| Identifier |
Hashimotos_Encephalopathy_Lee |
| Title |
Hashimoto's Encephalopathy |
| Creator |
Andrew G. Lee, MD; Jeremy Auerbach |
| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (JA) Baylor College of Medicine, Houston, Texas |
| Subject |
Thyroid; Encephalopathy; Hashimoto |
| Description |
Dr. Lee lectures medical students on Hashimoto's encephalopathy. |
| Transcript |
"So I want to talk to you about Hashimoto's. And as you know Hashimoto's disease in terms of autoimmune disease of the thyroid produces autoimmune thyroiditis, and that autoimmune thyroiditis causes low thyroid in Hashimoto's although it can be transiently high because the colloid is damaged. And that's thyrotoxicosis. It's different than Graves' disease where the target is the TSH receptor and produces T3 and T4 excess leading to Graves' hyperthyroidism. So, in Hashimoto's autoimmune thyroiditis just like in Graves' autoimmune thyroiditis we can get thyroid eye disease and that thyroid eye disease usually results in proptosis and lid retraction, lid lag, diplopia, and rarely it can cause compressive optic neuropathy at the orbital apex and loss of vision. So, those are the well-known things. The thing you need to know and what we're talking about today is that it can also be associated with an encephalopathy. So, when I was a resident we called this Hashimoto encephalopathy. However, because it's not clearly related to the thyroid function - in fact usually the thyroid function is normal or near normal because they're treated with Synthroid - this is now called steroid responsive encephalopathy of autoimmune thyroiditis. So, it's SREAT. So, the steroid responsiveness is the key diagnostic feature. They have to get better with the steroids. The encephalopathy can manifest as seizure, mental status change, hallucinations, memory loss. And it's sub-acute so it's not like the slowly progressive neurodegenerative disorders. It happens in like weeks to months. So, a sub-acute encephalopathy. They have to have an imaging study that is negative or is compatible with only encephalitis. Lumbar puncture can show elevated CSF protein but shouldn't show meningitis or white cells or anything like that and the usual checks for the normal things that cause encephalopathy have to be all negative. And that means we need to have an EEG as well. So, we have an EEG, the usual suspects, a spinal tap, a negative MRI or MRI only compatible with encephalopathy, and the antibody is positive. So, TPO antibody or TSI. So, we have to have antibody positive, typically the thyroid functions are normal, they're encephalopathic, it's sub-acute, negative imaging, lumbar puncture only elevated CSF protein, EEG negative, work up otherwise negative. And, the most important thing, it has to respond to steroids. So, in patients who present to me with thyroid eye disease who are also encephalopathic, a better single unifying diagnosis is Hashimoto's encephalopathy. You can also present with ataxia alone. And, steroid responsiveness is the key. Give the steroid trial. Work it up, and if you have a steroid responsive encephalopathy that is associated with autoimmune thyroiditis, that is SREAT, what we used to call Hashimoto's encephalopathy." |
| 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/s6pfht68 |
| Setname |
ehsl_novel_lee |
| ID |
1751078 |
| Reference URL |
https://collections.lib.utah.edu/ark:/87278/s6pfht68 |
