 introduction. Like you said, I'm Kevin Meyer. I'm one of the PGY3 neuro residents. I've been on the neuro ophthalmology rotation for three and a half weeks. I'm a little far from where I want to end up. I'm playing on doing a critical care fellowship in a year and a half. But at least I know what the back of the eyeball looks like now. And I'd like to thank my BFF and she who has listened to me practice this. And she was also mentioned. But I love this dog. So this is a patient that I saw with Dr. Warner. He was a 65 year old right handed male who was referred to the clinic for Diplopia. The Diplopia is vertical and strictly binocular. And he's a dentist and his primary concern is whether or not he's going to... What did I say? Oh, yeah, binocular. So he's worried about his ability to continue practicing. He first noticed that in 2009 and kind of over the years it's become more and more constant. He's seen other ophthalmologists who have tried prisms that did not help significantly. And the main issue is he's able to focus through his loops. But when looking off laterally he gets the double vision. And through the loops his depth perception is impaired. He's a pretty healthy guy. He's wore glasses or contacts all his life. He has atrial fibrillation for which he's on aspirin 325. He was on warfarin, but his chest to score was low enough that he got demoted to just an aspirin. No prior neurologic history and no alcohol to back or drugs. On exam his visual acuity was 20-20. Color vision was normal. Stereo vision was slightly impaired and no afferent peoplary defect. And visual fields were intact bilaterally. His eye movements were intact. On down gaze and when looking laterally he did have downbeat nystagmus. Also when looking through the slit lamp we were able to detect a very subtle downbeat nystagmus in primary gaze. In primary gaze he had a right hyperphoria of two and it increased when looking to the right and he had a left hyperphoria of one when looking to the left. And his optic nerves were normal. So here's a video of his nystagmus. He's going to look down into the left in one second. It's a little bit more evident there off to the right. And like I mentioned we were able to detect it in primary gaze through the slit lamp. So to summarize he has the downbeat nystagmus, the alternating skew deviation and then the remainder of his neurologic exam was normal. No ptosis no fatigability specifically looking for myasthenia and no cerebellar findings and I was two neurologists looking. And so to talk about a few of these things downbeat nystagmus it's felt to result from an interruption of the vestibular or the vertical vestibular ocular pathway. This would localize to the cranial medullary junction and the and or the cerebellum and then there's various medical causes that can contribute. So in just an imaging study of 24 patients with downbeat nystagmus six of them had an Arnold Kiari malformation six had cerebellar atrophy two had demyelinating disease and in the remainder there was no no obvious imaging finding. So the differential includes primary cerebellar degeneration various congenital or structural malformations specifically those that are compressing the the brainstem or or cerebellar or the cerebellum such as an Arnold Kiari malformation or various vascular abnormalities that can compress the brainstem or demyelinating disease or ischemic lesions in in those areas. Thinking about other causes toxicity with lithium, phenytoin, carbamazepine or alcohol can contribute low magnesium or a Wernicke's encephalopathy. Alternating skewed deviation when looking in one direction you have a hyperphoria of one eye and in the other direction a hyperphoria of the other eye. Most often when looking to the right the right eye is hyperforic but it's not not always like that. And this is thought to result from a bilateral injury to the central gravisceptive pathways that run from the midbrain down to the medulla and in a study of 47 cases 29 of them had pre-tecto lesions in the midbrain and five had lower brainstem lesions. So the differential diagnosis here includes hydrocephalus and tumors anything really anything that can compress in the posterior fossa. Strokes and demyelinating disease in those locations. Spinal cerebellar disease such as atrophy and then herniation syndromes and other chiarin malformations or vascular abnormalities that can compress as well. So combining these two really we just drop off the the medical causes. Those aren't really thought to be related to alternating skewed deviation so the differential is left with cerebellar degeneration cranioservical compression demyelinating disease and a stroke. So for this guy our first step in evaluation was to get a brain MRI and also we know he's not we knew he was not on any of the meds that are known to to contribute to the the down gaze or the downbeat nystagmus. So we got the brain MRI and it was normal. There was no cerebellar atrophy no chiarin malformation no signs of demyelination and and no ischemia. Here is a mid sagittal cut from his his brain MRI. So for him the the next step is is some some labs to further work it up. The Wernicke's was on the the differential of the downbeat nystagmus. He's walking talking practicing dinner so it's a little less likely but we'll get a thiamine level a b12 level anti-gad antibodies and vitamin E can both affect the cerebellum and then a cmp and a magnesium level is is on the docket for his further work out and we'll see what happens.