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Abstract Details

Reversible focal neurologic deficits as a complication of diagnostic cerebral angiogram
Cerebrovascular Disease and Interventional Neurology
P14 - Poster Session 14 (11:45 AM-12:45 PM)
13-007

Contrast-induced encephalopathy (CIE) is a rare complication of coronary angiography/diagnostic cerebral angiogram (DCA) presenting with focal neurologic deficits and neuroimaging evidence of cerebral edema with focal contrast extravasation in the subarachnoid space. Here, we describe a case of reversible focal neurological deficits (RFND) post-DCA (without intervention) without the aforementioned neuroimaging features.

A 79-year-old woman underwent routine biannual DCA for monitoring of basilar artery aneurysm coiling. Four hours post-DCA, global aphasia was noted. Magnetic resonance (MR) brain was negative for acute intracranial pathology. EEG demonstrated focal slowing in the left hemisphere. Nine hours post-DCA, patient additionally developed left gaze deviation and right hemiparesis. EEG remained unchanged. Repeat neuroimaging with computed tomography (CT) of head without contrast was unrevealing. CT angiogram of head and neck demonstrated decreased flow to distal vasculature in the left hemisphere. CT perfusion demonstrated increased mean transit time to the left hemisphere. Repeat MR brain with and without contrast at 24 hours post-DCA was unrevealing however MR perfusion imaging continued to show decreased perfusion to the left cerebral hemisphere. Intravenous nimodipine was initiated due to suspected cerebral vasospasm. Clinical improvement was noted within 48 hours and complete symptom resolution within five days post-treatment.

Case report
One week post-DCA, repeat MR perfusion and EEG demonstrated resolution of previously noted findings with no residual deficits on the MR brain with and without contrast.

RFND as complication of DCA in the absence of neuroimaging evidence of contrast extravasation and cerebral edema was not previously described to best of our knowledge. Given the temporal course, we suspect focal hypoperfusion due to cerebral vasospasm as the likely etiology, possibly attributable to iodinated contrast agent. Further studies are needed to clarify whether this represents an entity separate from previously described CIE, where contrast staining and cerebral edema are seen on neuroimaging.

Authors/Disclosures
Anusha Mangalampalli, MD
PRESENTER
Dr. Mangalampalli has nothing to disclose.
Sri Raghav S. Sista, MD (UTHouston) Dr. Sista has nothing to disclose.
Elias Samaha, MD (OSF Multispecialty Group) Dr. Samaha has nothing to disclose.