Diagnosis History and clinical examination in NTG is similar to PAOG with special attention to some differences.
1) History
Special attention should be made to systemic associations and predisposing factors, including migraine, Raynaud’s phenomenon, episodes of shock, systemic hypotension and obstructive sleep apnea. All these factors may contribute to compromised ocular blood flow. (Kanski & Bowling, 2011).
2) Clinical examination
There is evidence that the left eye is 2.5 times more likely to be affected first. However, with increasing age, it becomes a bilateral disease. The IOP is within the normal range. The eye with the higher IOP usually corresponds to more glaucomatous damage. Although the IOP remains normal in most of the patients, …show more content…
(Firat et al., 2013). Also GCC loss was found to be more localized in NTG, compared to diffuse loss in PAOG. (Kim et al., 2013).
Differential Diagnosis:
1) POAG with apparently normal IOP due to diurnal fluctuation.
2) Previous episodes of high IOP due to trauma, uveitis or steroids therapy.
3) High IOP masked by systemic treatment, such as systemic beta blockers, started after glaucomatous damage has already happened.
4) Retinal nerve fiber layer defects due to myopic degeneration or optic disc drusen.
5) Congenital disc anomalies simulating cupping, such as disc pit or coloboma.
6) Neurological lesions causing compression on optic nerve or chiasma, and producing visual field defects simulating glaucoma. Therefore, neuroimaging is important if any suspicion arises.
7) Previous anterior ischemic optic neuropathy (AION), or optic nerve insult due to hypovolemia and shock. (Kanski & Bowling, …show more content…
Prostaglandin analogues are considered the gold standard for medical treatment of glaucoma. They are effective in IOP reduction with adequate diurnal control. Topical beta blockers have the risk of systemic hypotension, which is of particular concern in NTG. Topical alpha agonists were shown to have a neuroprotective effect in animal models. (Song & Caprioli, 2014).
Several prostaglandin analogues like travoprost 0.004% (Naito et al., 2016) and tafluprost 0.0015% (Keating, 2016) showed effective and sustained reduction of IOP. Combination of prostaglandin analogs with timolol also showed greater reduction of IOP than prostaglandin monotherapy. (Igarashi et al., 2014).
However, a study conducted on 4 prostaglandin analogues: latanoprost, travoprost, tafluprost, and bimatoprost, showed that up to 15% of NTG patients receiving prostaglandin analogues were non-responders. The percentage of non-responders was significantly lower with bimatoprost. (Inoue et al., 2016).
The Low-Pressure Glaucoma Treatment Study (LoGTS) followed up patients using either timolol or brimonidine as monotherapy for NTG. Patients on brimonidine showed lower incidence of visual field progression, although the reduction in IOP was similar between both groups. This could be related to the neuroprotective effect of brimonidine. (Krupin et al.,
1) History
Special attention should be made to systemic associations and predisposing factors, including migraine, Raynaud’s phenomenon, episodes of shock, systemic hypotension and obstructive sleep apnea. All these factors may contribute to compromised ocular blood flow. (Kanski & Bowling, 2011).
2) Clinical examination
There is evidence that the left eye is 2.5 times more likely to be affected first. However, with increasing age, it becomes a bilateral disease. The IOP is within the normal range. The eye with the higher IOP usually corresponds to more glaucomatous damage. Although the IOP remains normal in most of the patients, …show more content…
(Firat et al., 2013). Also GCC loss was found to be more localized in NTG, compared to diffuse loss in PAOG. (Kim et al., 2013).
Differential Diagnosis:
1) POAG with apparently normal IOP due to diurnal fluctuation.
2) Previous episodes of high IOP due to trauma, uveitis or steroids therapy.
3) High IOP masked by systemic treatment, such as systemic beta blockers, started after glaucomatous damage has already happened.
4) Retinal nerve fiber layer defects due to myopic degeneration or optic disc drusen.
5) Congenital disc anomalies simulating cupping, such as disc pit or coloboma.
6) Neurological lesions causing compression on optic nerve or chiasma, and producing visual field defects simulating glaucoma. Therefore, neuroimaging is important if any suspicion arises.
7) Previous anterior ischemic optic neuropathy (AION), or optic nerve insult due to hypovolemia and shock. (Kanski & Bowling, …show more content…
Prostaglandin analogues are considered the gold standard for medical treatment of glaucoma. They are effective in IOP reduction with adequate diurnal control. Topical beta blockers have the risk of systemic hypotension, which is of particular concern in NTG. Topical alpha agonists were shown to have a neuroprotective effect in animal models. (Song & Caprioli, 2014).
Several prostaglandin analogues like travoprost 0.004% (Naito et al., 2016) and tafluprost 0.0015% (Keating, 2016) showed effective and sustained reduction of IOP. Combination of prostaglandin analogs with timolol also showed greater reduction of IOP than prostaglandin monotherapy. (Igarashi et al., 2014).
However, a study conducted on 4 prostaglandin analogues: latanoprost, travoprost, tafluprost, and bimatoprost, showed that up to 15% of NTG patients receiving prostaglandin analogues were non-responders. The percentage of non-responders was significantly lower with bimatoprost. (Inoue et al., 2016).
The Low-Pressure Glaucoma Treatment Study (LoGTS) followed up patients using either timolol or brimonidine as monotherapy for NTG. Patients on brimonidine showed lower incidence of visual field progression, although the reduction in IOP was similar between both groups. This could be related to the neuroprotective effect of brimonidine. (Krupin et al.,