II. Improved dark adaptation after carotid endarterectomy. Evidence of a long-term ischemic penumbra?

We have reported that dark vision is impaired in symptomatic carotid artery disease and that the impairment correlates with internal carotid artery stenosis. To find out whether this impairment is reversible after carotid endarterectomy, dark adaptation was examined pre- and postoperatively. Twenty-one consecutive patients were examined by dark adaptometry. Two examinations were done for each eye on two consecutive days pre- and postoperatively. Thirty-one matched control subjects were examined under identical conditions. The control subjects did not have clinical evidence of carotid artery disease. Patients and control subjects were free of ophthalmologic disorders. Dark vision frequently improved remarkably after endarterectomy. The average retinal sensitivity to light in darkness on the operated side doubled, and there was also improvement on the nonoperated side. There was no significant change in dark vision in the control subjects, negating a learning effect. The findings suggest the existence of reversible neuronal ischemia secondary to hemodynamic causes or frequent subclinical microembolization. Because the circulatory conditions are optimized, formerly inactive, surviving neurons may regain function.

I. Impaired dark adaptation in symptomatic carotid artery disease.

It has been known for more than a century that even slight hypoxemia reduces dark adaptation. We studied dark adaptation in symptomatic carotid artery disease. Twenty-one consecutive patients scheduled for first-time carotid endarterectomy and 31 age-matched control subjects with normal carotid arteries were examined by dark adaptometry monocularly and were tested repeatedly on consecutive days. The average degree of internal carotid stenosis on the symptomatic side was much greater than that on the contralateral side. Dark adaptation was markedly impaired in the patients as compared with the control subjects. In the patients there was no difference in dark adaptation between the symptomatic and nonsymptomatic sides. The existence of carotid stenosis correlated to the level of dark adaptation. Pupillary size and age correlated to the dark adaptational level but did not affect the effect of carotid stenosis on dark adaptation. The decreased dark adaptation may be due to insufficient blood supply or repeated subclinical microembolization to the retinae, the brain, or both.

Intraocular pressure-dependent light sensitivity in glaucoma.

The intraocular pressure-dependent light sensitivity of discrete retinal points was measured using the Heijl-Krakau automated light-emitting diode perimeter with an appropriate software program. A total of 300 measurements of light sensitivity were recorded from six retinal points during the test period of 8-10 min; increased intraocular pressure was induced using a Langham scleral suction-cup system. The ocular pulsatile blood flow and the ophthalmic arterial pressure were measured in the same patients. The fluctuation of the light sensitivity was less than 5% over the test period in healthy eyes and remained unaffected by an intraocular-pressure increment of 20 mm Hg; a small decrease of sensitivity occurred at a pressure increment of 30 mm Hg. In glaucomatous eyes the light sensitivity was lower and the fluctuation of the light sensitivity at some but not all retinal points was substantially greater than in the controls. In the glaucomatous eyes, and intraocular-pressure increment of 20 mm Hg increased the fluctuation and decreased the light sensitivity. The pulsatile ocular blood flow was lower in the glaucomatous eyes but not severe enough to be solely responsible for the loss of vision. The coexistence of retinal points with normal and abnormal stabilities of light sensitivity in glaucomatous eyes was consistent with impaired blood flow in the lamina cribrosa.

Human ocular vasodynamic changes in light and darkness.

PURPOSE: To determine whether changes in the retinal blood flow in light and darkness occur in humans. METHODS; The systolic and diastolic flow velocities were measured by color Doppler in the ophthalmic and the central retinal arteries in 12 healthy individuals in light and darkness. RESULTS: In the ophthalmic artery there was a trend toward lower systolic velocity in darkness compared with that in the light, but there was no change in diastolic velocity. In the central retinal artery the systolic and the diastolic flow velocities were markedly increased in darkness. After re-exposure to light the systolic flow velocity decreased. CONCLUSIONS: Darkness is associated with increased blood flow velocity in the central retinal artery, probably reflecting increased retinal metabolic demands by the photoreceptors.

Disc haemorrhages and the etiology of glaucoma.

As a consequence of the hypothesis that all open angle glaucomas at some time exhibit a disc haemorrhage, it is proposed that both low and high tension glaucomas have the same etiology. That the primary lesion should be sought in the small vessels of the optic disc seems to be a reasonable suggestion.

Impaired dark adaptation in polycythemia. Improvement after treatment.

PURPOSE: To determine if dark adaptation is reduced in individuals with polycythemia and if so whether there is any improvement in dark adaptation after treatment. METHODS: Dark adaptation was recorded monocularly by automatic dark adaptometry in ten consecutive patients with polycythemia before and after treatment. Analogue investigations were performed in 31 healthy control subjects. RESULTS: Dark adaptation was markedly impaired in the patients as compared with the control subjects. After reduction of the red cell count and normalization of the hematocrit and hemoglobin the dark adaptation was markedly improved. There was no significant change in dark vision in the control subjects negating a confounding learning effect. CONCLUSION: The findings indicate a sustained but reversible neuronal hypofunction secondary to polycythemia. As the rheological abnormality was normalized, dark adaptation was improved, probably secondary to normalized microcirculation within the retina or the brain, or both, possibly with reactivation of formerly inactive neuronal cells.