CONCEPT exist in the diagnosis and treatment of glaucoma
(Published by Cipla India, the Indian eye doctors will be distributed)
Dr. M. Jain, a leading specialist in glaucoma, is currently Medical Director and Chief Ophthalmologist J R. Jain Institute and Department of Ophthalmology Jaipur, India. He has published textbooks on a book about glaucoma and ocular inflammation, and published 130 scientific papers in India and abroad. In 2007 he published a book of public education in Hindi on “EYES: Safety and Treatment”
He Life Time Achievement Award Rajasthan Ophthalmological Society was awarded in 2002 Career Award and time by each company in India Ophthalmological <2006
/ p> Dr. Jain is the gold medal of the National Academy of Medical Sciences’ research and clinical work awarded in the field of “glaucoma and distribution of drugs on the eye.”
Dr. Jain Currently, the chairman, Dr. MR J Charitable Trust, President, Lucky Seventh, Medicos SMS and state coordinator of the National Academy of Medical Sciences.current concepts of diagnosis and
management of glaucoma <
PROF. MRJAIN, MS, FICS (USA), FAMS, FACLP (London) Medical Director MRJINSTITUTE
& ; JAIN JAIPUR Eye Hospital
E-mail:
/ p>
It has a revolutionary change in the understanding, diagnosis and treatment glaucoma of been. Prior glaucoma was as a condition of intraocular pressure, defined not compatible with the health and function of the eye. Currently, the American Academy of Ophthalmology defined glaucoma as an optic neuropathy, damage to the optic nerve structural feature associated with the progressive death of retinal ganglion cells, loss of nerve fibers and loss of vision. The importance of intraocular pressure over 21.0 mm Hg as a singular factor was could be reduced for about a third of patients show glaucomatous damage to the classical normal intraocular pressure (1.2) or controls despite IOP after glaucoma surgery, it may be the gradual loss of the fields.
The definition of glaucoma in visual important target organ damage (3) is based. It is strictly the opinion that IOP-related damage can occur at all levels of IOP, and so that nearly 50 percent of patients with glaucoma not recognized (4-6). However reveal Baltimore Eye Survey, Aravind Eye comprehensive study that the relationship between IOP and the prevalence of glaucoma is positive. In general, 21mm Hg as cutoff point.
<
/ p> <
/ p> <
/ p> Top
/ p> / p>
optic nerve head IMMAGING
In addition to direct ophthalmoscopy well established and slit lamp indirect ophthalmoscope with a 90 diopter lens to look at new diagnostic tools, and precisely the changes documented subtly into the disc, such as contour, color, cupping and healthy neuroretinal rim. (7-10) are the following:
(a) Photographs STEREO
/ p> 2
(a), optical coherence tomography (OCT)
/ p> (b) confocal laser scanning tomography (sctl)
(c) scanning laser polarimetry (SLP).
These methods are particularly useful to assess quantitatively retinal nerve fiber layer (RNFL) thickness in addition to the changes in the disc in suspected glaucoma. It is established that the retinal show nerve fiber layer in glaucoma may thinning even before the changes in the field (11-14) are detected.
/ p>
optical coherence tomography (OCT) analysis of a normal eye with glaucoma 2, shows the thickness of the nerve fibers.
Heidelberg retina tomograph (HRT and HRT II) is a confocal laser-scanning system for the collection and analysis of three-dimensional images of the optic nerve head. HRT imaging system, the highest diagnostic accuracy, precision, reproducibility, and is able to diagnose glaucoma before confirmed visual field change has. (15,16 <)
/ p> and Kamal al (17) and Greaney et al (18) noted that imaging techniques are no better than the quantitative assessment of disc photographs. In addition to the progressive erosion of the optic disc, the neuroretinal rim of the Health reflects the width and the color is very important (8). Localized unilateral notch in the lower part or superiority in temporal neuroretinal rim is an excellent indicator of glaucoma. Several other symptoms such as slight asymmetry ratio Cup / disc of 0.2, peripapillary halo, disc hemorrhage, Herschler exposed character ships ground, ovality vertical optic cup with a ratio greater than 3 and a few others when he is present, the suspect, adding to glaucoma. In recent years more emphasis on a drainage channel from the edge of the optic nerve be assigned and is regarded as connected with acquired pit of the optic nerve (ON), what ‘a very strong association of glaucoma (16 19).
