What Is Normal-Tension Glaucoma?

At present, normal intraocular pressure glaucoma refers to optic disc damage similar to other glaucoma, retinal nerve fiber layer defects and corresponding visual field damage. Without any intraocular pressure-reducing drug, the intraocular pressure does not exceed 21mmHg in 24 hours. The structure is normal and completely open, and there is no other eye and systemic glaucoma that may cause the above diseases.

Basic Information

nickname

Hypotonic glaucoma

English name

normal tension glaucoma

English alias

low-tension glaucoma)

Visiting department

Ophthalmology

Common causes

It is related to genetic factors, vascular diseases and local anatomic factors.

Common symptoms

Sore eyes, bloating, eye pain, easy fatigue with eyes, etc.

Causes of normal intraocular pressure glaucoma

It is related to genetic factors, vascular diseases and local anatomic factors.

Clinical manifestations of normal intraocular pressure glaucoma

Medical history

The incidence of normal intraocular pressure glaucoma is concealed, and most of them have no obvious conscious symptoms in the early stage, such as acid eyes, eye swelling, eye pain, and easy fatigue with the eyes. Vision loss or visual impairment, because these patients have normal intraocular pressure, and central vision is usually better without other eye diseases. Therefore, if the disc, cup, retinal nerve fiber layer and visual field cannot be checked in detail and closely followed up It is easy to miss the diagnosis, and many patients are found during routine fundus examinations or routine health examinations for other eye diseases.

Some NPG patients have myopic refractive error, hypotension, and other systemic vascular disorders, such as migraine, diabetes, etc. A few patients have hemodynamic crisis, such as acute hypotension caused by shock, myocardial infarction, and major bleeding. History, but there are many patients who do not have the above medical history, and the family history of NPG patients is difficult to study, but there are still many studies that report that NPG patients have a strong family genetic tendency, and there are often multiple NPG and HPG patients in the same family, suggesting that both There is an unknown relationship.

2. Signs

It mainly focuses on the following 4 aspects:

(1) Although the intraocular pressure of normal intraocular pressure glaucoma is in the normal range, but the specific levels are different. Clinically, the intraocular pressure level in different patients is close to the upper limit of the normal range and close to the lower limit. The average is around 16mmHg. It is the average value of the intraocular pressure range of the normal population. Foreign literature reports that the intraocular pressure of most patients is close to the upper limit. From a physiological point of view, whether the intraocular pressure is normal, in addition to the absolute value, is also reflected in the fluctuation range of the diurnal curve and the symmetry of the eyes. In terms of sex, etc., so far, it has mainly focused on its highest value. Most of the peak intraocular pressure is believed to occur at night, because the position of the sleeping state causes the suprascleral venous pressure to increase. As for the latter two indicators, from the limited clinical data, The patient's diurnal IOP distribution is symmetrical in both eyes, and the wave shape is a unimodal curve. The difference between the highest value and the lowest value is about 4mmHg. The performance of IOP in normal tonoscopy glaucoma is completely consistent with the physiological state of normal IOP in the general population. To remain normal and stable during the course of the disease.

(2) Fundus changes Fundamental changes are structural changes, including changes in the optic disc and RNFL. There are similarities and differences in fundus changes between normal intraocular pressure glaucoma and HPG. The results of various studies are different. In normal intraocular pressure glaucoma, Optic disc damage is more commonly manifested as disc narrowing and notching, and lateral disc choroidal retinal atrophy (PPCA) and disc bleeding. Clinically, disc bleeding is relatively common in optic pressure glaucoma optic disc damage, sometimes it is The earliest visible sign can be recurring. It is more common in the subtemporal or superior temporal disc area of the optic disc, which is a strip or flame. Riding across the disc margin, bleeding and its repeated indications of the occurrence or progression of optic nerve tissue damage. In some studies, normal intraocular pressure glaucoma is divided into two cases according to the optic disc performance: senile sclerosis is mainly seen in elderly patients with vascular disease, and the pale edge is pale shallow slope. Focal ischemic type There are focal deep notches along the disc, located at the upper pole or lower pole.

