Low tension glaucoma (LTG), also known as normal tension glaucoma (NTG), is a condition where the optic nerve is damaged, leading to progressive vision loss. Glaucoma is generally defined by the gradual deterioration of the optic nerve, which transmits visual information to the brain. In LTG, however, this damage occurs despite the internal eye pressure being within the statistically normal range. Confirming the diagnosis requires a detailed process to distinguish it from other causes of nerve damage.
The Paradox of Normal Eye Pressure
Glaucoma is primarily characterized as a disease of high intraocular pressure (IOP), which physically stresses the optic nerve fibers. The standard range for a “normal” IOP is considered to be between 10 and 21 millimeters of mercury (mmHg). In the most common form, Primary Open-Angle Glaucoma (POAG), the IOP is consistently above this threshold, causing the damage.
LTG patients, by contrast, have IOP measurements that never exceed 21 mmHg and are often in the mid-to-low teens. The existence of nerve damage at these safe pressure levels suggests the optic nerve is either unusually vulnerable or that other, non-pressure factors are causing the damage. Because a routine eye check may not flag any pressure concerns, the condition can be overlooked until significant vision loss has occurred.
The visual field defects in LTG often present closer to the center of vision than in POAG, which affects peripheral vision earlier. A common finding in LTG is the presence of small hemorrhages on the surface of the optic disc, known as splinter hemorrhages. These differences in clinical presentation suggest that LTG may represent a distinct variant of the disease, even though it is often treated similarly to POAG.
Non-Pressure Factors Contributing to Optic Nerve Damage
Research into LTG focuses on factors that compromise the optic nerve’s health independent of IOP, primarily vascular dysregulation (poor or unstable blood flow). The nerve’s high metabolic demand makes it sensitive to fluctuations in oxygen and nutrient supply.
Systemic issues, such as low nocturnal blood pressure, are a concern because they can lead to hypoperfusion, or reduced blood flow, to the optic nerve while a person sleeps. This drop in blood pressure, particularly the diastolic reading, can be a risk factor for progression in LTG patients. Another linked phenomenon is vasospasm, where blood vessels temporarily constrict, which is seen in associated conditions like migraine headaches and Raynaud’s phenomenon.
The structural vulnerability of the optic nerve itself also plays a role. It is theorized that some individuals have a naturally weaker structure that cannot withstand even normal forces. Genetic predisposition is a factor, as a family history of glaucoma increases the risk, and LTG is prevalent in certain populations, such as those of Japanese ancestry. Other non-IOP mechanisms studied include chronic inflammation, oxidative stress, and autoimmune responses.
The Diagnostic Process
A diagnosis of LTG is not made solely by a normal IOP reading. The first step involves a comprehensive eye examination to rule out other, non-glaucomatous causes of optic nerve damage, such as tumors, past trauma, or systemic neurological disorders that can mimic glaucoma. True LTG is considered a diagnosis of exclusion.
Specialized testing documents the characteristic structural and functional damage. Visual field testing assesses the extent of vision loss, which typically presents as arcuate defects closer to the center of fixation in LTG than in other forms of glaucoma. This functional test is complemented by advanced imaging of the optic nerve.
Optical Coherence Tomography (OCT) measures the thickness of the retinal nerve fiber layer (RNFL), which thins as the disease progresses. OCT can detect the specific arcuate patterns of nerve loss associated with LTG, often before visual field changes are noticeable. Doctors may also recommend 24-hour IOP monitoring, which sometimes reveals pressure spikes that occur outside of a standard office visit, particularly at night.
Treatment and Long-Term Management Strategies
The primary goal of managing LTG is to lower the IOP to a level that prevents further optic nerve deterioration. Even though the pressure is in the normal range, clinical trials show that reducing the IOP still slows or halts the progression of the disease. Physicians often aim for an IOP reduction of at least 20 to 30 percent below the patient’s baseline pressure.
Achieving this target often requires medicated eye drops (the first-line treatment), with laser or surgical procedures reserved for insufficient cases. The target IOP is frequently set in the low teens or high single digits, sometimes as low as 8 to 12 mmHg, depending on the damage severity.
Management also involves addressing the non-pressure risk factors contributing to the condition. This includes collaboration with a primary care physician to manage systemic issues like nocturnal hypotension or severe migraines. Some medications, such as the alpha-2 agonist brimonidine, have been studied for potential neuroprotective effects, meaning they may protect nerve cells independent of their pressure-lowering ability. Consistent monitoring of the optic nerve and visual fields is necessary to ensure the treatment is stabilizing the condition.