GAD in Neuro-Ophthalmology

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Identifier GAD_in_Neuro_ophthalmology_Lee
Title GAD in Neuro-Ophthalmology
Creator Andrew G. Lee, MD
Affiliation (AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York
Subject Glutamic Acid Decarboxylase (GAD); Nystagmus; Endocrine and Neurologic Pathologies
Description Dr. Lee lectures medical students on the role of GAD.
Transcript "So, today I'm going to talk to you about GAD, and GAD is glutamic acid decarboxylase. So, it's an enzyme -ase that removes the carboxyl group from glutamic acid and so glutamate is converted to GABA via GAD. And the reason we know need to know a little bit about GAD the enzyme is we can have antibodies against GAD, so if you have anti-GAD antibody, you are blocking the conversion of glutamate to GABA. And because GABA is an inhibitory neurotransmitter, if you inhibit the inhibitor, you'll get excitatory phenomenon and so for neuro-op, the kinds of things that we see in patients who have anti-GAD antibody are oscillopsia, and that's the sensation that things are jumping because your eyes are jumping and that's nystagmus. The typical nystagmus that we see in GABA-related anti-GAD antibodies is downbeat nystagmus but it can be PAN, which is periodic alternating nystagmus, or it can just be gaze evoked nystagmus so the type of nystagmus is not that localizing. But the most common one that we see is downbeating nystagmus. It can also cause diplopia and that diplopia can be from a number of central mechanisms, including skewed deviation, and it can affect cerebellar function. And so when you have cerebellar eye signs, that's going to be psychotic abnormalities, cogwheels psychotic pursuit, slow saccades, hypermetric saccades, and any kind of saccadic abnormality. And neurologically, they might have ataxia so they have these cerebellar ataxia people also get from the GAD antibody. And it can cause convergence, spasm, and supernuclear type of ophthalmoplegia. So that's basically how the gad comes to be. And you need to know that GAD is associated with other neurologic and systemic findings. One of them is latent autoimmune diabetes of adulthood (LADA). It kind of looks like diabetes type 2 plus diabetes type 1, so it's kind of a diabetes 1.5. So it's a older patient who's thin so it looks like type one but they actually have no insulin-dependence yet. So it's like a type two an adult but a thin person. And in the case of LADA, you should test for anit-GAD, the other antibodies, and their thyroid should be checked to make the diagnosis. This should probably lead to endocrinology. So the other neurologic thing that we see is stiff person syndrome. So stiff person syndrome is also a GAD-associated phenomenon and some of the patients have limbic encephalitis and that means they can present with neuropsych manifestations. So I'm ordering the gad when there's stiff person, unexplained limbic encephalitis, and unexplained cerebellar ataxia. I'm going to ask about diabetes type 2 because it might be diabetes type 1.5 which is LADA, an autoimmune latent adult version of diabetes. We're going to be thinking about it when we have unexplained downbeat nystagmus but any kind of nystagmus including PAN or gaze-evoked. And any unexplained diplopia in association with any of the other GAD findings, you should be thinking about glutamic acid decarboxylase antibody GAD."
Date 2022-03
Language eng
Format video/mp4
Type Image/MovingImage
Collection Neuro-Ophthalmology Virtual Education Library: Andrew G. Lee Collection: https://novel.utah.edu/Lee/
Publisher North American Neuro-Ophthalmology Society
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah, 10 N 1900 E SLC, UT 84112-5890
Rights Management Copyright 2019. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
ARK ark:/87278/s67yda24
Setname ehsl_novel_lee
ID 1751077
Reference URL https://collections.lib.utah.edu/ark:/87278/s67yda24
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