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Results for “Low Tension Glaucoma”

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At least 19 recordsLinked to original sources
PubMed1988

Correlation of asymmetric damage with asymmetric intraocular pressure in normal-tension glaucoma (low-tension glaucoma).

If intraocular pressure plays a role in producing visual field loss in normal-tension glaucoma, there may be a possible benefit from therapeutic efforts to lower the pressure. To see whether pressure plays a role in the production of damage, we studied 14 cases of normal-tension glaucoma with asymmetric intraocular pressure (1- to 6-mm Hg interocular difference in pressure). In 12 of these 14 cases, we found that glaucomatous cupping and field loss (damage) was greater in the eye with higher pressure. This statistically significant correspondence of the higher pressure with the greater visual damage suggests that the level of pressure is a factor in producing optic nerve damage. Other factors also must contribute to account for the few instances in which damage asymmetry did not reflect interocular pressure-difference and for the occurrence of injury at such low levels of pressure in the first place. Although benefit may be expected from therapeutic lowering of pressure in this condition, the degree of benefit, as well as the side effects from treatment required for successful lowering of pressure, remains to be documented by a future clinical trial.

Glaucoma↗
PubMed1994

Visual and blood flow responses in low-tension glaucoma.

Low or normal-tension glaucoma (NTG) is a rare clinical condition characterized by a glaucomatous cupping of the optic disk associated with the appearance of typical visual field defects, without ocular hypertension. According to several authors, NTG accounts for 5-15% of primary open angle glaucomas (POAG). In our open study we obtained a complete documentation of clinical and instrumental data-tonometric curve, computerized perimetry, pattern electroretinogram, pulsatile ocular blood flow (POBF) and retinography--on 10 consecutive patients (18 eyes) affected by NTG. We found that the NTG patients were similar to the controls as regards arterial systemic pressure and heart rate, but that POBF values were lower in the NTG patients.

Aged↗
PubMed1993

Optic nerve compression by carotid arteries in low-tension glaucoma.

Low-tension glaucoma (LTG) is manifested by glaucomatous optic nerve damage and visual field loss despite normal intraocular pressure (IOP). We describe 62 patients with classical signs of LTG. Computed tomography (CT) was performed in all patients. In 56 of the patients (90.3%), pathology of the intracavernous carotid arteries adjacent to the intracranial opening of the optic canal could be demonstrated. In 28 patients (45.2%) a clear asymmetry of the optic nerve cupping was found and could be correlated with the severity of the carotid artery pathology. A control group of 24 age-matched patients included five (20.8%) with intracavernous carotid artery calcification and only one (4.2%) with intracavernous ectasia. We suggest that calcification, dilatation and ectasia of the carotid artery into the optic canal may play an important role in the pathogenesis of many cases of LTG. The close proximity of the carotid artery to the optic nerve at this location may result in compressive neuropathy with subsequent glaucomatous damage of the optic nerve head.

Aged↗
PubMed1982

Visual field defects in low-tension glaucoma. Comparison of defects in low-tension glaucoma and chronic open angle glaucoma.

In a study of the visual fields of 160 eyes with low-tension glaucoma (LTG) and 154 eyes with chronic open angle glaucoma with the same degree of optic nerve change, no differences in the qualitative or quantitative characteristics were found. The field defects in those eyes with LTG in which a major hemodynamic crisis had occurred were not different from those in which no crisis had been documented.

Aged↗
PubMed1992

[Primary open angle glaucoma and low tension glaucoma--pathogenesis and mechanism of optic nerve damage].

The etiology, pathogenesis and mechanism of optic nerve damage in primary open angle glaucoma (POAG) and low tension glaucoma (LTG) were investigated by experimental glaucoma in monkey and by follow-up studies of many patients over 15 years, by pathohistological and immunohistochemical analysis. 1) LTG was proved to be a real glaucoma, showing pressure-dependent optic nerve damage. The pathological entity was a primary weakness of the lamina cribrosa (LC), and therefore even normal pressure could deform the LC. Due to backward distortion of LC the channels were disarranged and twisted, inducing mechanical optic nerve damage. There was no active vascular damage or vascular constriction at the site of the optic nerve damage. The filling defects of the advanced glaucomatous optic disc were not the cause of optic nerve damage, but the result of regressive vascular change after axon bundle loss. Splinter hemorrhage of the optic disc might be the result of the same process. 2) The weakness of LC might be induced by the abnormal metabolism of the extracellular matrix of the LC. 3) To arrest the progressive optic nerve damage in LTG, the intraocular pressure (IOP) should be maintained under 12, or ideally, 10 mmHg. 4) The optic nerve damage in POAG was not only pressure-dependent, but also dependent on the weakness of the LC, as in the case of LTG. In the early stage the IOP should be under 19 mmHg, in the advanced stage under 14 mmHg in order to arrest progression for over 15 years. 5) In advanced experimental glaucoma of monkeys, the LC showed reduction of elastin, fragmentation of collagen, and change of proteoglycans. 6) As in the LC, the trabecular meshwork also showed abnormal metabolism and abnormal deposits on the extracellular matrix in POAG, and LTG as well. 7) POAG and LTG might belong to the same family in which common abnormal metabolism of LC and trabecular meshwork induce various clinical features.

