POSTERIOR REVERSIBLE ENCEPHALOPATHY

POSTERIOR REVERSIBLE ENCEPHALOPATHY - keywords
PRES references to PRES r e f e r e n c e s n a v i g a t o r < Casey SO, Sampaio RC, Michel E, Truwit CL (2000) Posterior reversible encephalopathy syndrome: utility of fluid-attenuated inversion recovery MR imaging in the detection of cortical and subcortical lesions. Am J Neuroradiol 21(7):1199-206. Covarrubias DJ, Luetmer PH, Campeau NG (2002) Posterior reversible encephalopathy syndrome: prognostic utility of quantitative diffusion-weighted MR images. Am J Neuroradiol 23(6):1038-48. Govaert, P., De Vries, L. (2010) An atlas of neonatal brain sonography, second edition . McKeith Press, Wiley, UK as Clinics in Developmental Medicine, nrs 182-183. ISBN 978-1-898683-56-. Keyserling HF, Provenzale JM (2007) Atypical imaging findings in a near-fatal case of posterior reversible encephalopathy syndrome in a child. Am J Roentgenol 188(1):219-21. McKinney AM, Short J, Truwit CL, McKinney ZJ, Kozak OS, SantaCruz KS, Teksam M (2007) Posterior reversible encephalopathy syndrome: incidence of atypical regions of involvement and imaging findings. Am J Roentgenol 189(4):904-12. Pavlakis SG, Frank Y, Chusid R (1999) Hypertensive encephalopathy, reversible occipitoparietal encephalopathy, or reversible posterior leukoencephalopathy: three names for an old syndrome. J Child Neurol 14(5):277-81. Prasad N, Gulati S, Gupta RK, Sharma K, Gulati K, Sharma RK, Gupta A (2007) Spectrum of radiological changes in hypertensive children with reversible posterior leucoencephalopathy. Br J Radiol 80(954):422-9. Stott VL, Hurrell MA, Anderson TJ (2005) Reversible posterior leukoencephalopathy syndrome: a misnomer reviewed. Intern Med J 35(2):83-90.Utsunomiya H (2011) Diffusion MRI abnormalities in pediatric neurological disorders. Brain Dev 33(3):235-42. https://radiopaedia.org/articles/posterior-reversible-encephalopathy-syndrome-1 Typical MRI changes in adults:T1: hypointense (darker) affected regions T1 + contrast (gadolinium): patchy variable enhancement T2/FLAIR: hyperintense (brighter) affected regions DWI: usually normal, sometimes restricted diffusion ADC: usually increased signal (brighter) due to increased diffusion, but restricted diffusion (darker) possible SWI: may show microhaemorrhages MRA: may show vessel irregularity consistent with vasoconstrictions/vasodilatation. DWMRI can distinguish in the acute stage between vasogenic (increased ADC) and cytotoxic (decreased ADC) oedema, which helps predict conversion to infarction (if ADC decreased) with irreversible tissue damage (Utsunomyia 2011). Purely vasogenic changes may be completely reversible and remain invisible on DWMRI, although some T2 shine-through is possible. Typical posterior reversible encephalopathy syndrome in adults manifests as bilateral vasogenic edema within the occipital and parietal regions (70-90% of cases), but also in watershed areas, including within the frontal, inferior temporal, cerebellar, and brainstem regions. Both cortical and subcortical areas are affected. Uncommon are purely unilateral PRES, brainstem (particularly pons) or basal ganglia involvement (central PRES), spinal cord PRES. The vertebrobasilar system may be particularly vulnerable because fo a lack of orthosympathic innervation in branches of the basilar artery. Ultrasound findings: To our knowledge the examples presente here are the only reported PRES conditions in neonates (courtesy de Vries Utrecht and Horsch Berlin). In one of them anterior and ventrolateral thalamus were involved. The areas are bilateral nearly symmetrical, especially affecting striatum and also thalamus. Associated plexus haemorrhage may fit with the mechanism of rupture of the BBB. The hyperechoic areas persist for days, later regress and do not leave cavitation. The disappearance and diffusion negativity are characteristic of PRES. The bilaterality and multiplicity on each side also exclude perforator stroke. In the children presented here no metabolic disorder was diagnosed. “Posterior reversible leukoencephalopathy syndrome” presents in children and adults with headache, altered mental status, seizures and visual loss. The term derives from imaging findings of predominantly posterior areas of vasogenic oedema [hypersignal on T2 and FLAIR (fluid-attenuated inversion-recovery)(Pavlakis et al. 1999, Covarrubias et al. 2002, Stott et al. 2005, Prasad et al. 2007, McKinney et al. 2007). The term is a misnomer because the condition is not always reversible, and not necessarily confined to the posterior cerebral regions (Keyserling et al. 2007). MRI has shown lesions in both grey and white matter (Casey et al. 2000). Most adult PRES occurs in association with hypertension and/or immunosuppression, and it is believed to result from the failure of vessels to compensate adequately for rapid unusual increase of blood pressure, resulting in fluid extravasation. Typical is the context of eclampsia with “hypertensive encephalopathy”. Although posterior reversible encephalopathy syndrome is most associated with hypertension, this does not appear to be obligatory. Alternative conditions may culminate in altered integrity of the blood-brain barrier: - high blood pressure leads to loss of autoregulation, hyperperfusion with endothelial damage and vasogenic edema - vasospasm - endothelial dysfunction secondary to endogenous or exogenous toxins. PRES is seen in children with hypertension, but after antihypertensive therapy, most improve. Some children have PRES associated with chemotherapy, transplantation, transfusion or HIV-1 infection. PRES: posterior reversible encephalopathy syndrome examples > preterm and term hypertension Term infant with hypertension due to coarctation of the aorta. Symmetrical hyperechoic change in striatum and thalamus was reversible. case by courtesy Horsch S, Berlin: 31w, eclampsia, secondary caesarean, Apgar 0/1, breathing after 5 minutes, resuscitation started at 5 minutes, blood lactate 11 mmol/l with fast normalisation, no neonatal seizures, no CP and Bayley MDI 94 and PDI 85 at 2 years. Hyperechoic changes due to PRES were associated with haemorrhage into choroid plexus. Preterm with severe hypertension bout. Changes within the basal ganglia in the acute (left) and subacute (right) stage. Development was normal at 2 years. ——> preterm, maternal eclampsia examples of PRES Mac OS X 2ÖATTRÜ,Ücom.apple.TextEncodingëcom.apple.provenanceöcom.apple.quarantineutf-8;134217984Â.Im0ÖWq/0081;00000000;;

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