Clinical and radiographic intersection of cerebral amyloid angiopathy with euglycemic diabetic ketoacidosis in the development of transient focal neurologic deficits: case report

TL;DR

An 81-year-old man with cerebral amyloid angiopathy and euglycemic diabetic ketoacidosis experienced transient neurological symptoms, possibly due to cortical spreading depolarization.

Contribution

This case report highlights a rare intersection of CAA and euglycemic DKA with reversible T2 FLAIR hypointensity and transient focal deficits.

Findings

The patient exhibited euglycemic DKA with transient neurological deficits and MRI findings consistent with probable CAA.

Reversible T2 FLAIR hypointensity was observed in brain regions with heavy microbleed burden from CAA.

Cortical spreading depolarization is speculated as a common pathway linking CAA and hyperglycemia-related deficits.

Abstract

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.

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.

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.

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.

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