NORMAL-TENSION RISKS

Apart from having a normal intraocular pressure (IOP), there is as yet no known diagnostic feature of normal-tension glaucoma (NTG) that separates it from high-tension glaucoma. However, some research suggests that vascular disease may play a direct or indirect role in some patients with the condition, said Antonio Fea MD, PhD, University Eye Hospital, Torino, Italy.
“There are two families of low-tension glaucoma, one which is probably more atherosclerotic and which has a slower pace of progression but which at the same time does not respond very well to IOP reduction, and another family that has a more vasospastic type of disease and responds better to IOP-lowering therapy,” Dr Fea told a session of the 11th European Glaucoma Society Congress in Nice.
He noted that optic nerve head pathology of both high- and normal-tension glaucoma share the same characteristic features. However, some features, like disc haemorrhages, pits and notches, occur more commonly in NTG.
In terms of visual field loss, again there are no diagnostic features to distinguish normal-tension from high-tension glaucoma, although as a rule, visual field loss in NTG tends to be more localised, denser in the superior quadrant and more prominent in the lower hemifield.
Localised deterioration
In addition, visual field loss in NTG tends to progress more slowly than high-tension glaucoma. A study into the natural history of the disease showed that after seven years only half of the cases had a confirmed localised deterioration. However, the rate of progression varied significantly between patients, ranging from -0.2dB to -2dB.
Although IOP is at normal levels in NTG, IOP is nonetheless an important factor in the disease. Research has shown that NTG patients in whom treatment brings about a 30 per cent reduction in IOP will have a better preservation of their visual field than untreated patients (Am J Ophthalmol. Jan 1999;127(1):120).
The more recent Low-Pressure Glaucoma Treatment Study (LOGTS) yielded similar results and showed that risk factors for progression included lower mean ocular perfusion pressure and the use of systemic antihypertensive agents (Krupin, Am J Ophthalmol. April 2011;151(4):671-681).
The LOGTS study also famously demonstrated that there was less progression among patients receiving brimonidine than in those receiving timolol, despite both groups achieving the same IOP reduction, suggesting that brimonidine may have a neuroprotective effect.
Dr Fea noted that several studies have shown that glaucoma patients have a lower cerebral spinal fluid pressure and a higher trans-lamina cribrosa pressure difference when compared to those without glaucoma.
“The cerebrospinal fluid is correlated to blood pressure, so it might be that in some way some of the circulatory issues that we are seeing in NTG are related to this parameter more than the circulation itself,” he added.
Dr Fea also highlighted that, although it is not included in the guidelines for the diagnosis of NTG, progression should be considered essential in the diagnosis of the disease because several other entities may mimic both the visual field defect and the optic nerve appearance.
Antonio Fea: antoniofea@interfree.it
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