Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 1994
[Perfusion time of the central retinal artery in normal pressure glaucoma. Initial results].
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Nasemann J E, Carl T, Pamer S, Scheider A
Аннотация
UNLABELLED: A possible explanation for the progressive visual field defects in normal tension glaucoma is reduced ocular blood flow. We have tried to answer this question using fluorescence perfusion scintigraphy that measures the circulation times between the subclavian vein, carotid artery, central retinal artery and central retinal vein.
PATIENTS: Eight normal subjects and eight age- and sex-matched normal tension glaucoma patients were compared. Inclusion criteria for NTG patients were an IOP below 23 mmHg, glaucomatous visual field defects, glaucomatous disk cupping, normal chamber angle and no neurologic deficits. The subclavian carotid time, the carotid retina time and the mean retinal perfusion time of the intravenously injected radioactive fluorescein bolus were measured using digitized scanning laser angiography and technetium scintigraphy.
RESULTS: Subclavian carotid time and mean retinal perfusion time were not significantly different between groups, whereas the carotid retina time was 1.6 s (min = 0.8, max = 2.6) in normals and 3.3 (min = 2.6, max = 4.2) in normal tension glaucoma. This difference was highly significant (P < 0.001).
CONCLUSIONS: The delay of the carotid retina circulation time in normal tension glaucoma patients may reflect a reduced blood flow velocity in the internal carotid artery, the ophthalmic artery and the central retinal artery. The subclavia carotid time and ultrasound investigation of the carotid artery were normal. This suggests that the delayed carotid retina time is an indicator of reduced blood flow velocity in ophthalmic and mainly central retinal artery. The good discrimination between normal subjects and NTG patients must be confirmed in a larger group of patients.
PATIENTS: Eight normal subjects and eight age- and sex-matched normal tension glaucoma patients were compared. Inclusion criteria for NTG patients were an IOP below 23 mmHg, glaucomatous visual field defects, glaucomatous disk cupping, normal chamber angle and no neurologic deficits. The subclavian carotid time, the carotid retina time and the mean retinal perfusion time of the intravenously injected radioactive fluorescein bolus were measured using digitized scanning laser angiography and technetium scintigraphy.
RESULTS: Subclavian carotid time and mean retinal perfusion time were not significantly different between groups, whereas the carotid retina time was 1.6 s (min = 0.8, max = 2.6) in normals and 3.3 (min = 2.6, max = 4.2) in normal tension glaucoma. This difference was highly significant (P < 0.001).
CONCLUSIONS: The delay of the carotid retina circulation time in normal tension glaucoma patients may reflect a reduced blood flow velocity in the internal carotid artery, the ophthalmic artery and the central retinal artery. The subclavia carotid time and ultrasound investigation of the carotid artery were normal. This suggests that the delayed carotid retina time is an indicator of reduced blood flow velocity in ophthalmic and mainly central retinal artery. The good discrimination between normal subjects and NTG patients must be confirmed in a larger group of patients.