/obesity (vs. moderate weight: hazard ratio, 1.04 [95% confidence interval, 1.02–1.07]). Another study from Taiwan, The Longitudinal Health Insurance Database (LHID) 2000 and LHID2005 from 2001 to 2010, analysed the participants. They found that the risk of open-angle glaucoma was significantly higher in obese adults than in non-obese adults after multivariable adjustment (adjusted hazard ratio (aHR): 1.43 (95% confidence interval (CI) 1.11–1.84)/aHR: 1.54 (95% CI 1.23–1.94) in the LHID2000/LHID2005).

Surprisingly, the China Health and Retirement Longitudinal Study found that obesity was significantly associated with a 10.2% reduced risk of glaucoma.

(ii). Age-Related Macular Degeneration (AMD):

   A meta-analysis of 15 studies found that obesity increases the risk of developing AMD by 25%.

(iii). Diabetic Retinopathy:

   A cohort study of over 100,000 participants found that obesity increases the risk of developing diabetic retinopathy by 50%.

(iv). Cataracts:

   A systematic review of 20 studies found that obesity increases the risk of developing cataracts by 15%.

3. SCIENTIFIC REPORTS:

The impact of obesity on eye health is increasingly recognized as significant. Reports from both the World Health Organization (WHO) and the National Eye Institute (NEI) highlight the association between obesity and various chronic eye diseases, which can lead to vision loss.

(1). WHO Report: This report underscores that obesity increases the risk of developing chronic eye conditions. These conditions can significantly impair vision and overall eye health, emphasizing the importance of managing obesity to protect against such risks.

(2). NEI Report: The National Eye Institute identifies obesity as a significant risk factor for several specific eye diseases, including:

   - Age-related macular Degeneration (AMD): A condition that affects the central part of the retina and can lead to vision loss.

   - Diabetic Retinopathy: A complication of diabetes that affects the blood vessels in the retina, potentially leading to blindness.

   - Cataracts: Clouding of the eye's lens can impair vision.

These reports highlight the broader implications of obesity beyond commonly discussed health issues, drawing attention to the need to maintain a healthy weight to prevent chronic eye diseases and preserve vision.

4. MECHANISMS:

Obesity can have significant impacts on eye health through various mechanisms:

A. Inflammation:

Chronic inflammation is a hallmark of obesity. The excessive adipose tissue in obese individuals releases pro-inflammatory cytokines, leading to chronic low-grade inflammation. This systemic inflammation can extend to ocular tissues and contribute to the development of chronic eye diseases, such as:

- Age-related macular degeneration (AMD): Inflammation can damage the macula, leading to progressive vision loss.

- Dry eye syndrome: Inflammatory mediators can affect the tear-producing glands, leading to inadequate tear production and dry eyes.

B. Insulin Resistance:

Obesity is a major risk factor for the development of insulin resistance, which can lead to type 2 diabetes. Elevated blood sugar levels in diabetes can damage the blood vessels in various organs, including the eyes. This vascular damage can lead to several eye conditions, such as:

- Diabetic retinopathy: High blood sugar levels can damage the tiny blood vessels in the retina, leading to leakage, bleeding, and the formation of scar tissue. This can result in vision loss if not properly managed.

- Diabetic macular edema: Fluid accumulation in the macula due to leaky blood vessels can cause swelling and vision distortion.

By addressing obesity through lifestyle changes, diet, and medical interventions, it is possible to reduce the risk of these ocular complications and improve overall eye health.

C. Other mechanisms:

Obesity can also affect the eyes in other ways, including:

- Raising blood pressure, which can damage blood vessels in the eyes

- Altering lipid profiles, which can affect the eyes

5. THE CONSEQUENCES OF OBESITY ON EYE HEALTH:

The consequences of obesity on eye health can be severe, including:

- Vision loss and blindness

- Reduced quality of life

- Increased risk of eye surgery

- Higher healthcare costs

6. IMPORTANCE OF MAINTAINING A HEALTHY WEIGHT AND LIFESTYLE:

Maintaining a healthy weight and lifestyle is crucial for protecting our eye health. By losing weight and adopting healthy habits, we can reduce the risk of developing chronic eye diseases and vision loss.

Tips for Maintaining a Healthy Weight and Lifestyle:

- Eat a balanced diet rich in fruits, vegetables, and whole grains

- Engage in regular physical activity, such as walking or swimming

- Get enough sleep and manage stress

- Avoid smoking and limit alcohol consumption

7. CONCLUSION:

Obesity is a major worry that impacts general health and specifically eye health. Understanding the relationship between obesity and eye health allows us to make efforts to safeguard eyesight and lower the risk of chronic eye illnesses. Maintaining a healthy weight and lifestyle is critical for protecting the eyes and preventing vision loss.

