Glaucoma is a group of eye diseases characterized by progressive damage to the optic nerve, which transmits visual information from the eye to the brain. This damage results in irreversible vision loss, starting with the periphery and potentially leading to blindness. Low-Tension Glaucoma (LTG), also known as Normal-Tension Glaucoma, is a specific form where this nerve damage occurs even though the intraocular pressure (IOP) is consistently measured within the statistically normal range (typically 10 to 21 millimeters of mercury, or mmHg). Despite the normal pressure, LTG is a serious condition requiring specialized diagnosis and management to halt its progression.
Understanding Low-Tension Glaucoma
The pathology of Low-Tension Glaucoma involves the physical deterioration of the optic nerve head, leading to the distinct “cupping” appearance and loss of peripheral vision, similar to high-pressure glaucoma. The core issue is that the optic nerve is unusually vulnerable to stress, meaning that even statistically normal pressure is too high for that specific eye. Reduced blood flow (hypoperfusion) to the optic nerve is thought to play a significant role, making the nerve tissue sensitive to damage at lower pressures.
This inadequate blood supply may stem from systemic circulatory issues or localized vascular dysfunction. The condition often remains silent because initial vision loss affects the outer edges of the visual field, which the brain compensates for. Patients rarely experience symptoms until the disease is advanced and central vision is affected. Routine comprehensive eye examinations are necessary to detect LTG early before substantial vision loss occurs.
How Low-Tension Glaucoma Differs from Standard Glaucoma
The defining distinction between Low-Tension Glaucoma and Primary Open-Angle Glaucoma (POAG), the most common form, is the level of intraocular pressure (IOP). POAG is characterized by IOP consistently above 21 mmHg, where elevated pressure drives optic nerve damage. In contrast, LTG shows all signs of glaucomatous damage—optic nerve cupping and visual field defects—while the IOP remains below this threshold.
Since high pressure is not the main cause, LTG is strongly associated with non-pressure related factors pointing toward a vascular mechanism of damage. These systemic risk factors affect blood flow and circulation throughout the body. Examples include Raynaud’s phenomenon, migraine headaches related to vascular instability, and nocturnal hypotension (excessively low blood pressure during sleep). These factors introduce complexity to diagnosis and management, requiring a broader assessment of the patient’s overall health.
Identifying Low-Tension Glaucoma Through Testing
Diagnosis depends on confirming optic nerve damage typical of glaucoma while ruling out other causes of optic neuropathy. Since IOP is not elevated, the focus shifts to detailed structural and functional testing.
Visual Field Testing, or perimetry, maps the patient’s central and peripheral vision to identify characteristic patterns of vision loss. In LTG, these defects are often deeper, more focal, and located closer to the center of vision compared to POAG.
Ocular Coherence Tomography (OCT) provides a high-resolution image of the retina and measures the thickness of the Retinal Nerve Fiber Layer (RNFL). A thinning RNFL confirms the loss of nerve fibers and provides objective evidence of structural damage.
Pachymetry measures the thickness of the cornea. This is important because a thinner cornea can cause the pressure reading to be artificially low, potentially masking true high IOP. This measurement helps confirm the accuracy of the low IOP reading.
Finally, a comprehensive medical history is collected to screen for systemic vascular factors. These include a history of low blood pressure, migraines, or severe blood loss, which contribute to the optic nerve’s vulnerability.
Management and Treatment Options
Treatment for Low-Tension Glaucoma focuses on reducing intraocular pressure (IOP), even if it is already normal, and addressing associated systemic risk factors. The goal for IOP reduction is typically to achieve a pressure at least 30% below the patient’s baseline measurement. This significant reduction is necessary to slow or stop the progression of optic nerve damage.
Medication, usually topical eye drops, is the first-line treatment. Prostaglandin analogues are often used to increase the outflow of fluid from the eye. Brimonidine is also a preferred choice because it may offer a neuroprotective effect that benefits the nerve cells, which is desirable in LTG.
Beta-blockers must be used with caution. Their systemic effect of lowering blood pressure could reduce blood flow to the optic nerve, which is already compromised in LTG patients.
If topical medications fail, laser procedures such as Selective Laser Trabeculoplasty (SLT) can improve the eye’s natural drainage system. For advanced cases or when a very low target pressure is needed, filtering surgeries like trabeculectomy may be performed to create a new drainage channel.
Addressing non-pressure factors is also essential alongside IOP management. This often involves working with other medical specialists to manage conditions like nocturnal hypotension. The goal is to ensure that systemic blood pressure does not drop to a level that compromises the optic nerve’s blood supply.