/ p>
PROMOTION IN AUTOMATIC field recording
Introduction of the field test automated computer helped us significantly to glaucoma to diagnose early this decade, and it offers a degree of documentation control and monitor the progression of glaucoma.
last great progress in testing policies that saw the process done quickly, accurately, reliably and reproducibly. (20:21)
SITA (Swedish Interactive Threshold Algorithm) and TOP (Tendency Oriented Perimetry) test strategies have reduced the test of time and the variability of unmanned tests perimeter.Frequency doubling technology (FDT) perimetry is very fast and effective method for the detection of glaucomatous field loss.
Automated Perimetry short wavelength (SWAP) is in a position to the development and progression of glaucomatous visual field defects much earlier than standard automated perimetry (SAP)
Recent studies suggest that the proceedings may be mfVEP glaucomatous damage earlier to detect than conventional perimetry <. Goldberg and Associates (22) states that 60 percent of the eyes of glaucoma patients, the normal visual field had been identified by Member Humphrey, the abnormal mfVEP.
/ p>
decade
load was not significant progress in the methodology of the compilation of the IOP. In spite of various kinds by applanation tonometer including Pneumatonograph, Marg electronic tonometer Mackay, (23-27), XL Tonopen (tonometer blood flow) (28) and even non-contact tonometer, Goldman tonometer is the most reliable tonometer clinic where he is able to use this technique. Non Contact tonometer is comfortable for the patient and the physician, but the values often do not compare well with the Goldman tonometer. The machine must be standardized and repeated this several limitations. Outside the scleral rigidity, abnormal central corneal thickness affect the reading of intraocular pressure (29, 30 ).
What has changed in the last ten years, the understanding of the ideal of the IOP. The target IOP IOP was labeled.
</ p> target IOP as IOP that is defined secure for the individual. It can be anywhere mmHg to between the bottom of Youth 21st
</ p> IOP goal is set to the following principles:
<
/ p a.
slight loss of land: reducing IOP less than 20% IOP
b. Moderate damage: reduction of 30% or more.
c. Severe damage: reduction of 40% or more.There are no IOP at which a person is completely immune to damage caused by glaucoma and therefore target IOP should be individualized on repeated examinations of records and fields. risk factors such as age, myopia, diabetes, etc . inheritance (31) have to bear in mind.
</ strong p> The result of the Advanced Glaucoma Intervention Study (AGIS) data suggest that the decrease in IOP player, regardless of Risk factors recognized clinically. In younger patients the IOP be kept relatively low (32).
Most in glaucoma treatment decisions are for the steady-state-based pressure. ophthalmologists rarely document or episodic transient spikes in press, or the damage that may cause the these spikes to be tested. But these episodic peaks are clearly detrimental to the Royal Geographical Society (33). change of posture in IOP when the IOP is reported in lying posture when sitting, in the usually in non-contact tonometry Goldmann will increase, may miss some cases of glaucoma (23-27).
/ p>
glaucoma damage range is associated with a decrease in perfusion pressure of the neuroretinal rim and lamina cribrosa. He believes that the deregulation of vascular disturb the automatic regulation of ocular perfusion and makes the eye more sensitive to increase or decrease blood pressure, IOP. This partly explains the theory of the field to lower intraocular pressure loss and emphasizes the importance of using only the anti-glaucoma that does not compromise the perfusion of the optic nerve (34,35).
perfusion pressure of the hard disk can be explained by the following techniques:
<
/ p> Heidelberg Retina FLOMET
<
be measured / strong p>
Scanning Doppler
Measures
Doppler color
/ p reported> some workers that the absence of infusion correction of optical disc is the main cause for the loss of field. Such a reduction in perfusion pressure due to increased eye pressure may, or may be independent of pressure, the appearance of low tension glaucoma (36-40), explains. Some patients with normal-tension glaucoma particularly vulnerable when they have a history of the vasospasm and migraine have that invoices to prevent the use of calcium antagonists for glaucomatous damage. It is worthy to be the reference perfusion of the optic nerve to the reduction of intraocular pressure to recover especially after trabeculectomy with success. (41)
/ p>
apoptosis (programmed cell death)
/ p>
A normal person loses about 10,000 ganglion cells per year and if they have they lost 80 years 30 percent of its ganglion cells. In the case of open-angle glaucoma, the loss of the vision of time is apparent, more than 50 percent of the ganglion cells are destroyed.
