FACTS
- epidemiology: can occur in all ages but more likely in adults, F > M, Black > White/Hispanic
- pathophysiology: acute HTN, systemic inflammation, endothelial dysfunction disrupt cerebral autoregulation
HPI
universal ROS, with emphasis on
- seizures
- encephalopathy
- HA
- visual disturbances
Risk factors
- acute HTN,
- eclampsia, pregnancy, HELLP, post-partum status,
- autoimmune disease (SLE, Crohn’s, autoimmune hemolytic anemia, hypothyroidism, RA, Sjogren’s, primary sclerosing cholangitis),
- renal failure,
- sepsis, hematological disorders (TTP)
- electrolyte disturbances
- medicinal toxins (tacrolimus, anti-angiogenic drugs e.g. bevacizumab, tyrosine kinase inhibitors, anti-CD19 CAR-T therapies)
- drugs: cocaine, amphetamine, synthetic cannabinoids (via acute HTN, direct neurotoxic effects, endothelial dysfunction)
IMAGING
MRI Brain without contrast
- FLAIR: symmetric subcortical vasogenic edema affecting parieto-occipital regions although can be anywhere (frontal lobes, temporal lobes, thalamus, brainstem, BG, cerebellar)
- DWI: can restrict diffusion
- T1 + c: can enhance
CT angiography
- vasoconstriction, especially posteriorly, can be seen (co-occurring RCVS)
CT perfusion
- can show hyperperfusion or reduced perfusion
A/P
Diagnosing PRES (Rabinestein et al 2025)
- LP: should show elevated protein concentration without pleocytosis
Treatment
- supportive care
- AED
- cEEG if mental status poor or fluctuating
- mannitol / HTS only if herniation imminent
- address underlying etiology
- most patients will get better with blood pressure control
- remove the triggering medicine
- delivery of baby/placenta
- Counsel:
- in absence of strokes / severe hemorrhage requiring CSF diversion, most will make a full recovery following prompt diagnosis and treatment