Vascular & Stroke
PRES: Reversible — If You Name the Complications
Fellowship-level neuroradiology teaching by E. Brooke Schrickel, MD. Open this topic in the interactive reading room →
Watch · concise explainerVisual summary
Core clinical idea
Both are treatable and usually reversible, so the value of the read is the prompt diagnosis plus naming the complications that flip prognosis. PRES is a clinico-radiologic pattern (risk factors + acute presentation + reversible vasogenic edema, not imaging alone); RCVS is defined by reversible segmental vasoconstriction read across serial studies.
Bottom line
PRES and RCVS are reversible and treatable — make the prompt diagnosis, then report the complications (diffusion restriction, hematoma, sulcal SAH, infarct) that decide the outcome.
Core workstation questions
- Is the edema vasogenic (high T2/FLAIR, elevated ADC) — and where (posterior, frontal-sulcus, deep gray, brainstem)?
- Are the worse-outcome features present: restricted diffusion, hematoma with mass effect?
- Do the risk factors and acute presentation support PRES (hypertension, chemo/immunosuppression, peripartum)?
- For thunderclap headache with segmental narrowing: is this RCVS — and will short-interval follow-up show reversibility?
- Is the SAH convexity/sulcal (RCVS) or basal-cistern (aneurysm)? Hemorrhage early, infarct later?
- Concomitant PRES + RCVS — and does a quiet (non-enhancing) wall steer me away from vasculitis?
What changes reporting / management
- Call PRES when risk factors + acute presentation + reversible-type vasogenic edema (high T2/FLAIR, elevated ADC, posterior-predominant +/- frontal-sulcus) line up; treatment is reverse the driver (BP control, withdraw/change offending drug, peripartum management).
- Explicitly flag PRES worse-outcome features: restricted diffusion (cytotoxic injury) and hematoma with mass effect.
- RCVS: multifocal segmental vasoconstriction, thunderclap headache + vasoactive trigger, young/middle-aged women; recommend short-interval follow-up to confirm reversibility, since initial luminal imaging can be normal.
- Separate RCVS SAH (convexity/sulcal) from aneurysmal basal-cistern SAH; watch hemorrhagic complications early and ischemic (TIA -> infarct) later.
- Read PRES/RCVS as an overlapping spectrum (can co-occur); CCB for RCVS vasoconstriction + withdraw agent; a quiet non-enhancing vessel wall and reversibility favor RCVS over vasculitis and spare immunosuppression.
Practical traps
- Excluding PRES because it's atypical/central (deep gray, brainstem-only, confluent periventricular) or because it hemorrhages/enhances — those don't exclude it.
- Missing the bad-actor PRES features (diffusion restriction, hematoma with mass effect) that change outcome.
- Committing an RCVS patient to a vasculitis workup/steroids — RCVS is non-inflammatory and reversible; biopsy is to exclude vasculitis, not diagnose RCVS.
- Reading RCVS SAH as aneurysmal because the thunderclap headache is identical — location (convexity vs. basal cistern) separates them.
Teaching pearls
- PRES is a clinico-radiologic diagnosis — risk factors plus reversible vasogenic edema, not imaging alone.
- Prove it's vasogenic: high T2/FLAIR with elevated ADC. Restricted diffusion is the bad actor.
- PRES isn't always posterior or pure — central, brainstem-only, hemorrhagic, and enhancing variants are still PRES.
- RCVS is the diagnosis of the time-course — reversibility on serial imaging, hemorrhage early, ischemia late.
- RCVS SAH is at the convexity, not the basal cisterns — and the quiet wall separates it from vasculitis.
Teaching visuals
Source lectures
- Posterior Reversible Encephalopathy Syndrome (PRES) & Reversible Cerebral Vasoconstriction Syndrome (RCVS)
Educational material for radiology residents and neuroradiology fellows. Nothing here drives individual patient care, and it contains no patient data.