/ p>
Apoptosis is a genetically programmed process, where cells commit suicide, characterized by condensation chromatic Intracellular fragmentation and internucleosomal DNA fragmentation. (42-44)
death of retinal ganglion cells is initiated when an abnormal event such as ischemia, axonal injury, or changes in the lamina cribrosa to the activation of the leading apoptosis (programmed cell death).
Apoptosis may be due to primary or secondary mechanisms.
are the most important mechanisms:
/ p> mechanical stress: increased eye pressure can with retrograde axoplasmic flow of the essential growth factors produced by the geniculate disturbing side.
circulatory disorders: Elevated IOP, vascular diseases or drugs may reduce the perfusion of the optic nerve, which ischemic diseases.
Genetic factors: Genetic factors may also the vulnerability of ganglion cell damage (45)
diseases such as diabetes also make neurons more susceptible to damage.secondary mechanisms:
In that damage neurons apparently caused by toxic factors such as high levels of glutamate (to be motivated to normal levels, there is a neurotransmitter), free radicals of oxygen or nitric oxide, which can be released by a primary insult, leading to further damage, even if the primary insult was controlled or removed.
glutamate, an amino acid when it is in excess toxic to nerve cells and thus the initiation of the apoptosis process. The dead cells are thought to glutamate and other amino acids, which keep the vicious circle of “programmed death of ganglion cells to release. We now know that one neurotransmitter glutamate damage likely in the normal retina, where s is also collecting for dead or dying cells living cells.
oxygen free radicals (OFR) are molecules containing oxygen that leads one or more unpaired electrons. These molecules react with lipids, nucleic acids and proteins and lead to cell death. Ischemia that may be independent of pressure, in the process of release of the OFR. <
/ p>
neuroprotective (enhanced cell survival)
The term “neuroprotection” refers to the protection of healthy but vulnerable neurons in the vicinity of the dead, and dead cells at risk of injury and also after the removal of the primary insult. In glaucoma, is to limit the goal of neuroprotection or delay of property-pressure dependent or independent of the pressure of the retinal ganglion cells (RGC) by interfering with the processes and substances that the cell death, or strengthening the neural pathways cause of this increase neuronal survival under stress conditions. (42,43, 45-47) <
/ p try to find> Researchers
intrinsic processes or natural ways to interrupt the process of apoptosis and promote survival of ganglion cell death by inhibiting the signals in the presence of ischemia induced by withdrawal of growth factors Released or caused by the accumulation of the excitatory amino acids such as glutamate (48). <
/ p> glutamate is shown to double the quantity in the vitreous with glaucoma. neuroprotective based on the principleReduction of risk factors: Lower IOP reduce ischemia. <
/ p> Promotion and / or inhibit cell
Excess glutamate can be toxic to normal stimulation RGSS more N-methyl-D- aspartate (NMDA). The NMDA receptor is an important type of glutamate receptor, which can kill most active when the retinal ganglion cells. Memantine of amantidine, Showing promise for neuroprotective effect in glaucoma. Memantine interaction with non-competitive NMDA receptor blockade results in the toxic effects of glutamate, without significant effect on normal cell function. Most of the activation of NMDA receptors by glutamate, the better the effect of memantine blocks glutamate and prevents the death of ganglion cells. (49) <
/ p> The protein Bcl-2 gene plays a central role in the regulation of apoptosis. The family members Bcl-2 genes that promote programmed cell death are poor and Bax, in contrast, the expression of Bcl-2 and Bcl-XL suppresses the apoptotic program. To date, A-2 signaling pathways have been identified to induce increased expression of bFGF, Bcl-2 and Bcl-XL genes, and improve the availability of the major neurotrophic factors. By activating alpha -2 in the retina, brimonidine (Brimodin) is shown that increasing the expression of anti-apoptotic genes, thereby preventing retinal ganglion cells death and promote axonal growth (50). Brimonidine also neutralizes the Kainic acid, which is toxic to nerve cells.
antioxidants, radical scavengers superoxide dismutase, catalase and vitamin E are also useful found neuroprotective effect. ‘/ P>
calcium channel blockers (diltiazem, nicardipine Nilvadipin, Nifedipine, etc.), semax (neuropeptide Russia), Citicoline, eliprodil, etc. riluzole and L deprenal be as neuroprotective agents studied.
