Unilateral Posterior Reversible Encephalopathy Syndrome in Chronic Intracranial Occlusion: A Case Report
Jayant Yadav1, Rafail Chionatos1, Sharanya Ramakrishnan1, Matthew Tilem2
1Tufts Medical Center, 2Lahey Clinic
Objective:
To highlight a pathophysiologic mechanism of a rare form of Posterior Reversible Encephalopathy Syndrome (PRES), leading to appropriate diagnosis and management.
Background:
The pathophysiology of PRES is not well understood but is thought to involve endothelial dysfunction with compromise of the blood–brain barrier (BBB). Unilateral PRES is a rare variant.
Results:
A 69-year-old female with recent left Middle Cerebral Artery (MCA) stroke, type 2 diabetes, peripheral vascular disease, obstructive sleep apnea, subdural hematoma and coronary artery disease presented from a rehabilitation facility with headache, nausea, vomiting, worsening right-sided weakness, facial droop, dysarthria, and aphasia. She had experienced severe frontal and retro-orbital headaches and poorly controlled blood pressure for several days. In the ED, her systolic blood pressure was 210 mmHg. Stroke code was activated. NIHSS was 8. CTA revealed chronic left MCA occlusion with moderate collaterals. CT perfusion revealed evidence of chronic left MCA occlusion with an 8-cc ischemic penumbra. MRI of the brain with contrast revealed extensive cortical and subcortical edema in the left temporal, parietal, and occipital lobes without corresponding diffusion restriction or abnormal enhancement consistent with PRES. EEG revealed LPDs (1Hz) without evidence of seizures or postictal slowing. She was hospitalized and systolic blood pressure gradually decreased to less than 140 mmHg with improvement in right-sided hemiparesis, aphasia, and moderate right visual field deficit at discharge. A new MRI 2 months after discharge revealed interval resolution of edema with stable encephalomalacia.
Conclusions:
Chronic intracranial arterial occlusion can promote extensive collateral formation. However, a significant rise in arterial blood pressure can disrupt cerebral autoregulation, leading to endothelial dysfunction and breakdown of the blood-brain barrier. This results in hemispheric vasogenic edema which can resolve with blood pressure control.
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