Contrast-Induced Cerebritis Leading to Acute Hemiparesis
Daniela Lozano1, Taleen Shahrigian1, Bradley Haveman-Gould1, Muhammad Farooq1
1Trinity Health Grand Rapids
Objective:
N/A
Background:

Contrast administration is a rare cause of cerebritis, which can lead to acute neurological deficits, headaches, confusion, or seizures. Head CT can show diffusely hyperdense parenchyma with sulcal effacement. Brain MRI will typically reveal restricted diffusion and cortical ribboning. Risk factors for developing cerebritis include the use of large amount of contrast, history of prior stroke, and acute hypertension at the time of contrast administration. This is thought to increase blood-brain barrier permeability, allowing contrast to leak into the brain parenchyma.  

Design/Methods:
N/A
Results:

A 93-year-old female with hypertension, dyslipidemia and prior amaurosis fugax presented with 2-hour symptoms of acute right monocular vision loss. Initial head CT was unrevealing. Neurological exam was only evident for complete vision loss in the right eye without any evidence of intraocular hemorrhage on fundoscopic exam. The patient was taken for conventional angiogram of the right carotid artery and received 4 mg intra-arterial IV alteplase to the right ophthalmic artery for central retinal artery occlusion.  

After the angiogram, the patient developed right gaze preference, left-sided facial droop, left hemiparesis, and neglect. CT head revealed right hemispheric sulcal effacement with diffusely hyperdense right hemisphere suggestive of cerebritis. CT angiogram revealed no occlusion. MRI brain showed restricted diffusion involving the right cerebrum with cortical ribboning, consistent with cerebritis. The patient was started on intravenous fluids and Decadron 4 mg every 6 hours. She improved clinically. Brain MRI 2 months later showed full resolution of prior inflammatory changes.  

Conclusions:
We highlight the importance of recognizing symptoms and imaging characteristics of contrast-induced cerebritis, as it can be a reversible cause of acute neurological focal deficits. Most cases are self-limiting, although a minority may develop permanent deficits or even fatal cerebral edema. Treatment is focused on decreasing inflammation, which can be accomplished with steroids or mannitol and IV fluids.  
10.1212/WNL.0000000000211551
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