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Show Poster 269 MRI Inquiry into the Anatomic Aspects of Alexia Without Agraphia Jeremy Shapiro 1, Aseem Sharma 2, Jonathan Trobe 2, Michael Lee 3, Ryan Walsh 4, Sangeeta Khanna 2 University of Michigan Medical School, 2 University of Michigan, 3 University of Minnesota Department of Ophthalmology & Visual Neurosciences, 4 Medical College of Wisconsin 1 Introduction: We reviewed brain MRI imaging in patients with alexia without agraphia (AWA) to better classify the pathophysiology of AWA as a disconnection syndrome or as a word form agnosia. AWA is primarily thought of as a disconnection syndrome in which a left occipital lobe lesion affects the callosal fibers of the splenium and disrupts access between the right striate cortex and the language regions for reading (Geschwind N 1965). Disconnection may also occur in unusual lesion combinations. Other authors have suggested that AWA may be word form agnosia from left fusiform gyrus damage (Warrington and Shallice 1980; Beversdorf et al 1997). The only systematic study of the neuro-anatomy of these lesions in a larger series of 16 patients with AWA was CT based (Damasio 1983). Methods: We performed a MRI study of 26 patients, 13 with right hemianopsia with AWA and 13 with right hemianopsia but without AWA. All patients were evaluated in neuro-ophthalmologic clinic at our institution and had brain MRI imaging available since the onset of the problem. MRIs were evaluated in a masked fashion by one neuroradiologist looking for changes in the occipital cortex, splenium, forceps major, and fusiform gyrus. Results: Of controls, 8 were female, average age was 64.4(34-84), and the etiology of all lesions was posterior cerebral artery (PCA) stroke. Of AWA cases, 5 were female, average age was 63.8(47-83) and lesion etiology was stroke in 11 cases and glioblastoma in 2 cases. 100% of AWA patients showed lesions in either splenium, left forceps major, or left fusiform gyrus with 69% showing lesions in both left fusiform gyrus and splenium/left forceps major. No controls showed lesions in these areas. Conclusions: Lesion combinations in these areas supports the word form agnosia hypothesis rather than the disconnection syndrome hypothesis alone. We plan on expanding our cohort with additional institutional collaboration. References: 1) Geschwind N. Disconnexion syndromes in animals and man. Brain 1965; 88: 17-294. 2) Beversdorf DQ, Ratcliffe NR, Rhodes CH, Reeves AG. Pure alexia: clinical-pathologic evidence for a lateralized visual language association cortex. Clin Neuropathol. 1997 Nov-Dec;16(6):328-31. PMID: 9401800. 3) Damasio AR, Damasio H. The anatomic basis of pure alexia. Neurology. 1983 Dec;33(12):1573-83. doi: 10.1212/wnl.33.12.1573. PMID: 6685830. 4) Warrington EK, Shallice T. Word-form dyslexia. Brain. 1980 Mar;103(1):99-112. doi: 10.1093/brain/103.1.99. PMID: 6244876 Keywords: Higher visual functions, Neuroimaging, Stroke, Visual fields Financial Disclosures: The authors had no disclosures. Grant Support: None. Contact Information: Dr. Sangeeta Khanna, khannasa@umich.edu 2023 Annual Meeting Syllabus | 457 |