https://www.youtube.com/watch?v=7FUFku4auJc&t=11s

1. PRES (POSTERIOR REVERSIBLE
ENCEPHALOPATHY SYNDROME )
https://www.youtube.com/watch?v=7FUFk
u4auJc&t=11s

2. PRES
1.DEFINITION
2.PATHOPHYSIOLOGY
3.CLINICAL FEATURES
4.IMAGING
5.DIAGNOSIS AND D.D
6.TREATMENT AND PROGNOSIS

3. DEFINITION
• It is a clinical & radiographic syndrome of
heterogeneous etiologies that are grouped
together because of similar findings on
neuroimaging studies.
• Reversible subcortical brain edema.

4. OTHER NAMES
1. Reversible posterior cerebral edema
syndrome
2. Posterior leukoencephalopathy syndrome
3. Hypeperfusion encephalopathy
4. Brain capillary leak syndrome

5. PATHOPHYSIOLOGY
1. Associated with disordered cerebral
bloodflow autoregulation
2. Cerebral ischemia
3. Endothelial dysfunction.

6. Autoregulatory failure
• Normal autoregulation maintains constant CBF
over a range BP , by means of arteriolar
constriction and dilatation . If it is exceeded,
arterioles dilate and CBF increases resulting in
brain hyperperfusion, may lead to breakdown of
the BBB allowing extravasation of fluid and
blood products.

7. Cerebral ischemia
• Disordered autoregulation may lead to
reactive focal vasoconstriction, thereby
resulting in local hypoperfusion, cytotoxic
edema, and cerebral infarction

8. Endothelial dysfunction
• Especially in cases - preeclampsia or cytotoxic
therapies.
direct toxicity on vascular endothelium, leading to
-Capillary leakage
-BBB disruption
-Axonal swelling
which may then trigger vasogenic edema

9. Why posterior mainly
• Heterogeneity in the sympathetic distribution
of the intracranial arterioles,
• Postulated that greater concentration of
adrenergic nerves around pial and
intracerebral vessels in the anterior circulation
than posteriorly.

10. Risk Factors
• Hypertensive encephalopathy
• Eclampsia
• Vasculitis
• Contrast media exposure (cerebral, coronary
angiography

11. Major medical illness
1. Organ transplantation
2. TTP ,HSP ,HUS
4. Autoimmune : systemic lupus,
scleroderma,
Wegener’s,
PAN
5. Sepsis/SIRS
6. Alcohol and drug withdrawal
7. Hypomagnesemia,
hypercalcemia,
8. Renal failure
9. Transfusion.
Neurologic illness
1. GBS
2. Spinal cord injury
with autonomic
dysreflexia
3. Head injury

12. Drugs
Immunosuppressive, chemotherapeutic drugs
Cyclosporine A
Intravenous immunoglobulin
Methotrexate
Rituximab
Sirolimus
Tacrolimus

13. CLINICAL FEATURES
• Any age group .
• Females are slightly more affected .
SEIZURES HEADACHE
VISUAL
DISTURBANCES
ALTERED
SENSORIUM

14. EXAMINATION
• Focal neurologic deficits are rare.
• Fundoscopic examination is often normal,
might –papilledema.
• The deep tendon reflexes are frequently brisk
with Babinski signs often present.

15. IMAGING
• CT
• MRI
1.watershed zones
2.superior frontal sulcus
3.parieto-occipital dominance

16. T1: hypo intense in affected regions
T1 C: patchy variable enhancement
T2: hyperintense in affected regions
DWI: usually normal

19. Vasogenic edema.
DWI
Findings usually resolve with treatment.

20. DIAGNOSIS
• No specific diagnostic criteria.

22. DD
• Stroke,
• Vasculitis
• Venous thrombosis,
• Toxic or metabolic encephalopathy,
• Demyelinating disorders,
• Encephalitis among others

23. TREATMENT
• IDENTIFY ETIOLOGY
• BP CONTROL
• ANTIEPILEPTICS
• IF DRUG A/O – REDUCE THE DRUG DOSE OR
STOP IT.

24. Prognosis
• Usually benign .

25. SUMMARY
• Reversible subcortical brain edema
• Disordered CBF and endothelial dysfunction
• Headache , seizure , Altered sensorium, visual
disturbance
• Hyperintense on T2w
• Supportive treatment.
THANK YOU …. .https://www.youtube.com/watch?v=7FUFku4a
uJc&t=11s