Glaucoma describes a group of eye conditions that damage the optic nerve, the bundle of nerve fibers transmitting visual information to the brain. This damage typically leads to progressive, irreversible vision loss. The most recognized risk factor is elevated intraocular pressure (IOP), the fluid pressure inside the eye. However, many individuals experience optic nerve damage despite having an IOP that consistently falls within the normal range (21 mmHg or lower). This specific condition is known as Low-Pressure Glaucoma (LPG) or Normal-Tension Glaucoma (NTG), and its paradoxical nature makes diagnosis and management challenging.
Defining Low-Pressure Glaucoma
Low-Pressure Glaucoma (LPG) is defined by characteristic optic nerve damage and visual field loss in patients whose intraocular pressure (IOP) never exceeds the conventional upper limit of 21 mmHg. Diagnosis requires ruling out secondary causes of nerve damage and confirming that the eye’s drainage angle is open. Many experts consider LPG a form of Primary Open-Angle Glaucoma (POAG) that simply occurs at the lower end of the pressure spectrum.
The standard IOP range is 10 to 21 mmHg, meaning LPG damage occurs even when pressure readings are in the mid- to low-teens. The resulting optic nerve damage is indistinguishable from that caused by high pressure, presenting as a loss of retinal ganglion cells and thinning of the nerve fiber layer. The key difference is the consistent finding of normal pressure measurements over time. Patients with LPG sometimes show unique clinical signs, such as small hemorrhages on the optic nerve head, which occur more frequently than in POAG.
Identifying the Symptoms and Risk Factors
Individuals affected by Low-Pressure Glaucoma typically do not experience noticeable symptoms early on. Progressive damage causes a gradual loss of peripheral vision first, which often goes undetected because the brain compensates for the missing information. Significant vision loss is usually only detected when the damage is advanced or affects the central visual field.
Since high IOP does not cause LPG, research focuses on non-pressure related factors. A leading theory involves vascular dysregulation, suggesting that unstable blood flow deprives the optic nerve of necessary oxygen and nutrients. Systemic conditions associated with LPG include migraine headaches, Raynaud’s phenomenon, and low systemic blood pressure. These are often grouped under Primary Vascular Dysregulation Syndrome (Flammer syndrome), which predisposes individuals to poor microvascular circulation.
Nocturnal hypotension, an excessive drop in systemic blood pressure while sleeping, is an important risk factor. This dip can severely compromise ocular perfusion pressure—the difference between the pressure pushing blood into the eye and the pressure inside the eye. When perfusion pressure drops too low, the blood supply to the optic nerve head can be temporarily interrupted, leading to ischemic damage. Structural weakness of the optic nerve tissue is also considered a contributing factor, making the nerve vulnerable even to normal pressure forces.
Diagnostic Procedures and Testing
Diagnosing Low-Pressure Glaucoma requires a comprehensive evaluation to confirm optic nerve damage while ruling out pressure spikes and other neurological causes. The initial step is tonometry, the measurement of intraocular pressure (IOP). Because IOP naturally fluctuates, multiple measurements are taken at different times, sometimes extended to 24-hour monitoring, to ensure no pressure spikes are missed.
Visual field testing (perimetry) maps the extent and pattern of vision loss, assessing function and tracking disease progression. To objectively measure structural damage, Optical Coherence Tomography (OCT) is used. OCT provides high-resolution images that precisely measure the thickness of the Retinal Nerve Fiber Layer (RNFL), identifying thinning indicative of nerve cell loss.
Pachymetry, the measurement of corneal thickness, is also performed, as a thinner cornea can lead to an artificially low tonometry reading. A neuro-imaging study, such as a brain MRI or CT scan, may be required to exclude non-glaucomatous causes of optic nerve damage, such as tumors or neurological conditions that mimic glaucoma. This thorough process ensures the damage is correctly attributed to LPG.
Current Treatment Approaches
The primary treatment for Low-Pressure Glaucoma remains the reduction of intraocular pressure (IOP). Studies show that lowering IOP, even from a normal baseline, can slow or halt the progression of vision loss. The target pressure is often set aggressively, aiming for a reduction of at least 30% below the patient’s pre-treatment baseline IOP.
Pressure reduction is typically achieved using prescription eye drops, such as prostaglandin analogs, which enhance fluid outflow. Medications like the alpha-adrenergic agonist brimonidine may be favored for their potential neuroprotective benefits beyond simple pressure lowering. If eye drops are insufficient, procedures like laser therapy or filtration surgery may be performed to achieve the required low target pressure.
Treatment also involves addressing systemic vascular risk factors. Collaboration between the ophthalmologist and the primary care physician is necessary to manage systemic blood pressure, especially nocturnal dips. Care must be taken to ensure blood pressure medications do not cause excessive drops at night, which could worsen ocular perfusion pressure and accelerate optic nerve damage. Regulating these systemic factors is integral to stabilizing the condition and preserving vision.