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MRI SPECTRUM OF POSTERIOR
REVERSIBLE ENCEPHALOPATHY
SYNDROME(PRES)
Dr Nirav Kadvani
Dr Chandresh Karnavat
Dr Ritu Kashikar
Dr Shrinivas Desai
JASLOK HOSPITAL AND RESEARCH CENTRE
AIM
To study the spectrum of PRES(Posterior
Reversible Encephalopathy Syndrome)
DEFINITION
Acute change in Blood
Pressure.
Inability of posterior
circulation to autoregulate
Neurotoxicity menifiested
as PRES
Hyperperfusion
Disruption of the blood
brain barrier
Vasogenic oedema, but not
infarction, commonly in
the parieto-occipital
regions
MATERIALS & METHODS
 Study Area: Radiology department, JHRC
 Age: All Age group
 Sex: 11 male 8 female
 Machine:3T SIEMENS MAGNETOM,
 Sequences:T1,T2, FLAIR,DWI,ADC Images
were obtained
 Duration: August 2014 to January 2016
CASE-1 PREGNANCY WITH
HYPERTENSION & HEADACHE
WATERSHED
AREA LESION
CASE-2 POST LSCS, HYPERTENSION &
SEIZURES, RIGHT UPPER LIMB
WEAKNESS
FRONTAL
LOBE LESION
CASE-3 POST RENAL TRANSPLANT,
VISUAL SYMPTOMS
OCCIPITAL
LOBE LESION
CASE-5 UNCONTROLLED
HYPERTENSION & HEADACHE
WITH
MICROBLEED
CASE-6 POST BONE MARROW
TRANSPLANT, HEADACHE &
APHASIA
SPLENIAL
LESION
CASE -7 POST RENAL TRANSPLANT,
ALTERED MENTATION
BASAL
GANGLIA
LESION
CASE-8 POST TRANSPLANT,
UNCONTROLLED HYPERTENSION &
ATAXIA
CEREBELLAR
LESION
CASE-9 POST TRANSPLANT H/O
SEIZURES
UNILATRRAL
LESION
LOCATIONS OF BRAIN LESIONS
Location % Patients
Occipital/parietal 98
Frontal lobe 68
Inferior temporal/occipital 40
Cerebellum 32
Brain stem 13
Basal ganglia 14
Deep white matter 18
Splenium corpus callosum 10
RESULTS
DISCUSSION
 PRES is also known as acute hypertensive
encephalopathy or reversible posterior
leukoencephalopathy.
 Presents with headache, seizures,
encephalopathy and/or visual disturbance.
 Two main theories
 High blood pressure: leads to loss of self-regulation,
 Endothelial dysfunction: leads to vasoconstriction and
hypoperfusion
ETIOLOGY
 Severe hypertension
◦ post partum
◦ eclampsia/preeclampsia
◦ acute
glomerulonephritis
 Haemolytic uraemic
syndrome (HUS)
 Thrombocytopaenic
thromboic purpura
(TTP)
 Systemic lupus
erythematosus (SLE)
 Drug toxicity
◦ cisplatin
◦ interferon
◦ erythropoietin
◦ tacrolimus
◦ cyclosporin
◦ azathioprine
◦ use of L-asparginase
◦ bone marrow or stem
cell or organ
transplantation
 Sepsis
 Hyperammonemia
MRI FEATURES
 T1: hypo intense in affected regions
 T1 C+ (Gd): patchy variable enhancement. It can be seen in ~35%
of patients, whether leptomeningeal or cortical pattern.
 T2: hyperintense in affected regions
 DWI: usually normal
 ADC: signal increased in affected regions due to increased diffusion
 GRE: may show hypointense signal in cases of haemorrhage
 SWI: may show microhemorrhages in up to 50%
DIFFERENTIALS
 Progressive multifocal leukoencephalopathy
(PML): immunocompromised, commonly affect
subcortical u-fibre
 Severe hypoglycaemia:diabetic and insulinoma,
typically bilateral,spares cerebellum brainstem
and thalami in adults
 Posterior circulation stroke
 Gliomatosis cerebri: Diffusely infiltrative glial
tumour that involves at least three lobes by
definition
 Sagital sinus thrombosis
 Hypoxic-ischaemic encephalopathy: Primarily
affects gray matter structure.
DIFFERENTIALS
 Progressive multifocal leukoencephalopathy
(PML)
 Severe hypoglycaemia
 Posterior circulation stroke
 Gliomatosis cerebri
 Sagital sinus thrombosis
 Hypoxic-ischaemic encephalopathy
TYPICAL PATTERNS
Dominant Parietal-Occipital Pattern
Superior Frontal Sulcus Pattern
Holohemispheric watershed pattern
TAKE HOME MESSAGE
Syndrome can involve or extend beyond the posterior
cerebrum, Like
 Frontal and temporal lobes
 Cerebellum
 Brain stem
 Basal ganglia
 Deep white matter
 Splenium
Some patients can progress to develop permanent
cerebral injury
Can be unilateral
May have associated microbleed
PRES CAN BE MISNOMER
REFERENCES
 Posterior Reversible Encephalopathy Syndrome,Part
1: Fundamental Imaging and ClinicalFeatures ,W.S.
Bartynski,Am J Neuroradiol 29:1036–42
 Posterior reversible encephalopathy syndrome:
clinical and radiological manifestations,
pathophysiology, and outstanding questions Jennifer
E Fugate Prof and Alejandro A Rabinstein ProfLancet
Neurology, The, 2015-09-01, Volume 14, Issue 9.