(3) Visual field damage Visual field damage is a functional damage. There is no difference in the location and morphology of normal visual pressure glaucoma and HPG, and there is no consensus so far. Compared to HPG, normal visual pressure glaucoma has more early visual field defects. It is focal, more dense, the border is steeper, and the part is closer to or even invades the central fixation zone.

(4) Room angle For normal intraocular pressure glaucoma, the room angle is undoubtedly open. From the pathophysiology analysis of the aqueous humor circulation, if the room angle is closed as a cause in advance, it is impossible to have a "normal IOP" as a result. It should be noted that there are two cases in which the angle of the opening of the room can be "wide" or "narrow" anatomically.

Acquired acquired POAG-like optic disc changes, retinal nerve fiber layer damage, and visual field damage. The intraocular pressure measurements within 24 hours before treatment were 21mmHg (2.79kPa), and the angle of the chamber was open, excluding optic nerve damage, visual field defects, and temporary Other ocular or systemic causes of hypotensive intraocular pressure can establish a diagnosis.

Normal intraocular pressure glaucoma

Immunological abnormalities: NPG patients have a higher incidence of immune-related diseases, such as hypothyroidism, arthritis or Raynaud's disease, etc. Some people have found that abnormal complement factors are higher in NPG patients, but some scholars have failed to confirm autoimmunity. The disease is related to glaucoma.

Fundus fluorescein angiography

Fundus fluorescein angiography (FFA) shows that most patients with NPG have filling defects in the optic cup, and most of them show segmental weak fluorescence, indicating that there is optic disc ischemia. Corresponding disc cuts often appear at the site of staged fluorescent filling defects. And retinal nerve fiber layer defect, and the filling defect of the optic disc appeared before the visual field damage.

2. Eye blood flow examination

Earlier scholars reported that the ocular arterial pressure and diastolic blood pressure in patients with NPG were lower than those in suspected glaucoma. It was also reported that the diastolic perfusion pressure in NPG patients may be low. Later, it was thought that the ocular arterial pressure and perfusion pressure in NPG patients were not significantly different from those in normal people. The difference is that the perfusion pressure is easily affected by blood pressure, and the ciliary choroidal blood vessel resistance measured according to the pulsation amplitude and arterial blood flow of the eye artery can better reflect the blood supply. Some studies have shown that the eye pulse amplitude of NPG patients is lower than that of normal eyes. The resistance of the ciliary choroidal vascular network is 2 to 3 times higher than that of normal people, and the blood flow is reduced due to the increase in resistance. Some scholars have reported that the eye pulse amplitude of NPG patients is not different from that of normal people. At present, the eye blood flow of NPG patients There is no more consensus, and the results reported by different companies are not very consistent, but most studies believe that the eye blood flow of NPG patients may be lower than that of normal people.

3. Excitation test

Provocation tests for NPG patients include corticosteroid booster test, drinking test, and cold stimulation challenge visual field test. The cold stimulation challenge test compares the patient's normal field of vision with the field of vision of a hand or foot after being placed in 4 ° C cold water for 10 minutes. The average defect reduction was 10% positive, and about 25% of NPG patients had a positive response. Because this test can detect the tension of the blood vessels, it may help determine whether the use of vasodilators is effective in NPG patients.

4. Other eye characteristics

The prevalence of myopia, especially high myopia, in NPG patients is higher than that in normal people and patients with primary open-angle glaucoma, and the posterior segment of the eyeball is larger than that of normal people. With a larger cup-to-disk ratio and greater susceptibility to glaucoma damage, patients with high myopia due to enlarged eyeballs, the optical disk is irregularly stretched and extended, resulting in abnormal shape of the optical disk, enlarged and tilted, and the pulling effect is reduced The tolerance threshold of the sieve plate to the intraocular pressure injury makes the intraocular pressure between or close to physiological values sufficient to cause damage to the optic disc and retinal nerve fibers.