Adolescent↗
PubMed1992

[Fluorescein fundus angiography of optic nerve head in primary open angle glaucoma and low tension glaucoma].

Fluorescein fundus angiography was performed at angle of 20 degrees in the 58 low tension glaucoma (LTG) eyes (30 cases) and 77 primary open angle glaucoma (POAG) eyes (41 cases) and the relation of the optic nerve head fluorescein changes to visual field disturbances (stage classification of Kosaki) was compared between POAG and LTG groups. The filling defect of fluorescein in the deep area and the decrease in number of superficial capillaries were observed in the optic nerve head. The filling defect area of fluorescein in the optic nerve head corresponding to Bjerrum scotoma was recognized even in the mild visual field disturbance cases of both LTG and POAG. The following findings were noted in both LTG and POAG cases; expansion of the filling defect area and the decrease in number of superficial capillaries in the same area with progression of visual field disturbances. Filling defect area of fluorescein of the optic nerve head accorded with visual field disturbance area in 19 LTG eyes (32.8%) and 61 POAG eyes (79.2%). On the contrary, the filling defect area of the optic nerve head was wider than the visual disturbance area in 37 LTG eyes (63.8%) and 16 POAG eyes (20.8%). These findings suggest that blood circulatory disorders of the optic nerve head occurred earlier in LTG than in POAG and that the development of LTG might be closely associated with the blood circulatory disorders.

Aged↗
PubMed1985

Inter-individual variation in blood supply of the optic nerve head. Its importance in various ischemic disorders of the optic nerve head, and glaucoma, low-tension glaucoma and allied disorders.

There is no one standard pattern of the blood supply of the optic nerve head in all human eyes. There is a marked inter-individual variation in the blood supply of the optic nerve head, and the various factors which produce this include variations in (I) the anatomical pattern of blood supply, (II) the pattern of posterior ciliary artery (PCA) circulation (the main source of blood supply to the optic nerve head), and (III) the blood flow. The variations in the pattern of PCA circulation include the variations in (a) number of PCAs supplying an eye, (b) area of supply to the optic nerve head by each PCA, (c) location of the watershed zones between the various PCAs in relation to the optic nerve head, and (d) blood pressure in various PCAs as well as short PCAs. The variations in the blood flow in the optic nerve head can be produced by changes in (i) the intraocular pressure, (ii) mean blood pressure in the capillaries of the optic nerve head and (iii) peripheral vascular resistance. These variations are discussed in detail. A lack of appreciation of these complexities of the blood supply of the optic nerve head in health and disease is responsible for many of the current problems in the understanding of the role of vascular disturbances in anterior ischemic optic neuropathy, glaucoma, low-tension glaucoma and various ischemic disorders of the optic nerve head.

Adolescent↗
PubMed1992

[Intraocular pressure and optic nerve damages in monocular early glaucoma: a comparative study of primary open angle glaucoma and low tension glaucoma].

The correlation of intraocular pressure (IOP) to optic nerve damages was studied in 17 patients of primary open angle glaucoma (POAG) and 24 patients of low tension glaucoma (LTG) both with monocular early glaucomatous damages. In the POAG group, the mean IOP was higher in the glaucomatous eye than in the other, while in the LTG group there was no significant IOP difference between the two eyes. Comparing the optic nerve damages in both groups, patients of POAG presented a concentrically enlarged cup with even disc rim and diffuse retinal nerve fiber layer defect (RNFLD), while patients of LTG exhibited a paracentrical cup with uneven disc rim and localized RNFLD. The results suggested that there could be different mechanisms of optic nerve damages in the two groups.