ROLE OF GOJI BERRY IN GLAUCOMA

 

DR. SAHRISH

BUMS, AJMAL KHAN TIBBIYA COLLEGE,

ALIGARH, INDIA

Vascular dysregulation is one of the major risk factors for glaucoma.

The vasoconstrictor peptide endothelin-1 (ET-1) and its G-protein coupled receptors, namely endothelin receptor A (ET-A) and endothelin receptor B (ET-B), are present abundantly in ocular structures. They play important roles in regulating IOP, ocular blood flow, and neuronal functions.

Dysregulation of ET-1 and its receptors has been associated with clinical glaucoma. Elevated ET-1 levels in plasma, aqueous humor, or following cold-induced vasospasm have been reported in patients with normal tension or open-angle glaucoma.

Lycium barbarum (LB), also known as wolfberry or goji berry has been studied for its retinal ganglion cell (RGC) neuroprotective role.

A study was performed at the Hong Kong Polytechnic University, to investigate the therapeutic efficacy of LB glycoproteins (LbGP) in ET-1 induced RGC degeneration.

The animals were given LB extract by mouth under pre- and post-treatment conditions and then intra-vitreal ET was injected. Subsequently, the structural and functional outcomes in the retina were characterized using clinical-based techniques.

ET-1 injection in vehicle control induced transient reductions in arterial flow and retinal functions, leading to significant RNFL thinning and RGC loss.

Although ET-1 induced a transient loss in blood flow or retinal functions in all LbGP groups, LbGP treatments facilitated better restoration of retinal flow and retinal functions as compared with the vehicle control.

The LbGP groups also had significantly preserved retinal nerve fiber layer (RNFL) thickness and RGC densities.

WHAT IS GOJI BERRY?

Lycium barbarum has been used in China for more than 2,000 years as a traditional medicinal herb and food supplement. Lycium barbarum contains abundant Lycium barbarum polysaccharides (LBPs), betaine, phenolics, carotenoids (zeaxanthin and β-carotene), cerebroside, 2-O-β-d-glucopyranosyl-l-ascorbic acid (AA-2βG), β-sitosterol, flavonoids and vitamins (in particular, riboflavin, thiamine, and ascorbic acid). LBPs are the primary active components of Lycium barbarum. 

Lycium barbarum belongs to the family of Solanaceae. The berry is fusiform or oblong shaped with a length ranging from 6-20 mm and a diameter 3-10 mm. The orange or dark red berry has a small stylar scar protruding from the top, and skin having shrunken appearance. The pulp is fleshy and soft with a bitter and sweet taste. The berry is eaten raw, consumed in juice form, or added to tea or wine.

REFERENCES:

Lakshmanan, Y., Wong, F.S.Y., So, KF. et al. Lycium barbarum glycopeptide promotes neuroprotection in ET-1 mediated retinal ganglion cell degeneration. J Transl Med 22, 727 (2024). https://doi.org/10.1186/s12967-024-05526-8.

 

Age and brain changes are more important than IOP in glaucoma

 

Neuronal degeneration in glaucoma is characterized by early distal transport loss and damage to axonal pathology.

Mouse experiments have shown that the site of termination of retinal ganglion cell (RGC) axons in the superior colliculus (SC) shows reduced active transport. This follows a retinotopic pattern resembling glaucomatous vision loss.

Distal transport loss appears early, where RGC axons terminate in the SC. Subsequently, the deficits progress to more anterior RGC brain targets, including the optic tract and nerve, and finally to the retina, where active uptake eventually fails.

The deprivation of trophic factors due to compromised axonal integrity and transport is integral to the neurodegenerative process.

Downstream apoptotic mechanisms contribute late in glaucoma, and axonal pathology precedes somatic degeneration.

Acute glaucoma models have also demonstrated that RGC targets in the brain atrophy associated with the loss of recipient neurons.

The DBA/2 mouse glaucoma model has shown that the loss of markers (labels) in the SC do not correlate with the IOP. It is seen that the older the mouse, the more the neural deficit in the brain.

According to this research, IOP cannot predict a deficit, but aging can influence the likelihood of one for a given IOP.

REFERENCE:

Crish SD, Sappington RM, Inman DM, Horner PJ, Calkins DJ. Distal axonopathy with structural persistence in glaucomatous neurodegeneration. Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):5196-201. doi: 10.1073/pnas.0913141107. Epub 2010 Mar 1. PMID: 20194762; PMCID: PMC2841892.

GLAUCOMA AND HEARING LOSS

 

DR FARHAT JAHAN

P.G. SCHOLAR

Department of Amraz Ain, Uzn, Anf, Halaq wa Asnan,

State Unani Medical College and Hospital

Prayagraj, India

A systematic literature review was performed by Meliante and colleagues to look into the association of glaucoma with hearing loss. Their review analyzed 30 studies across various databases.

