Optic nerve damage

Adverse reactions associated with administration of the corticosteroid ophthalmic preparations include elevated IOP with optic nerve damage, loss of visual acuity, cataract formation, delayed wound healing, secondary ocular infection, exacerbation of comeal infections, dry eyes, ptosis, blurred vision, discharge, ocular pain, foreign body sensation, and pruritus. 

The goals of therapy are to prevent further loss of visual function minimize adverse effects of therapy and its impact on the patient s vision, general health, and quality of life control intraocular pressure in order to reduce or prevent further optic nerve damage and educate and involve the patient in the management of their disease. 

The goal of drug therapy in patients with glaucoma is to preserve visual function by reducing the IOP to a level at which no further optic nerve damage occurs. 

There is no specific target IOP because the correlation between IOP and optic nerve damage is poor. Typically, a 25% to 30% reduction is desired. 

Tolterodine can only affect the narrow-angle glaucoma (primary closed-angle glaucoma) and is contraindicated in uncontrolled cases of this type of glaucoma. It is therefore necessary to establish if the deterioration in the patient s vision is due to tolterodine use. In order to prevent optical nerve damage, an earlier appointment with the consultant is possibly warranted and therefore the patient should be advised to contact the consultant for further advice. 

SAFETY PROFILE Poison by ingestion. Moderately toxic by intraperitoneal route. Human systemic effects by ingestion change in central nervous system electrical function, optic nerve damage, and changes in vision. Experimental teratogenic and reproductive effects. Human mutation data reported. When heated to decomposition it emits very toxic fumes of Cl", I", and NOx. 

Jonas JB, et al. Ranking of optic disc variables for detection of glaucomatous optic nerve damage. Invest Ophthalmol Vis Sci 2000 41 1764-1773. 

Mechanisms that might contribute to optic nerve damage in glaucoma include ... 

Quigley HA, Addicks EM, Green WR, Maumenee AE (1981) Optic nerve damage in hnman glancoma. II. The site of injury and susceptibility to damage. Arch Ophthalmol 99 635-649. 

The syndrome includes headache, nausea and vomiting, dizziness, tinnitus, papilledema, and visual disturbances caused by scotoma or optic nerve damage. In babies, the first symptoms appear during the first 3 days of treatment while in older children and adults symptoms may not appear before a second or even later exposure. In adults, peripheral paresis or severe pyramidal and extrapyramidal symptoms, occasionally followed by a transitory psychosis, have been observed (7). 

The mechanisms through which the cannabis reduces intraocular pressure have not been determined. Cohen and Andrysiak (1982) suggested that cannabis dilates die vessels that drain excess fluids from the eyeball. This draining is thought to prevent fluid buildup and the resultant pressure that causes optic nerve damage. 

It is thought that high pressure within the eye (intraocular OP) is the main cause of the optic nerve damage. Although elevated IOP is clearly a risk factor, other factors must also be involved because even people with normal levels of pressure can experience vision loss from glaucoma. The Tajimi study in Japan revealed that a substantial number of... 

Tafluprost significantly increases retinal blood flow and blood velocity in animal models. The improvement of ocular blood flow is thought to be relevant in glaucoma therapy, especially for normal-tension glaucoma patients since it is assumed that optic nerve damage is involved not only in mechanical compression caused by IOPbut also in impairment of ocular blood flow. 

Fechtner RD, Weinreb RN. 1994. Mechanisms of optic nerve damage in primary open angle glaucoma. Surv Ophthalmol 39 23-42. 

The mechanism of lOP elevation in CAG is clearer than that of POAG. In CAG, a physical blockage of trabecular meshwork is present. In many cases, single or multiple episodes of excessively high lOP (>40 mm Hg) result in optic nerve damage. Very high lOP (>60 mm Hg) may resnlt in permanent loss of visual field within a matter of hours to days. 

The goal of therapy is to lower the lOP to a level associated with a decreased risk of optic nerve damage, usually at least a 20% if not a 25% to 30% decrease from the baseline lOP. Greater decreases may be required in high-risk patients or those with higher... 

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