Glaucoma, Open-Angle↗
PubMed1984

Postural change of IOP in normal persons and in patients with primary wide open-angle glaucoma and low-tension glaucoma.

The values of intraocular pressure (IOP) measurements by an Alcon pneumatic tonometer and a Goldmann applanation tonometer were found to be close, with a correlation coefficient of 0.92. Measured by the pneumatonograph the IOP after 30 minutes in the supine position was highest in normal persons, in patients with primary wide open-angle glaucoma and low-tension glaucoma. The greatest difference in IOP between subjects sitting and supine was observed in patients with low-tension glaucoma.

Aged↗
PubMed1993

[The central visual field defects in low-tension glaucoma. A comparison of the central visual field defects in low-tension glaucoma with those in primary open angle glaucoma].

To discover if there is difference in central visual field damage between low-tension glaucoma (LTG) and primary open angle glaucoma (POAG) eyes, the data obtained with the 10-2 threshold program of the Humphrey visual field analyzer were analysed using logistic discriminant analysis. One hundred and four LTG eyes from 65 case (maximum IOP < or = 21 mmHg) and 48 POAG eyes from 34 cases (maximum IOP > or = 25 mmHg) with early to moderately advanced visual field damage were included. There was no significant difference in mean deviation (MD, STATPAC), refraction, or age between the 2 groups. The analysis demonstrated that an arcuate area in the upper central 5-10 degrees of the visual field was significantly more depressed in LTG than in POAG eyes.

Aged↗
PubMed1989

Co-existence of empty sella syndrome and low tension glaucoma.

In 15 low-tension glaucoma patients computed tomography of the head was re-evaluated in order to find the possible empty-sella syndrome. Fourteen CT-scans were normal, and empty sella was found in one patient with progressive low tension glaucoma. The possible role of empty sella syndrome in glaucomatous visual field defects is discussed.

Aged↗
PubMed1996

Differences in optic discs in low-tension glaucoma patients with relatively low or high pressures.

We evaluated the differences in the optic nerve head in patients with chronic open-angle glaucoma (HTG) and those with low-tension glaucoma with either relatively high (between 16 and 21 mmHg [LTGH]) or low (< or = 15 mmHg [LTGL]) intraocular pressures. We included 36 patients in this study. We found that LTGL patients had a significantly greater mean area of peripapillary atrophy inferior to the optic disc (0.65 +/- 0.38 mm2) than LTGH (0.40 +/- 0.38 mm2) or HTG (0.34 +/- 0.25 mm2) patients (p < 0.005). No significant difference was found between groups for the area of the neural rim, optic disc, cup/pallor discrepancy, or peripapillary halo, or in the diameter of the largest artery or vein in the inferior and superior peripapillary area. This study raises the question of whether a separate mechanism of damage could exist at the optic disc in patients whose intraocular pressure is < or = 15 mmHg because of a greater extent of peripapillary atrophy than in patients with higher intraocular pressures.

Aged↗
PubMed1982

Open angle glaucoma, ocular hypertension, low-tension glaucoma, and refraction.

An analysis of the refractions of patients with primary open angle glaucoma, ocular hypertension (OH), and low-tension glaucoma showed that myopia occurred more frequently in each group than would be expected in a normal population of similar age. One in three of the myopes with OH had glaucomatous field defects on follow-up examination, whereas the defects developed in only one in 20 of the emmetropes and in one in 40 of the hypermetropes. These results suggest that myopic eyes are more susceptible to the effects of raised intraocular pressure than are nonmyopic eyes and that myopes with OH have a particularly high risk of the development of field defects.

Adolescent↗
PubMed1985

The neurologic evaluation of patients with low-tension glaucoma.

One hypothesized cause of low-tension glaucoma is chronic or intermittent ischemia of the optic nerve. Since the optic nerve and brain are both parts of the central nervous system and share a common blood supply, the authors wondered if patients with low-tension glaucoma might also have clinical or radiographic evidence of cerebral atrophy. In this study, 27 patients with low-tension glaucoma were examined using neurobehavioral testing, electroencephalography, computerized tomographic scan, neurological history, and physical examination. In only a small number of patients were these tests abnormal. However, 12 of the 27 patients gave a history of common or classic migraine. This unexpected finding raises the possibility that migraine-related ischemia might be the pathogenic mechanism in some cases of low-tension glaucoma.

Aged↗