WHAT IS SENSORINEURAL HEARING LOSS?:

• Sensorineural hearing loss (SNHL) refers to hearing impairment secondary to cochlear abnormalities and/or damage to the cochlear nerve or the central auditory pathways.
• The most common form of SNHL is age-related hearing loss, characterized by a gradual and symmetrical decrease in hearing sensitivity, particularly at higher frequencies.
• It affects over 60% of individuals aged sixty-five and above.
• SNHL is a complex condition influenced by various factors, including gender, ethnicity, noise exposure, ototoxic medications, lifestyle choices, comorbidities, and genetic predisposition.
• SNHL is associated with a higher prevalence of neurodegenerative or neurological diseases like Alzheimer’s, cognitive impairment, or general dementia, through both common and causal mechanisms.
• These factors are also associated with the development of glaucoma.

SNHL AND PSEUDOEXFOLIATIVE GLAUCOMA:

• Several studies have reported increased pure tone audiometry (PTA) thresholds at speech frequencies (0.25, 0.5, 1 and 2 kHz) in patients with pseudoexfoliative syndrome (XFS)
• Singham et al. found a higher prevalence of hearing loss in individuals with XFS and significantly higher hearing thresholds at 0.5 and 1 kHz compared to controls (p < 0.05).
• Temporale et al. (2016), detected abnormal PTA at 2 kHz in 87% of XFS patients compared to 64.3% of controls (p = 0.008), and Lee et al. (2017) found XFS patients to have moderate to severe SNHL in 64% of cases (vs. 40.3% in controls) with an average hearing threshold of 47.93 dB, corresponding to the moderate hearing loss category according to the ISO 1964 and significantly decreased PTA at 1 and 2 kHz.
• Others have found an association between SNHL and pseudoexfoliation at all frequencies. SNHL at speech frequencies (mean value of 0.5, 1 and 2 kHz) in 69% of XFS patients vs. 52% of controls (p = 0.03) with a significantly higher mean threshold value (33.6 ± 18.5 dB vs. 28.4 ± 15.0 dB, p = 0.01).
• Papadopoulos et al. found a higher prevalence of PTA hearing loss in XFS patients at both low frequencies (0.25 & 0.5 Hz—57% vs. 41%, p = 0.07), medium frequencies (1 & 2 kHz—81% vs. 59%, p = 0.007) and high frequencies (4 & 8 kHz—98% vs. 86%, p = 0.007), with more severe hearing loss noted at 4 and 8 Hz.
• However, Muhafiz and also Tryggvason did not find any association between SNHL and pseudoexfoliation.
• The mechanism of association between SNHL and pseudoexfoliation can be explained by the dysfunction of hearing mechanoreceptors due to the deposition of fibrillar material in either or both the tectorial and basilar membranes, impairing the transmission of vibrating energy to the sensory hair cells, hence the conversion of the vibration energy to bioelectric energy. An alternative mechanism is vascular compromise due to the deposition of pseudo-exfoliative fibrils in the vessel walls.

SNHL AND PRIMARY OPEN ANGLE GLAUCOMA (POAG):

• In the study by Meliante and colleagues, 36% of POAG participants experienced difficulty differentiating low-frequency sounds. These findings indicate that some individuals with POAG may have an increased central nervous system vulnerability to damage, leading to auditory and visual processing dysfunction.
• A study by Kim et al. on the Korean population showed that aging and increased triglyceride levels were independent risk factors for the simultaneous occurrence of POAG and hearing impairment.

SNHL AND NORMAL TENSION GLAUCOMA (NTG):

• Regarding the potential correlation between NTG and progressive SNHL, some authors have focused on the role of autoantibodies against antigens in the inner ear.
• Patients with NTG had significantly higher concentrations of IgG APSA compared to controls (p<0.05), and elevated APSA concentrations showed significantly higher concentrations in NTG with progressive SNHL compared to NTG patients with normal hearing (p<0.01). Significantly higher concentrations of IgG APSA in NTG with progressive SNHL compared to normal hearing and controls were also found by Bachor et al., who additionally found the concentrations of IgM APSA were significantly elevated in all subgroups of NTG patients, as well as in NTG patients with normoacusis, compared to controls.

CONCLUSION:

These studies show a significant association of glaucoma with SNHL. Therefore, all patients having SNHL should be investigated for glaucoma and vice versa.

REFERENCE:

Meliante LA, Piccotti G, Tanga L, Giammaria S, Manni G, Coco G. Glaucoma, Pseudoexfoliation and Hearing Loss: A Systematic Literature Review. J Clin Med. 2024;13:1379.