Is symptomatic atherosclerotic cerebrovascular disease a risk factor for normal-tension glaucoma?

To compare the incidence of glaucomatous optic disk appearance between patients with symptomatic atherosclerotic stroke and healthy individuals with normal intraocular pressures [IOP]. 46 patients with ischemic stroke with evident lacunar infarction or large vessel atherosclerosis, and 93 age- and sex-matched healthy individuals, all with normal IOP, were included. Patients and controls were examined for the presence of high cup-to-disk ratios [>0.5]. Seven patients [15.22%] in the ischemic cerebrovascular disease [CVD] group and 3 controls [3.23%] had glaucomatous optic disk appearance. All subjects with glaucomatous optic disk appearance in the control group and 3 patients in the study group had visual field defects in concordance with normal-tension glaucoma [NTG]. The incidence of glaucomatous optic disk appearance was significantly higher in the group with symptomatic atherosclerotic CVD. Atherosclerotic CVD is a risk factor for having glaucomatous optic disk appearance. Symptomatic atherosclerosis involving the brain vasculature may also affect the eye and lead to NTG. Patients with ischemic strokes due to large artery atherosclerosis or small artery occlusion must be examined and followed for NTG

Visual Evoked Potentials in Guillain-Barre Syndrome

BACKGROUND AND PURPOSE: Guillain-Barre syndrome (GBS) is an acute demyelinating polyneuropathy with various clinical features. Optic neuritis occurs in rare cases. In this study we determined the incidence and patterns of visual evoked potential (VEP) abnormality in GBS in association with ophthalmologic findings. METHODS: Thirty-two patients with a diagnosis of GBS were included in the study. The correlation between pathologic VEPs and categories of neurologic deficit and electrophysiological findings were examined statistically. RESULTS: The patients ranged in age from 19 to 77 years. Five cases (16%) had abnormal VEPs. All five of these patients exhibited increased P100 latency differences between the two eyes. Other abnormalities were prolonged p100 latency, increased interocular amplitude difference, and distorted p100 configuration. Pathologic signs on ophthalmologic examination were observed in 80% of patients with abnormal VEPs. VEP abnormality was never present in pure axonal forms. There was no significant correlation between pathologic VEP and cerebrospinal fluid protein level or categories of neurologic deficits. CONCLUSIONS: Involvement of the optic pathways is not a frequent finding in GBS. When present it is always asymmetric and generally accompanied with pathologic findings on ophthalmologic examination. VEPs may be abnormal in different clinical variants of GBS, and especially in demyelinating forms.