Abstract
This prospective study tests the hypotheses that: 1) glaucoma is associated with evidence of cerebral small vessel disease; 2) that imaging biomarkers of cerebral small vessel disease in POAG and NTG will show different characteristics. 12 normal controls, 7 patients with primary open angle glaucoma (POAG) and 9 patients with normal tension glaucoma (NTG) were recruited. Ophthalmological clinical assessment and MR imaging of the brain were performed. MR imaging was used to quantify white matter lesion load, frequency of dilated perivascular spaces (PVS) and abnormalities in cerebral hydrodynamics. Patients with POAG had significantly greater white matter lesion load (p < 0.05), more PVS in the centrum semiovale (p < 0.05) and had higher overall PVS scores than controls (p < 0.05). In the POAG group, optic cup-to-disc ratio (CDR) was positively correlated with deep white matter hyperintensities (R2 = 0.928, p < 0.01). Mean deviation on the Humphrey visual field assessment was negatively correlated with deep white matter lesion load (R2 = −0.840, p < 0.01), total white matter lesion load (R2 = −0.928, p < 0.01) and total PVS (R2 = −0.820, p < 0.01). MR evidence of cerebral small vessel disease is strongly associated with a diagnosis of POAG and with the severity of abnormalities in CDR and visual field.
Highlights
Glaucoma describes a group of optic neuropathies, characterised by slow progressive degeneration of retinal ganglion cells and their axons
In one recent large scale prospective study of 246 subjects perivascular spaces (PVS) were associated with lacunar stroke subtype (p < 0.0001) age and white matter lesion load and these authors concluded that the findings were “consistent with the hypothesis that PVS reflect small vessel disease”[27]
In addition dilation of PVS in the centrum semiovale (CSOV) can be seen in severe cerebral atrophy no such relationship has been reported with PVS in the basal ganglia
Summary
Glaucoma describes a group of optic neuropathies, characterised by slow progressive degeneration of retinal ganglion cells and their axons. Patients with POAG showed significantly greater white matter lesion load (p < 0.05), more PVS in the CSOV (p < 0.05) and had higher overall PVS scores than controls (p < 0.05, Fig. 2). Patients with NTG had a trend towards decreased total cerebral blood flow, decreased aqueductal stroke volume and decreased arterial aqueductal delay compared to controls and patients with POAG these failed to reach statistical significance.
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