Frontiers in neuroimaging · 2026
Clinical and radiographic intersection of cerebral amyloid angiopathy with euglycemic diabetic ketoacidosis in the development of transient focal neurologic deficits: case report.
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Aboubechara John Paul, Saggio Michael, Campa Olivia, Oguz Kader Karli, Nguyen Ivy
Аннотация
OBJECTIVES: This study aimed to describe a case of transient neurologic deficits triggered by euglycemic diabetic ketoacidosis (DKA) in brain tissue at risk due to heavy cerebral amyloid angiopathy (CAA) microbleed burden, while demonstrating the rare imaging finding of reversible T2 fluid-attenuated inversion recovery (FLAIR) subcortical hypointensity.
METHODS: We present the clinical course, laboratory findings, and neuroimaging features of an 81-year-old man who presented with acute altered mental status and transient focal neurologic deficits.
RESULTS: The patient presented with encephalopathy, headache, left hemianopsia, left sensory neglect, and mild left upper extremity weakness. Laboratory examination showed euglycemic DKA. Brain MRI revealed findings consistent with probable CAA according to Boston Criteria 2.0, including innumerable cortical microbleeds predominantly in the right temporo-parieto-occipital lobes, with superimposed diffuse T2 FLAIR-weighted hypointensity in this region.
DISCUSSION: Reversible T2 FLAIR hypointensity has been described in hyperglycemia-associated syndromes. In this case, T2 FLAIR hypointensity likely represented metabolic dysregulation that triggered cortical dysfunction within brain regions at risk due to heavy CAA-related microbleed burden. We speculate that a common pathway for the development of the patient's transient deficits resulted from cortical spreading depolarization (CSD), which has been associated with both CAA and hyperglycemia.
METHODS: We present the clinical course, laboratory findings, and neuroimaging features of an 81-year-old man who presented with acute altered mental status and transient focal neurologic deficits.
RESULTS: The patient presented with encephalopathy, headache, left hemianopsia, left sensory neglect, and mild left upper extremity weakness. Laboratory examination showed euglycemic DKA. Brain MRI revealed findings consistent with probable CAA according to Boston Criteria 2.0, including innumerable cortical microbleeds predominantly in the right temporo-parieto-occipital lobes, with superimposed diffuse T2 FLAIR-weighted hypointensity in this region.
DISCUSSION: Reversible T2 FLAIR hypointensity has been described in hyperglycemia-associated syndromes. In this case, T2 FLAIR hypointensity likely represented metabolic dysregulation that triggered cortical dysfunction within brain regions at risk due to heavy CAA-related microbleed burden. We speculate that a common pathway for the development of the patient's transient deficits resulted from cortical spreading depolarization (CSD), which has been associated with both CAA and hyperglycemia.