2011 Volume 39 Issue 2 Pages 138-143
We report a case of posterior reversible encephalopathy syndrome (PRES) with subarachnoid hemorrhage in eclampsia. A 31-year-old female presented with a sudden severe headache and generalized convulsive seizure 6 days after delivery. Initial blood pressure was 198/100 (mean 133). Moderate disturbance of consciousness was observed. A brain CT scan was performed by her gynecologist and revealed subarachnoid hemorrhage. Therefore she was referred to our neurosurgery department. A 3D-CTA and MRA were performed on the day of admission, and no ruptured aneurysm and only very mild segmental vasoconstrictions at the vertebral artery and posterior cerebral artery were shown. A FLAIR image revealed multiple vasogenic edema in the cerebellar hemisphere, cerebral cortices and basal ganglia bilaterally. PRES was the most likely diagnosis. The sedative Propofol was administered for 3 days, and the patient recovered clinically. A follow-up MRI and MRA were performed 3, 10, and 21 days and 1 and 2 months after admission. Although a continuous reduction of the vasogenic edemas was shown by a follow-up FLAIR image, the severest diffuse vasoconstrictions in multiple cerebral arteries appeared 3 days after admission. Vasoconstrictions gradually improved during 2 months of follow-up.
Concerning the clinical cause of vasogenic edema in PRES, Bertynski mentioned 2 theories in his review. One theory is “Injury of the endothelium caused by altered autoregulation of cerebral arteries following excessive hypertension results in vasogenic edema,” and the other is “Vasogenic edema caused by the cerebral infarction after vasoconstriction.” In the present case, an elevated initial blood pressure was shown, but the mean arterial pressure did not seem high enough to injure the endothelium. Besides, the severest vasoconstriction of cerebral arteries did not occur until 3 days after the peak of the vasogenic edema. This means vasoconstriction did not precede vasogenic edema. Both theories are still controversial, and our case does not correspond to either theory.
We conclude that the present case shows a new theory for the clinical cause of vasogenic edema in PRES should be considered.