 The many faces of posterior reversible
encephalopathy syndrome C J Stevens, MD and M K S
Heran, MD, FRCPC,Br J Radiol.2012 Dec
THANK YOU

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MRI SPECTRUM OF POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME

  • 1. MRI SPECTRUM OF POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME(PRES) Dr Nirav Kadvani Dr Chandresh Karnavat Dr Ritu Kashikar Dr Shrinivas Desai JASLOK HOSPITAL AND RESEARCH CENTRE
  • 2. AIM To study the spectrum of PRES(Posterior Reversible Encephalopathy Syndrome)
  • 3. DEFINITION Acute change in Blood Pressure. Inability of posterior circulation to autoregulate Neurotoxicity menifiested as PRES Hyperperfusion Disruption of the blood brain barrier Vasogenic oedema, but not infarction, commonly in the parieto-occipital regions
  • 4. MATERIALS & METHODS  Study Area: Radiology department, JHRC  Age: All Age group  Sex: 11 male 8 female  Machine:3T SIEMENS MAGNETOM,  Sequences:T1,T2, FLAIR,DWI,ADC Images were obtained  Duration: August 2014 to January 2016
  • 5. CASE-1 PREGNANCY WITH HYPERTENSION & HEADACHE WATERSHED AREA LESION
  • 6. CASE-2 POST LSCS, HYPERTENSION & SEIZURES, RIGHT UPPER LIMB WEAKNESS FRONTAL LOBE LESION
  • 7. CASE-3 POST RENAL TRANSPLANT, VISUAL SYMPTOMS OCCIPITAL LOBE LESION
  • 8. CASE-5 UNCONTROLLED HYPERTENSION & HEADACHE WITH MICROBLEED
  • 9. CASE-6 POST BONE MARROW TRANSPLANT, HEADACHE & APHASIA SPLENIAL LESION
  • 10. CASE -7 POST RENAL TRANSPLANT, ALTERED MENTATION BASAL GANGLIA LESION
  • 11. CASE-8 POST TRANSPLANT, UNCONTROLLED HYPERTENSION & ATAXIA CEREBELLAR LESION
  • 12. CASE-9 POST TRANSPLANT H/O SEIZURES UNILATRRAL LESION
  • 13. LOCATIONS OF BRAIN LESIONS Location % Patients Occipital/parietal 98 Frontal lobe 68 Inferior temporal/occipital 40 Cerebellum 32 Brain stem 13 Basal ganglia 14 Deep white matter 18 Splenium corpus callosum 10 RESULTS
  • 14. DISCUSSION  PRES is also known as acute hypertensive encephalopathy or reversible posterior leukoencephalopathy.  Presents with headache, seizures, encephalopathy and/or visual disturbance.  Two main theories  High blood pressure: leads to loss of self-regulation,  Endothelial dysfunction: leads to vasoconstriction and hypoperfusion
  • 15. ETIOLOGY  Severe hypertension ◦ post partum ◦ eclampsia/preeclampsia ◦ acute glomerulonephritis  Haemolytic uraemic syndrome (HUS)  Thrombocytopaenic thromboic purpura (TTP)  Systemic lupus erythematosus (SLE)  Drug toxicity ◦ cisplatin ◦ interferon ◦ erythropoietin ◦ tacrolimus ◦ cyclosporin ◦ azathioprine ◦ use of L-asparginase ◦ bone marrow or stem cell or organ transplantation  Sepsis  Hyperammonemia
  • 16. MRI FEATURES  T1: hypo intense in affected regions  T1 C+ (Gd): patchy variable enhancement. It can be seen in ~35% of patients, whether leptomeningeal or cortical pattern.  T2: hyperintense in affected regions  DWI: usually normal  ADC: signal increased in affected regions due to increased diffusion  GRE: may show hypointense signal in cases of haemorrhage  SWI: may show microhemorrhages in up to 50%
  • 17. DIFFERENTIALS  Progressive multifocal leukoencephalopathy (PML): immunocompromised, commonly affect subcortical u-fibre  Severe hypoglycaemia:diabetic and insulinoma, typically bilateral,spares cerebellum brainstem and thalami in adults  Posterior circulation stroke  Gliomatosis cerebri: Diffusely infiltrative glial tumour that involves at least three lobes by definition  Sagital sinus thrombosis  Hypoxic-ischaemic encephalopathy: Primarily affects gray matter structure.
  • 18. DIFFERENTIALS  Progressive multifocal leukoencephalopathy (PML)  Severe hypoglycaemia  Posterior circulation stroke  Gliomatosis cerebri  Sagital sinus thrombosis  Hypoxic-ischaemic encephalopathy
  • 19. TYPICAL PATTERNS Dominant Parietal-Occipital Pattern Superior Frontal Sulcus Pattern Holohemispheric watershed pattern
  • 20. TAKE HOME MESSAGE Syndrome can involve or extend beyond the posterior cerebrum, Like  Frontal and temporal lobes  Cerebellum  Brain stem  Basal ganglia  Deep white matter  Splenium Some patients can progress to develop permanent cerebral injury Can be unilateral May have associated microbleed PRES CAN BE MISNOMER
  • 21. REFERENCES  Posterior Reversible Encephalopathy Syndrome,Part 1: Fundamental Imaging and ClinicalFeatures ,W.S. Bartynski,Am J Neuroradiol 29:1036–42  Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions Jennifer E Fugate Prof and Alejandro A Rabinstein ProfLancet Neurology, The, 2015-09-01, Volume 14, Issue 9.  The many faces of posterior reversible encephalopathy syndrome C J Stevens, MD and M K S Heran, MD, FRCPC,Br J Radiol.2012 Dec