Normal tension glaucoma

Introduction to normal tension glaucoma Normal tension glaucoma is also known as low intraocular pressure glaucoma. It is a glaucoma with typical glaucomatous papillary lesions and visual field defects, open angles, and intraocular pressure always within the normal range of statistics. More common in people over the age of 40, single or double eyes. Normal tension glaucoma is an open-angle glaucoma with normal intraocular pressure. The pathogenic factors are complex and the exact cause is still unclear. Many studies have shown that the disease is associated with systemic cardiovascular disease, hypotension, anemia, or other blood abnormalities. Because the disease has no symptoms, it is not easy to find early. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: myopia

The cause of normal tension glaucoma

(1) Causes of the disease

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

(two) pathogenesis

The statistics of intraocular pressure in the normal group showed that the intraocular pressure level was not the standard normal distribution, but was slightly left-biased, especially in people older than 40 years. The normal or not the intraocular pressure was no longer based on the normal range of general population statistics. The meaning of the need to pay attention to "individual tolerance to intraocular pressure", therefore, for any patient, the normal intraocular pressure is defined as not exceeding the upper limit of the normal group of intraocular pressure statistics, has a strong human nature, and, in turn, consider The span of the normal range is 10 to 21 mmHg (the upper limit is twice the lower limit), and it is obviously biased to measure the normal or not the intraocular pressure of all patients by the upper limit.

Normal tension glaucoma challenges the traditional theory of "causal relationship between elevated intraocular pressure and optic nerve damage" and is considered a supporter of vascular or ischemic theory, but the ischemic theory itself is characterized by pathophysiology of the optic nerve. Sexual damage can not give a reasonable explanation. Perhaps the role of vascular lesions is only to reduce the resistance of the optic nerve to stress damage. In recent years, basic research has shown that the pathological changes of optic nerve damage are essentially retinal ganglion cell apoptosis. Clinical studies have shown that optic nerve damage in normal tension glaucoma is also intraocular pressure-dependent. Analysis of various research results to date: histological differences in the discs and their developmental defects and degenerative changes and their relationship with intraocular pressure The imbalance of relationship may be the initial factor of optic nerve damage in normal tension glaucoma, that is, the structure of the upper and lower areas of the sieve is so weak that it can not withstand the normal level of intraocular pressure, resulting in axoplasmic transmission block here, which leads to brain source. Deprivation of the neurotrophic factor, the results start the apoptosis of the ganglion cells in the upper and lower arcuate regions, in the fundus Presented on the upper and lower arcuate cross-sectional morphology of the nerve fiber layer defect region and narrowing down optic disc along the longitudinal expansion of the optic cup and deeper, as presented visual field defects and corresponding parts functionally form.

Regarding the pathogenic gene of normal tension glaucoma, the optic neuropathy-inducible protein gene (optinurin, OPTN) was found in 2002, and the gene locus was 10p13. In addition, the GLCIE discovered in 1998 belongs to the normal open-angle type with normal intraocular pressure. For glaucoma, the gene locus is 10p14~p15.

Normal tension glaucoma prevention

1. Pay attention to proper rest, do not master the combination of movement and static, rest well, is conducive to the recovery of the body; exercise can enhance physical strength and enhance disease resistance, and the combination of the two can better recover.

2. Continue taking the medicine and take care of it.

3. It is very important to maintain a good attitude, to maintain a good mood, to have an optimistic, open-minded spirit, and to be confident in the fight against disease. Don't be afraid, only in this way can you mobilize your subjective initiative and improve your body's immune function.

4. Appropriate nutrient supply, under today's living conditions, it is not appropriate to emphasize too much high sugar, high protein, high vitamin and low fat diet. However, the nutrition should be balanced, and the vegetarian diet should be accompanied by vegetables, fruits, meat, egg milk, etc. The intake is determined by the fatness of the person.

Normal tension glaucoma complications Complications

Optic disc hemorrhage, retinal nerve fiber layer defects, etc.

Symptoms of normal tension glaucoma Common symptoms Internal oblique A sign of visual impairment Eye dryness, soreness, fatigue, fundus changes, eye pain, sudden increase in visual pressure, visual field defect, eye swelling

The clinical manifestations of normal tension glaucoma are similar in all respects to HPG except for no increase in intraocular pressure.

Symptom

The incidence of normal intraocular pressure glaucoma is concealed. Most of the early cases have no obvious symptoms, such as eye acid, eye swelling, eye pain, and easy fatigue with the eye. Patients often visit for other reasons. In the late stage, when the visual field is seriously deficient, the patient can complain. Vision loss or visual impairment, because these patients have normal intraocular pressure, and the central vision is often better without other eye diseases, so if the optic disc, cup, retinal nerve fiber layer and visual field can not be examined in detail and closely followed up observation It is easily missed, and many patients are found during routine fundus examinations or routine health examinations for other eye diseases.

