Abstract Number ‐ 215: Distinct presentation of RCVS and PRES co‐existence and overlap of their pathophysiology

Abstract

Introduction Reversible cerebral vasoconstriction syndrome (RCVS), is characterized by reversible segmental and multifocal vasoconstrictionof cerebral arteries leading to infarcts and cytotoxic edema. Posterior reversible encephalopathy syndrome (PRES) is characterized by vasogenic edema predominantly in the parieto‐occipital regions associated with acute onset encephalopathy, seizures, headache, and visual disturbances.Whether PRES and RCVS are independent syndromes and sometimes overlapped or part of a continuum process, these theories are still debated. We report a case of a patient with distinct overlapping of RCVS and PRES. Methods Case Report Results 52‐year‐old woman with past medical Hx of Hypertension, Diabetes, Migraines and cocaine use, initially presented with hypertensive emergency andsubacute headaches with worsening confusion. Initial CT head was negative for bleed but showed evolving subcortical hypodensities in the right parietal and left frontal lobes. CTA head and neck showed multifocal intracranial irregularities of bilateral ACAs and MCAs with paucity of left anterior M2 branch, left V3/V4 steno‐occlusion. This vasculopathy and clinical presentation is very consistent with RCVS.MRI of brain showed multiple acute / subacute punctate infarcts in the left corona radiata, bilateral basal ganglia, right greater than left thalami, right dorsal pons, right mesial temporal lobe, bilateral occipital regions. Vasogenic edema was noted in the bilateral border zone regions, right parietal being most prominent with some contrast enhancement. The MRI showed vasogenic edema and cytotoxic edema with multiple infarcts which is consistent with PRES and RCVS vasculopathy. CSF analysis was negative for pleocytosis and showed mildly elevated protein. The patient was started on Verapamil and Aspirin and Atorvastatin for secondary stroke prevention. With improvement in mental status was discharged to Rehab. Conclusions The pathophysiological mechanisms of PRES and RCVS are still unknown. Theories whether RCVS and PRES are independent syndromes and sometimes overlap or part of spectrum, are still debated. However, some common characteristics make conceivable a common origin linked with impaired cerebral autoregulation, endothelial dysfunction, and BBB breakdown. Increased clinical awareness of their co‐existence may help in quickerdiagnosis and treatment.