5. General condition

(1) Whether the optic nerve damage in blood pressure NPG patients is related to abnormal blood pressure is inconclusive. People with low blood pressure, especially those with low diastolic blood pressure or normal blood pressure, are more common in patients with NPG than other types of glaucoma patients, and patients with NPG have acute low blood pressure. The incidence of blood pressure history or hemodynamic crisis was higher than that of NPG control group.

(2) Vascular diseases It is generally believed that NPG is related to vascular diseases. The incidence of cardiovascular and cerebrovascular diseases in NPG patients is significantly higher than that in normal people. Carotid artery disease (stenosis or calcification) is closely related to NPG. Flow confirms that decreased blood flow to the eye is associated with optic nerve damage, but the relationship between the two is not well understood.

(3) Hemorheology Studies have shown that the whole blood viscosity, plasma viscosity, and hematocrit of NPG patients are higher than those of normal people, and the incidence of abnormalities of the coagulation and fibrinolytic system is also high, and the blood is hypercoagulable.

Diagnosis of normal intraocular pressure glaucoma

(I) NPG diagnostic criteria in 8 countries including the United States and Japan

1. Goldmann applanation tonometer for 24h IOP 22mmHg, no record of IOP exceeding 24mmHg;

2. Corner angle examination showed wide angle of both rooms;

3. After stopping all IOP or systemic drugs for 1 month, at least two 24h IOP measurements, peak IOP 22mmHg, each time average value <20mmHg, and at least 4 from 5:00 pm to 7:00 am Times measurement

4 Typical glaucomatous optic disc changes;

5. Typical glaucoma visual field defect;

6. No other eye diseases that cause changes in the optic disc and visual field;

7. X-ray, CT, MRI, etc. showed no abnormalities in the skull and orbit;

8. Exclude neurological diseases, no hypotension.

(2) The diagnostic criteria for the glaucoma group of Moorfields Eye Hospital in the UK are as follows

1. The untreated 24h mean IOP is less than or equal to 21mmHg, and no IOP is greater than 24mmHg;

2. Corner is open;

3. There are no secondary causes of glaucomatous optic neuropathy, such as previous traumatic intraocular pressure increase, long-term history of corticosteroids, uveitis, etc .;

4. There is typical optic disc damage (glaucoma cup formation and disc edge loss);

5. Visual field defect consistent with glaucoma optic cup;

6. Glaucoma damage is progressive.

Treatment of normal intraocular pressure glaucoma

Reduce intraocular pressure

Although the disease of most NTG patients is progressive, some patients can be stable for a long period of time. It has been suggested that patients with a stable condition can be observed regularly every six months to a year. If the condition develops, consider medication, because of glaucoma Longer duration of medication may sometimes require lifelong medication, which can reduce the adverse consequences caused by prolonged medication and side effects. It is also believed that intraocular pressure is a major risk factor leading to the development of lesions. Lowering intraocular pressure can protect the optic nerve. Without treatment, due to various reasons, the patient's compliance with follow-up is reduced. Once the follow-up is lost, The consequences are unimaginable. In addition, there are still some unpredictable factors, such as how long this stability can be maintained, when it develops, how fast it develops, whether the stability after treatment is natural or drug, and before these unknown factors are not clear, active treatment It is more stable. During the treatment process, regular follow-up should be performed, and the type and dose of the drug should be adjusted according to the situation. Surgery should be considered when the drug treatment fails. Patients with vascular risk factors, such as hypertension, hypotension, diabetes, abnormal blood rheology, vasospasm, and elderly NTG patients, should be treated in a timely manner. Although the effect of drug treatment is not satisfactory, there is currently no better option.