Some patients with NPG have myopic refractive error, hypotension and other systemic vascular diseases, such as migraine, diabetes, etc., a few patients have hemodynamic crisis, such as shock, myocardial infarction, major bleeding and other acute hypotension History, but there are many patients without the above medical history. Family history studies of NPG patients are difficult, but many studies have reported that NPG patients have a strong family genetic predisposition, often with multiple NPG and HPG patients in the same family, suggesting that both There is something that is still unclear.

2. Signs

Referring to HPG, the main focus is on the following four aspects:

(1) Intraocular pressure: Although the intraocular pressure of normal intraocular glaucoma is in the normal range, the specific level is different. In clinically different patients, the intraocular pressure level is close to the upper limit of the normal range, and also close to the lower boundary, with an average of 16 mmHg. Nearby, it is the mean value of the intraocular pressure range of the normal group. The foreign literature reports that the intraocular pressure of most patients is close to the upper boundary. From the 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 both eyes. Symmetry and other aspects, but so far mainly focused on its highest value, most of the peak intraocular pressure is considered to occur at night, because the position of the sleep state causes the supracondional venous pressure to rise, as for the latter two indicators, from limited clinical data. See, the distribution of the eye pressure of the patient's day and night is bilaterally symmetrical, and the fluctuation pattern is a single-peak curve. The highest value differs from the lowest value by about 4 mmHg. The various manifestations of intraocular pressure in normal tension glaucoma are completely different from the normal physiological state of normal eye pressure in the general population. Consistent, staying normal and stable during the disease process.

(2) fundus changes: fundus changes as a structural change, including optic disc changes and RNFL changes, normal intraocular glaucoma relative to HPG, fundus changes have similarities and differences, different research results, normal tension glaucoma The medial disc damage is more manifested as narrowing and incision of the disc and choroidal retinal atrophy (PPCA) and disc edge bleeding. Clinically, disc hemorrhage is relatively common in normal optic glaucoma optic disc damage, sometimes It is the earliest visible sign that can be repeated. It is more common in the armpit of the optic disc or in the area along the upper disc. It is strip or flaming. It rides across the edge of the disc, and the bleeding and its repeated suggestion of the occurrence or progression of optic nerve tissue damage. Some studies divide normal tension glaucoma into two cases based on optic disc performance:

1 senile sclerosing type: mainly seen in elderly patients with vascular disease, the disc edge is pale and shallow slope.

2 focal ischemic type: there is a focal deep incision along the disc, located in the upper or lower pole.

(3) Visual field damage: visual field damage is a functional impairment. There is no difference in the location and morphology between normal tension glaucoma and HPG. There is no consensus on normal intraocular pressure glaucoma relative to HPG, early visual field defect. Most of them are focal, denser, steeper, and closer to the central fixation zone.

(4) iris corneal angle: For normal tension glaucoma, the iris cornea angle is undoubtedly open. From the pathophysiological analysis of the aqueous humor cycle, if the iris corneal angle is closed as a cause, it is impossible to have a result. The intraocular pressure is normal. It should be noted that there are two cases in which the iris corneal angle is open and can be "wide" or "narrow".

Examination of normal tension glaucoma

Immunological abnormalities: NPG patients have a higher incidence of immune-related diseases, such as hypothyroidism, arthritis or Raynaud's disease. Some people have found that NPG patients have higher complement factor, but some scholars have failed to confirm their own immunity. The disease is related to glaucoma.

Fundus fluorescein angiography

Fundus fluorescein angiography (FFA) showed that most patients with NPG had a filling defect of the optic cup, and most of them had segmental weak fluorescence, indicating that there was optic disc ischemia, and the corresponding disc edge was often present at the site of the staged fluorescence filling defect. And the location of the retinal nerve fiber layer defect, and the filling defect of the optic disc appears before the visual field damage.

2. Eye blood flow check

Some early scholars reported that the ocular pressure of the patients with NPG, the diastolic pressure of the eye was lower than that of the suspected glaucoma. It was also reported that the diastolic perfusion pressure of NPG may be low. Later, the arterial pressure and perfusion pressure of NPG patients were not obvious to normal people. The difference, and the perfusion pressure is easily affected by blood pressure, and the resistance of the ciliary choroid vasculature measured according to the amplitude of the eye artery beat and the arterial blood flow can reflect the blood supply. Some studies have shown that the pulse amplitude of the eye of NPG patients is lower than that of the normal eye. The ciliary choroidal vascular network resistance is 2 to 3 times higher than that of normal people. The blood flow is reduced due to the increase of resistance. Some scholars have reported that the pulse amplitude of the eye in NPG patients is not different from that of normal people. The current blood flow of patients with NPG is different. There is no consensus, and the results of the reports are not very consistent, but most studies suggest that the blood flow to the eyes of NPG patients may be lower than normal.

