Magnetic resonance imaging in patients with low-tension glaucoma.

OBJECTIVE: To study diagnoses and anatomic findings found on magnetic resonance imaging in patients with low-tension glaucoma. PATIENTS: We included in this study magnetic resonance images of 20 consecutive patients with low-tension glaucoma. We individually matched each patient with low-tension glaucoma to a control with normal ocular findings who had magnetic resonance imaging for reasons unrelated to the visual pathway. DESIGN: We studied axial and coronal images of the orbit and optic nerve with digitizing software (Image-Pro Plus, Media Cybernetics, Silver Spring, Md). Statistical evaluation was with a Wilcoxon Signed Rank Test for anatomic findings and a McNemar Test for diagnosis. RESULTS: We found no difference between groups in the optic nerve diameter or length, the carotid artery area, or the distance from the optic nerve to the carotid artery (P > .05). Left optic nerve area was greater in the control patients than patients with low-tension glaucoma (P = .026). The prevalence of intracranial abnormalities, including meningioma, aneurysm, and arteriovenous abnormality, was similar between groups (P > .05). However, diffuse cerebral small-vessel ischemic changes were found more in patients with low-tension glaucoma (n = 8) than control patients (n = 1) (P = .0196). CONCLUSIONS: This study proposes a hypothesis that cerebral small-vessel ischemia is more common in patients with low-tension glaucoma and potentially reflects indirectly a vascular cause of the optic nerve head damage at least in a subgroup of patients. Importantly, further research still is required to provide direct evidence for a vascular cause involved in low-tension glaucoma.

Cortical nicotinamide adenine dinucleotide (NADH) kinetics in patients undergoing extracranial-intracranial bypass.

Nicotinamide adenine dinucleotide (NADH) kinetics were measured in 76 cortical areas in 26 patients with transient ischemic attacks (TIAs) undergoing extracranial-intracranial bypass. Direct cortical stimulation was utilized to induce changes in surface fluorescence corresponding to a brief oxidation and reduction of mitochondrial NADH. Preoperative studies of cerebral blood flow in gray matter (CBF)g) demonstrated normal perfusion in 11 patients and ischemic changes ((CBF)g less than 43.5 ml/100 g/minute) in 15 patients. In 30 normally perfused areas within the craniotomy, the mean half-time for reduction (t1/2(red)) of cortical NAD was 21.5 +/- 2.6 seconds. In 39 ischemic areas, the mean t1/2(red) was 5.6 +/- 1.2 seconds. These rapid reduction rates were associated with supernormal overshoots of the base line indicative of a transient oxygen debt. Kinetic responses could not be elicited from 7 areas adjacent to foci of decreased attenuation on compound tomography. Bypass resulted in normalization of the t1/2(red) in 24 of 28 areas of ischemia. The dependence of NADH kinetics on blood flow through the graft was demonstrated in 15 of 19 areas of mild ischemia by the reapplication of a clip to the donor artery. It is concluded that persistent reversible abnormalities of cortical mitochondrial metabolism exit in a significant number of patients with a history of TIAs who are suitable candidates for bypass surgery. In such patients bypass may effectively augment the nutrient supply to meet the bioenergetic demands associated with increased electrophysiological activity.