NORMAL TENSION GLAUCOMA
Signs and Symptoms
The pathophysiological process underlying NTG is unclear and is, at best, speculative. For quite some time, it was unclear if IOP played a role in the pathogenesis of NTG or whether IOP reduction benefited patients with the condition. However, results of the Collaborative Normal Tension Glaucoma Study (CNTGS) indicated that IOP played at least a role in the development of NTG, and IOP reduction without causing cataracts could benefit a number of patients at risk of progression.4,5 Patients determined to be more at risk of progression included females, migraine suffers (many of whom were female), and those manifesting a disc hemorrhage.6 Interestingly, older age, higher average IOP, and field loss threatening fixation were not seen as risk factors for progression.6
While there has been some thought that NTG was a vascular perfusion problem, new research seems to indicate a potential autoimmune involvement in pathogenesis. Patients with NTG may have increased prevalence of monoclonal paraproteinemias.7 Paraprotein-emias have been seen in patients with peripheral motor and sensory neuropathies and are considered causative agents in several peripheral neuropathies in which antineuronal targets of these proteins have been identified.8 Kremmer and associates found greater incidence of antiphospholipid antibodies (particularly IgG anticardiolipin antibodies) in patients with NTG compared to those with POAG and age-matched control patients.9
Wax and associates10 and Tezel and associates11 found that serum from patients with NTG contained high titers of antibodies against retinal proteins, including rhodop-sin and heat shock proteins (HSP). HSPs are a family of cellular chaperone proteins considered neuroprotective because their expression is induced in neurons to ameliorate damage caused by various stress conditions, such as ischemia and excitotoxicity. Heat shock proteins are significant autoantigens and have been implicated in a number of human autoimmune diseases.
Before embarking on any therapeutic management of patients suspected of having NTG, remember that many other conditions can be confused with and misdiagnosed as NTG. These include congenital nerve anomalies such as tilted disc and morning glory syndrome, chronic angle closure, compressive lesions, and undiscovered POAG. The thorough examination includes gonioscopy to eliminate angle closure as a possibility and pachymetry to identify thin corneas (which by themselves may offer increased risk as well as the possibility that they may cause falsely lower IOP measurements). If the disc is unusual, a second opinion may be warranted to identify possible congenital anomalies.
Should NTG be strongly suspected, early treatment may not be prudent. Results of the CNTGS have shown that NTG is slowly- or non-progressive in the majority of cases. Thus, those patients destined to be slowly progressive or non-progressive derive no benefit from treatment, only risks. It is advocated that patients with NTG be observed for a period to establish the rate of progression or stability in each individual patient.6 Patients who manifest risk factors for progression such as migraine and disc hemorrhage may need to be monitored more closely. When progression has been conclusively demonstrated, IOP-lowering therapy may be initiated. However, should fixation be split or threatened, early treatment may be employed, though the CNTGS has shown that these patients are at no greater risk of progression. A 30% reduction in IOP from the mean baseline is advocated by most. Medications that have been typically avoided are the beta-blockers and alpha-adrenergic agonists, mostly due to a fear of diminishing perfusion to the optic nerve. It is interesting to note that the CNTGS avoided these medications. Brimonidine, however, has been used recently due to a perceived (though not clinically proven) neuroprotective effect. Prostaglandins have been recently advocated in the management of NTG, as they have the potential to lower IOP within the statistically normal range demonstrated in NTG. Pressure reductions of 15% to 30% have been seen in NTG in response to prostaglandin therapy.12,13
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Neuro-Ophthalmic Disease | Oculosystemic Disease
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