3. Excitation test

The challenge test of NPG patients was corticosteroid boost test and drinking water test and cold stimulation challenge field test. The cold stimulus challenge test was to compare the normal field of vision of the patient with the field of view of one hand or foot placed in cold water at 4 ° C for 10 min. The mean defect was reduced by 10% for positive, and about 25% of patients with NPG had a positive reaction because this test can detect vascular tone and therefore may help to determine whether vasodilators are effective in patients with NPG.

4. Other eye features

The prevalence of myopia, especially high myopia in NPG patients is higher than that in normal people and primary open angle glaucoma patients, and the posterior segment of the eyeball is larger than normal people. The longer axial axis tends to make the eye wall hardness lower and tends to There is a large cup-to-plate ratio, and the susceptibility to glaucoma damage is also large. In high myopia patients, the optic disc is irregularly pulled and extended due to the expansion of the eyeball, resulting in abnormal optic disc shape, enlargement and tilting, and the pulling effect is reduced. The tolerance threshold of the sieve plate for ocular pressure injury is such that the intraocular pressure at or near physiological value is sufficient to cause damage to the optic disc and retinal nerve fibers.

5. General condition

(1) Blood pressure: Whether optic nerve damage in NPG patients is related to abnormal blood pressure, it is still unclear. People with low blood pressure, especially low diastolic blood pressure or normal blood pressure, are more common in patients with NPG than in other types of glaucoma patients. The incidence of hypotension or hemodynamic crisis was higher than that of the NPG control group.

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

(3) Hemorheology: Studies have shown that the whole blood viscosity, plasma viscosity and hematocrit of patients with NPG are higher than normal, the incidence of abnormal blood coagulation and fibrinolysis system is higher, and the blood is hypercoagulable.

Diagnosis and identification of normal tension glaucoma

diagnosis

The optic disc changes similar to POAG with acquired acquiredness, retinal nerve fiber layer damage and visual field damage, intraocular pressure measurement at 24 h before treatment were all 21 mmHg (2.79 kPa), the angle of the anterior chamber was open, and the optic nerve damage, visual field defect and temporaryity were excluded. Diagnosis can be established by other ocular or systemic causes of decreased intraocular pressure.

NPG diagnostic criteria for 8 countries including the United States and Japan:

A 1Goldmann applanation tonometer measures 24h intraocular pressure 22mmHg, no intraocular pressure exceeds 24mmHg.

The 2 corner mirrors have a wide angle at the double angle.

3 After stopping all intraocular pressure or systemic drugs for 1 month, at least twice 24h intraocular pressure measurement, intraocular pressure peak 22mmHg, each average <20mmHg, and at least 4 times from 5:00 pm to 7:00 pm measuring.

4 typical glaucomatous optic disc changes.

5 typical glaucomatous visual field defects.

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

7X line, CT, MRI, etc. showed no abnormalities in the intracranial and sacral.

8 exclude neurological diseases, no hypotension.

The diagnostic criteria for the glaucoma group at the Moorfields Eye Hospital in the United Kingdom are as follows:

1 untreated 24h mean intraocular pressure 21mmHg, and no intraocular pressure > 24mmHg.

2 corners are open.

3 no secondary causes of glaucomatous optic neuropathy, such as increased traumatic intraocular pressure, long-term application of corticosteroids, uveitis and other medical history.

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

5 visual field defects consistent with glaucoma.

6 glaucomatous lesions are progressive.

Differential diagnosis

1. Primary open angle glaucoma Primary open angle glaucoma is easily misdiagnosed as NPG in the following cases. The intraocular pressure fluctuation is large, and no intraocular pressure peak is found because 24 hours of intraocular pressure is not measured. Some patients have occasional Increased intraocular pressure, and a single daily curve examination failed to measure; POAG patients with myopia have low intraocular pressure due to low scleral stiffness and Sichötz tonometer; taking beta blockers or cardiac glycosides The drug reduces the intraocular pressure, so it should be emphasized that the intraocular pressure measurement and the daily curve should be repeated under the condition of stopping all local or systemic medication with suspicious intraocular pressure reduction, and the intraocular pressure should be measured by the applanation tonometer as much as possible. It is confirmed that the intraocular pressure is indeed within the normal range to diagnose NPG.

