On this episode of the NeuroOp Guru video blog, Andy Lee, MD, and Drew Carey, MD, discuss the use of fluoxetine in patients with visual field loss after suffering a stroke.
Editor's note - This transcript has been edited for clarity.
Hello, and welcome again to another edition of the NeuroOp Guru. I'm very happy to have my good friend and colleague Drew Carey from Johns Hopkins with us. Hey, Drew,
And today we're going to be talking about a new hope for visual field loss from stroke, in a pilot randomized control trial. And so Drew, maybe you could just give us a little bit [of] background on how they decided to use fluoxetine, and then we can dive right into the data.
That is a great question, Andy. You know, I think for a long time, we see patients who have visual field loss from occipital strokes and some people get better and some people don't, and we're not really great at predicting that. And animal models suggest that, you know, there's maybe different pathways, biochemical pathways, we could use to help harness this. And there's been some animal models looking at selective serotonin reuptake inhibitors [SSRI] for post-stroke recovery in different neurologic domains. That's what they were hoping would be a mechanism in this pathway, so they decided to use fluoxetine. Which is you know, a generic medication that has been around for a while with a really good safety profile. It's commonly used in patients with post-stroke depression. So they thought it would be a safe option for trying for this trial.
So they were actually looking at a hard endpoint hemangiomas visual field loss from occipital stroke. And they repeated the field just to make sure that it really was stable, and then they did it again as the outcome measure and did it work?
That's a great question. Yeah. So patients were randomized, they had to be randomized within 10 days of visual field loss. And some got placebo and some got fluoxetine, and they did repeat the visual field test at 6 months. And you know, it was really small study, they had 17 patients included. Eight were randomized to fluoxetine, 9 were randomized to placebo, there was some loss to follow up or withdrawal. So they only ended up with 12 patients, 5 on the fluoxetine, and 7 in the placebo group. They did see like we see in our regular patients that some people got better and some people didn't. And because of the small numbers, it was hard to draw a really strong conclusion primary endpoint, they did not see a difference. There was a little bit of a trend towards more improvement with fluoxetine. And then they did a secondary analysis for patients who had complete resolution of their visual field defect, and that was higher in the fluoxetine group. But again, really small numbers.
What should our audience take away from this? Is it a success or a failure? Or stay tuned to this channel?
That's the most important question. Right? I think the most important take home point is that there's potential, and we definitely need some more research, larger cohorts. We would need to make sure the visual fields are comparable between the two groups, and the lesions of the occipital strokes are comparable between the two groups, because we don't want to have any common founders. You know, is this primary, occipital, you know, primary visual cortex? Was it more peripheral? You know, was there hemorrhagic involvement, and maybe that's why some patients got better and other patients didn't. But I think this is the first thing we've seen where it looks like there might be something we could offer our patients and we will look forward to further trials.
And do you think It's because they just were less depressed and they did the field better?
Well, we do worry about depression on our visual field, but not that kind of depression. So um, you know, I don't know the underlying mechanism and I think that would be difficult to say for certain we don't want to go in and biopsy these patients, occipital lobes to see the structural change that occurred. But, you know, we're hopeful that in this field of neuroplasticity, that there are things that are modifiable, and patients learn to rewire other parts of their brain after stroke, right? They recover from their hemiplegias, they can have improvement in auditory processing domains. So why not vision? You know, I think that's the hope.
Well, as fascinating as always, Drew and I thank you for participating. That concludes yet another edition of the NeuroOp Guru.