(1) Drug treatment The effect of reducing the intraocular pressure of NTG with drugs is not ideal. In the normal range of intraocular pressure, it is difficult to reduce the average intraocular pressure by 30% even with the maximum tolerated drug. Conventional medication can only Reducing the intraocular pressure by 2.5mmHg can reduce the intraocular pressure of 44% of NTG patients by up to 20%, so it cannot effectively prevent the development of the disease. In addition, commonly used -blockers such as timolol, betagan, etc., mainly By inhibiting the production of aqueous humor and reducing intraocular pressure, in addition to lowering blood pressure, slowing heart rate, and inducing asthma, it may also reduce blood flow in the eye. The safety of long-term use is worth considering. 1-blockers such as shellfish Special (Betarolol hydrochloride), which has less effect on cardiopulmonary function, can increase eye blood flow and neuroprotection, and is relatively safe. At present, some prostaglandin preparations such as Shilida (latanoprost) and Suweitan (travoprost) have a good effect on reducing intraocular pressure. By increasing the drainage of aqueous humor in the uveal scleral channel, the intraocular pressure can be reduced. It has little effect on the production of aqueous humor and the dynamics of aqueous humor. It can be used once a day to improve medication compliance. Local side effects are mainly irritation symptoms, conjunctival hyperemia, deepening of iris pigments, darkening and lengthening of eyelashes. Macular cystoid edema and allergic reactions mostly do not affect the treatment effect, and have less systemic side effects, such as increased upper respiratory infections, chest pain, joint pain, etc., are relatively safe to use, and it has been reported that intraocular pressure can be reduced by 21% after one day of dripping POAG and ocular hypertension can be reduced by 30%. Studies have shown that Shilida and Timoxan have a synergistic effect, 0.5% Timoxan drops twice a day, 0.005% Shilida drops once a day can make the eyes The pressure is reduced by 30%.

(2) Surgical treatment Surgical treatment should be considered when drug treatment cannot control the development of the condition. Argon laser miniplasty can effectively reduce the intraocular pressure by about 4mmHg. There are also reports that the intraocular pressure can be reduced to 12mmHg. However, strict control of laser energy, spot size, number and location is required. The disadvantage is that there may be sharp intraocular pressure in the short term after surgery. Increase, long-term (2 to 3 years) effect is not stable enough. Filtering surgery, such as trabeculectomy, should be considered when drug treatment and laser treatment cannot prevent the development of the disease, which can effectively reduce intraocular pressure by 30%. At the current level of technological development, the success rate of surgery has been greatly improved. It can effectively prevent optic nerve damage. It is necessary to know that any surgery has certain risks, and filtering surgery is no exception, such as postoperative scar adhesion, thin filtering bubbles, ruptured follicles, and intraocular infections. Because surgery cannot be accurately quantified, a few Patients may have low intraocular pressure (IOP below 8mmHg) after surgery. Low IOP can still be compensated in a short period of time (within 5 months). If IOP is lower than 6mmHg, a longer period of time can cause intraocular veins to expand and tissues Edema, macular edema, choroidal retinal detachment, and abnormal nutritional metabolism in the eye can also cause corneal sclera collapse and vision loss. Patients with low intraocular pressure before surgery should be carefully considered. Although the incidence of postoperative complications is low and there are remedial measures, it will affect the surgical effect to a certain extent.

2. Other adjunctive therapies

For patients with normal intraocular pressure glaucoma, especially in the middle and advanced stages, when the intraocular pressure drops to an acceptable level, attention should be paid to the medical treatment of relevant risk factors, while giving nutritional nerves and drugs to improve blood flow. Calcium channel blockers (Nimodipine Equality) can improve optic nerve function and blood flow. Studies have shown that patients with systemic calcium channel blockers have improved contrast sensitivity or reduced visual field damage after treatment. However, some studies have failed to confirm the above effects, and the systemic application of calcium channel blockers has adverse effects on blood pressure in patients, and the incidence is high. In view of this, calcium channel blockers should be used only after the patient's condition has deteriorated despite local drugs and surgery. In addition, the selective beta ₁ blocker, Betaxon, not only has a certain effect on reducing intraocular pressure, but also improves optic nerve blood flow, thereby protecting the visual field. Compared with systemic calcium channel blocker therapy, it has greater safety and can be used when necessary. Optional.