Posterior Reversible Encephalopathy Syndrome (PRES)

Posterior Reversible Encephalopathy Syndrome (PRES) is a clinicoradiological syndrome characterized by:

• Acute neurological symptoms
• Vasogenic cerebral edema (predominantly posterior circulation territory)
• Reversible changes on neuroimaging

It is not always posterior and not always reversible

• Frontal lobes may be involved
• Basal ganglia involvement possible
• Brainstem and cerebellar involvement possible
• Can even be unilateral

Pathophysiology of PRES

Two major competing (but complementary) theories:

1️⃣ Failure of Cerebral Autoregulation (Hyperperfusion Theory)

When BP exceeds autoregulatory limits:

• Loss of arteriolar vasoconstriction
• Hyperperfusion
• Blood–brain barrier breakdown
• Extravasation of plasma → vasogenic edema

Posterior circulation more vulnerable because:

• Less sympathetic innervation
• Vertebrobasilar system less protected

2️⃣ Endothelial Dysfunction Theory (More accepted in ICU patients)

Seen in:

• Sepsis
• Cytotoxic drugs
• Eclampsia
• Transplant patients

Mechanism:

• Endothelial activation
• Capillary leakage
• Vasogenic edema
• Sometimes microthrombosis

Etiology & Risk Factors 

1️⃣ Hypertensive Emergencies

• Malignant hypertension
• Rapid BP fluctuations

2️⃣ Eclampsia / Preeclampsia

• Classic board question

3️⃣ Sepsis / Septic Shock

• Endothelial injury
• Cytokine storm

4️⃣ Renal Failure

• Fluid overload
• Uremia
• Dialysis disequilibrium

5️⃣ Immunosuppressive Drugs

• Cyclosporine
• Tacrolimus
• Chemotherapy
• Anti-VEGF agents

6️⃣ Autoimmune Disease

• SLE
• TTP

Clinical Presentation

Classic Tetrad

1. Headache (throbbing)
2. Seizures (often generalized tonic–clonic)
3. Visual disturbances
4. Altered sensorium

Detailed Symptomatology

Imaging 

CT Brain(Not sensitive)

• May be normal early
• Hypodensities in posterior regions

MRI Brain 

Typical Findings:

• Bilateral symmetrical
• Parieto-occipital white matter hyperintensity
• FLAIR hyperintensity
• No restricted diffusion (vasogenic, not cytotoxic)

DWI / ADC Pattern

• Vasogenic edema → ↑ ADC
• Cytotoxic edema → ↓ ADC (poor prognosis)

 Important  differentiation from ischemic stroke.

Atypical Imaging Patterns

• Frontal lobe involvement
• Basal ganglia involvement
• Brainstem involvement
• Hemorrhagic PRES (15–20%)

Differential Diagnosis

Critical Care Management

Step 1: Control Blood Pressure

Goal:

• Reduce MAP by 20–25% in first hour
• Avoid rapid overcorrection

Preferred agents:

• Nicardipine infusion
• Labetalol infusion

Avoid:

• Nitroprusside (↑ ICP risk)

 Step 2: Seizure Management

Follow status epilepticus protocol:

1. Benzodiazepines
2. Levetiracetam (preferred in ICU)
3. Valproate (avoid in liver failure)
4. Phenytoin (less preferred)

Long-term AED usually not required if reversible.

Step 3: Remove Trigger

• Stop offending drug (tacrolimus, cyclosporine)
• Deliver fetus in eclampsia
• Treat sepsis aggressively
• Dialysis optimization in renal failure

 Step 4: ICP Control (if needed)

• Head elevation
• Osmotherapy (mannitol / hypertonic saline)
• Controlled ventilation if intubated

Complications

• Intracerebral hemorrhage
• Status epilepticus
• Brain herniation (rare)
• Persistent deficits (if delayed treatment)

 Is It Always Reversible?—>No.

Reversibility depends on:

• Early recognition
• Prompt BP control
• Removal of trigger
• Absence of cytotoxic edema

Poor prognostic markers:

• Diffusion restriction
• Brainstem involvement
• Severe hypertension
• Delayed management

Prognosis

• Most improve within 1 week
• Radiological resolution within weeks
• Mortality: ~5–15% in ICU cohorts
• Recurrence possible

PRES vs RCVS 

Reversible Cerebral Vasoconstriction Syndrome (RCVS)