Visual evoked potentials of the blue-sensitive pathway under cold provocation in normals and glaucomas

Vascular dysregulation in open-angle glaucomas can be identified by measuring the blood circulation during exposure to cold water. Aim of this study was to find out whether the same cold stimulus would lead to functional changes in the visual evoked potentials (VEP) of the short-sensitive pathway in normals and glaucoma patients.

Blue-on-yellow pattern-visual evoked potentials were studied in 22 healthy control persons and 47 patients with primary open-angle glaucoma (25 high-pressure glaucomas, 22 normal pressure glaucomas with clinical signs of vasospastic hyperreactivity). A blue stripe pattern, presented in onset-offset mode on a yellow adaptation light served as the stimulus. Cold provocation was initiated by dipping one hand of the patient into cold water of 3 degrees C to 5 degrees C. The onset amplitudes and peak times were measured without cold exposition as well as two and four minutes after the cold exposition began.

In the group of vasospastic glaucoma patients a significant reduction of visual evoked potential-amplitudes was observed during cold provocation (amplitude before ice exposition: 4.17 microV, amplitude following two minutes of ice exposition: 3.52 microV; paired test: P < 0.01). Other subject groups showed no significant amplitude reductions after cold provocation. Peak times of both open-angle glaucoma groups (132.3 +/- 18.7 milliseconds in high pressure, 132.7 +/- 14.5 milliseconds in normal pressure) were significantly increased in comparison to normals (117.4 +/- 8.0 milliseconds). However, no significant influence of the cold provocation on peak times could be found in all groups.

Peak times of the blue-on-yellow visual evoked potentials are significantly prolonged in patients with primary open-angle glaucomas. Cold provocation causes a significant amplitude reduction of the blue-on-yellow visual evoked potential in the present normal-pressure glaucoma patients and reflects vascular dysregulation in patients with vasospastic hyperreactivity.