2. Other types of glaucoma such as early stage of chronic angle-closure glaucoma, glaucoma ciliary body syndrome, hormonal glaucoma, pigment dissemination syndrome, ocular trauma and uveitis may have transient eyes Increased pressure, causing glaucomatous optic nerve and optic disc damage, and then the intraocular pressure returned to normal, easily misdiagnosed as NPG, detailed history, detailed eye examination, including angle examination to identify, such as pigmentation syndrome For example, in the young patients with typical pigment disseminated syndrome, the pigmented Krukenberg spindle and trabecular mesh dense pigment are visible in the corneal endothelium. The intraocular pressure is high and it is easy to distinguish from NPG. However, some elderly patients with pigmented glaucoma stop releasing pigment. Trabecular mesh function and intraocular pressure returned to normal, corneal and trabecular pigmentation decreased, but optic disc and visual field damage still exist, easy to be misdiagnosed as NPG, need to be identified by detailed medical history, careful examination and follow-up observation.

Some scholars have proposed the concept of "burned-out glaucoma" and considered it an important consideration in the differential diagnosis of NPG. This glaucoma is usually seen only in the elderly, with glaucomatous optic disc damage and visual field defects, and normal intraocular pressure. The fluency coefficient of aqueous humor is very low. These patients have had elevated intraocular pressure before. However, due to the normalization of ciliary body atrophy and low secretion, the intraocular pressure is normal. However, there are not many cases in which patients with POAG are not treated with normal intraocular pressure. See, therefore, some scholars are skeptical about the existence of this glaucoma, but in any case in the diagnosis of NPG, it is very important to ask the patient's previous history of high intraocular pressure.

3. Ischemic optic neuropathy This disease often occurs in the optic disc atrophy or partial atrophy, generally no sag enlargement, but some patients also have a glaucoma-like expansion of the optic cup after acute ischemic damage of the optic nerve, especially Patients with giant cell arteritis are more common and need to be differentiated from NPG patients. However, patients with ischemic optic neuropathy have the following characteristics:

1 onset more acute, acute or subacute, often with a history of sudden decline in vision, may be accompanied by headaches or eye pain and other discomfort.

2 The optic disc shrinks with the pale color of the affected area, and the pale range is significantly larger than the concave range.

3 visual field defects often involve fixation points, which are arc-shaped defects connected to physiological blind spots that are not bounded by horizontal midline or vertical midline, and are horizontally semi-blind or quadrant blind.

4FFA early manifestations of small blood vessel dilation, abnormal fluorescence leakage, the visual disc boundary is blurred and strong fluorescence, to the late stage can be characterized as slow filling and weak fluorescence.

5 often accompanied by giant cell arteritis, syphilitic arteritis, collagen disease and diabetes, hypertension arteriosclerosis, etc., therefore, carefully ask the history and combined with fundus examination and fluorescein angiography, if necessary, dynamic observation of the optic disc changes can be excluded.

4. Optic disc and optic nerve compression lesions Optic disc atrophy caused by optic nerve and optic chiasm is generally different from glaucoma ocular cup enlargement, but there are also a few non-glaucoma optic atrophy patients with large cups of sight, easily misdiagnosed as NPG, In patients with non-selective optic atrophy, 6% are misdiagnosed as glaucoma, and some intracranial lesions can also cause visual field defects similar to glaucoma. Therefore, the possibility of intracranial compression lesions should be excluded in the diagnosis of NPG patients.

5. Myopia myopia, especially in high myopia, is often larger than the average person. It is easy to mistaken for glaucomatous optic disc depression, and some patients may have mis-diagnosis due to visual field defects due to chorioretinal degeneration and atrophy. Some patients with high myopia have optic discs. There is a slope, the cup is sloped, so the glaucoma is difficult to identify when the cup is enlarged, and it is easy to miss the diagnosis. The shape of the optic disc depression and the location of the retinal choroidal atrophy should be carefully examined and compared with the visual field defect to evaluate the diagnostic value of visual field defect. If necessary, FFA can be used to assist diagnosis. Because the optic disc depression of myopia does not have the absolute filling defect of the optic disc of NPG patients, if it can not be excluded at one time, the dynamic changes of the optic disc and visual field can be closely followed, and the optic disc depression of general myopia is generally observed. Will not expand sexually.

6. Some other systemic diseases or conditions are also easily misdiagnosed as NPG, such as optic nerve fasciitis, arachnoiditis, non-specific giant cell arteritis, carotid calcification plaque compression nerve and alcoholism caused by optic disc atrophy and sag enlargement Need to pay attention to exclusion.

7. Empty sella syndrome is a type of disease in which the arachnoid membrane protrudes into the sella and the anatomical defects of the pituitary are caused by incomplete or missing saddle septum. It is characterized by endocrine disorders, headaches and visual field defects. X-ray visible saddle enlargement In some patients, the fundus changes and visual field defects are similar to those in glaucoma patients. Because of normal intraocular pressure, they are often misdiagnosed as NPG. The visual field damage of this disease is not progressing. There is no need for treatment. It can be diagnosed by X-ray, CT and MRI.

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