<
/ p>
with the many existing and new drugs classes of drugs are now available to lower IOP practitioners with complex decisions about treatment strategies for patients with glaucoma face. Traditionally, beta-blockers were used as the standard treatment for glaucoma, but other means, such as A-2-agonists, carbonic anhydrase inhibitors and prostaglandins have other options available to the clinician. More recently, a new group, namely, the group came on stage prostamides demands safety, efficacy and dosage of the treatment of patients, compliance to intermediaries that are already available.
</ p>
selected in the general anti-glaucoma compared to the following criteria:
efficiency of the most vital
systemic safety
The convenience of Local / p> After the above criteria , beta-blockers, especially timolol, which is the most effective means outside the group, dominated the anti-glaucoma treatment. The drug is highly effective at reducing beat them 15-30 percent IOP, relatively inexpensive, with excellent tolerance of eye tissue is still very primary therapy for glaucoma recommended in the world. (What term systemic adverse effects on respiratory and cardiovascular systems, and issues such as depression, powerlessness, lack of libido, diabetes, and nocturnal hypo tension (51,52)). The lack of vigilance on the part of physicians can lead patients to death from cardio-vascular status asthmaticus or complications. Since the introduction of drugs in 1978 were 40 deaths were reported due to drugs. Systemic toxicity may be greatly reduced if the doctor is wise to advise the use of these drugs and take measures to prevent systemic absorption through specific distributors, the pressure on the lower puncta, or daily with once-a gel (Timolet JRC) application form. Selective beta-blockers such as betaxolol is relatively safe in patients with diseases of the respiratory tract, but is less effective than timolol. pilocarpine continue to maintain its relevance in glaucoma, primary angle closure. The drug has a synergistic effect with beta-blockers, brimonidine group, and systemic acetazolamide and topical treatments. “/ P> adrenergic agents (agonists) as dipivefrine, clonidine and apraclonidine limited concrete evidence, as it often involves the conjunctiva, allergies and other side effects, ‘including the reduction of the pressure infusion of the papilla. / p> Top / p> / p> Latanoprost <<0.005% / p> / p> Bimatoprost <0.03% / p> Travoprost 0.004% Isopropyl Unoprostone
<0.12% / P> 1% brinzolamide (Azopt) “/ P> brimonidine tartrate Brimonidine is a selective 2-agonists. It is an analogue of clonidine. It is about 30 times more selective -2 and has a very low affinity for a -1. For this reason, mydriasis and lid was found with nonselective agonists such as clonidine. The most important mechanism of action removed the suppression of aqueous formation, but it was also to some extent, thus increasing the flow of uvéoscléral -. (The principal merit brimodine (Brimodin) is its safety profile relative position and demands for neuroprotection by upregulation of applied cell survival factors and nervous as bFGF1 in response to the activation of the A-2 adrenergic receptors and ocular to increase blood flow. (53-55)) The drug must be instilled twice daily and its effect will IOP reduction can be compared with timolol. The demerit is higher than low IOP. The limiting factor is their brimonidine allergic reactions such as follicular conjunctivitis and contact dermatoconjunctivis (about 30 percent of the eyes) which can be justified to stop the drug. shown in recent years, few reports of occurrence of uveitis after prolonged use of brimonidine tartrate. Other occasional side effects reported were fatigue, drowsiness and dry mouth. The recent introduction of brimonidine without preservatives would be far fewer allergies (50%) from the place of benzalkonium chloride, sodium chloride was used as a preservative. Therapeutics, it is as effective as briomonidine. < / p> Top Prostaglandin analogues and prostamides < / p> prostaglandins and prostamides are newer group of drugs . Despite their high cost, they gain a great importance due to their greater efficacy in reducing IOP only require instillation in 24 hours, and have a relatively safe profile, systemic (56-62) < / p> prostamides prostaglandin and have a common origin in the membranes of cells, but they come from different membrane lipids are mobilized and undergo their biosynthesis connections. Analogues of prostaglandin F2 alpha are coming from