An unexpected finding may lead to a new way to assess stroke patients, according to scientists at the National Institutes of Health (NIH).
Acute stroke patients who had MRI with gadolinium at baseline and another MRI with fluid-attenuated inversion recovery (FLAIR) imaging 2 or 24 hours later had a high frequency of gadolinium leakage into ocular structures (GLOS), according to Richard Leigh, MD, of NIH's National Institute of Neurological Disorders and Stroke (NINDS), and colleagues.
- Acute stroke patients who had MRI with gadolinium at baseline and another MRI with fluid-attenuated inversion recovery (FLAIR) imaging 2 or 24 hours later had a high frequency of gadolinium leakage into ocular structures.
- Patients who had gadolinium in the vitreous chamber 24 hours after their baseline MRI tended to be older, had a history of hypertension, and had more white matter hyperintensities.
Blood-ocular barrier disruption occurred in 76% of the stroke patients they evaluated and appeared to follow a temporal pattern: GLOS was in aqueous fluid within minutes to hours, and in vitreous fluid within hours to days, they reported in Neurology.
"In a subset of the population, both the aqueous and vitreous chambers had rapid GLOS," Leigh said. These patients had larger infarcts and a higher degree of blood-brain permeability than patients with a slower pattern of gadolinium leakage or no leakage at all.
Patients who had gadolinium in the vitreous chamber 24 hours after their baseline MRI tended to be older, had a history of hypertension, and had more white matter hyperintensities.
The patients were part of the NIH's Natural History of Stroke study, an ongoing project that follows stroke patients through serial scans. Participants agreed to have baseline MRIs and follow-up imaging 2 and/or 24 hours later.
"We stumbled on this finding when we were looking at our MRI scans," he told MedPage Today. "We noticed that in some patients, gadolinium had gone into the fluids of the eye, which was something that hadn't really been described before. When we went back and we looked though the records of our stroke patients over a 2-year period, we found the leakage to be surprisingly common."
Of 167 patients studied, 64% had gadolinium leakage into their eyes on a 2-hour scan, and 75% showed it on a 24-hour scan. Tissue plasminogen activator (tPA) treatment did not seem to make a difference; GLOS was present in 79% of tPA patients and 71% of untreated patients.
The mechanism behind this was unclear, but may be a remote effect of acute cerebral injury on the blood–ocular barrier, Leigh noted.
The findings raise more questions than they answer, he observed.
"When we see something in the brain affects the eye, is it because of a direct relationship from the brain injury, or does it reflect a more diffuse process, a more systemic reaction that also has a negative impact on eye?" he asked. "And if we looked at patients who did not have a stroke, would we find similar patterns? We don't really know."
The findings also raise the possibility that something observed in the eye might help evaluate stroke severity quickly, Leigh added.
"Looking in the eye is something that can be done in the field," he said. "We might be able to use some of these findings if we can demonstrate that in a low-tech fashion, we could have information that would allow us to change the way we deliver care."
The study was funded by the NIH's National Institute of Neurological Disorders and Stroke. The authors disclosed no relevant relationships.
Source Reference: Hitomi E "Blood–ocular barrier disruption in acute stroke patients" Neurology 2018; DOI: 10.1212/WNL.0000000000005123; DOI: 10.1212/WNL.0000000000005123.