the derived arachidonic acid, an intermediate in the metabolism and education, but prostamides from a path where anandamide are different enzymes involved. Prostamides Although structurally similar in some respects, prostaglandins, prostamides different functional. latanoprost, bimatoprost and travoprost are reported to reduce IOP by 30-40 percent and can the drug of choice as monotherapy in the eyes requiring IOP below target. Superior daily control (control 24 hours) with these medications, preventing spikes in connection with damage to eyes (56). A comparison of bimatoprost with timolol showed a statistically significant number of patients with bimatoprost specific target IOP reached at any moment to the use of timolol compared. (63) target IOP Latamoprost achieved, but often reached bimatoprost lowered IOP. Prostaglandin analogues release of trabecular uvéoscléral without compromising performance or the production of aqueous humor. Outflows rose seems to be uvéoscléral by changes in the extracellular matrix and gives a relaxation of the ciliary. Latanoprost is essentially a drug to improve performance. It is 50% better performance uvéoscléral (64-68) and 30% increase in trabecular output through a mechanism to explain the still. There is slight increase in flows, and (69). Latanoprost is indicated to increase the flow of blood to the optic nerve. (67, 68) < / p> Recent comparative studies Lataoprost be more effective than timolol Unoprostone and show less brimatoprost (56). Bimatoprost lowered IOP by 30% to around 78% of patients, whereas timolol achieved a reduction of 30% in 61% of patients. (56) Moreover, 62% of patients receiving bimatoprost are receive a 40% reduction in IOP compared to 35% of patients treated with timolol. The combination of latanoprost with timolol used once a day if a better IOP reduction of latanoprost to be alone. (69) only a few workers (70.71) represented a further decrease in IOP was used during pilocarpine four times daily with a single application of latanoprost. The biggest disadvantage of prostaglandins prostamides and is significant ocular side effects such as conjunctival hyperemia (15%), stinging and burning (30-40%) and foreign body sensation (20-22%), manifested the eyelash growth, increased pigmentation of the iris and periorbital tissue, including eyes, cystoid macular edema, herpes simplex keratitis and uveitis. These drugs are reported to the effectiveness of 10-20% for UV exposed brimatoprost, except in opaque bottles or latanoprost refrigerator. < / p> News CAIs have been developed which significantly systemic side effect profile as compared with oral counterparts. However, CAIS d the media are not as effective as oral medications. Dorzolamide and brinzolamide reduces IOP by about 15-24% and are not effective in all patients. serious side effects such as burning eyes, stinging, foreign body sensation, superficial punctate keratitis, etc. are noted. Moreover, could in some cases, sulfonamides, such as systemic effects can be determined. For these reasons, these drugs are used mainly as an alternative or third line treatment. / p> <
/ p> in the booster brimonidine (Brimodin) is just as effective, if used pilocarpine as adjunctive therapy with beta blockers, decrease the IOP by about 15% more. Dorzolamide timolol has no significant effect on IOP. Prostamides prostaglandins and can be used as second line treatment with beta-blockers (69), brimonidine (Brimodin), clonidine and representatives CAI can be used. Pilocarpine used if four times daily with latanoprost, provides further reduction in IOP. (71) Prostamides cause relaxation of the ciliary muscle and thus is pilocarpine / p> Much has been made in the diagnosis and treatment of glaucoma, but some cases can not be classified as suspect and marked medical care still remains a challenge. cholinergic effect and non-selective antagonist of the A-receptors have been replaced largely by new agents, better tolerated and have fewer side effects, ocular and systemic. Although antagonists of the beta-adrenergic antagonists are very effective in reducing IOP officers, the standard line of treatment in the last 20 years, but their side effects severe cardiopulmonary limitations of their use. Concept of apoptosis perfusion pressure, the papilla, neuroprotection, metabolic toxins, autoimmune processes and genetic mutation, a new dimension to the medical treatment of glaucoma has started. Brimonidine (Brimodin), an A-2 adrenergic receptor agonist, has a good” / p “‘tolerances