There may be signs of vasospasm or arteritis 3: The affected regions, as outlined above, are hypoattenuating. The presence of contrast enhancement, no matter the pattern or how avid, does not portend the clinical outcome. Parenchymal infarctions and hemorrhages are associated with posterior reversible encephalopathy syndrome in respectively 10-25% and 15% of cases. Other uncommon patterns of posterior reversible encephalopathy syndrome in <5% include: purely unilateral, or "central" (brainstem or basal ganglia lacking cortical or subcortical white matter involvement), or spinal cord involvement. Both cortical and subcortical locations are affected. Despite its name, however, posterior reversible encephalopathy syndrome can be found in a non-posterior distribution, mainly in watershed areas, including within the frontal, inferior temporal, cerebellar, and brainstem regions 2,19. Typical posterior reversible encephalopathy syndrome manifests as bilateral vasogenic edema within the occipital and parietal regions (70-90% of cases), perhaps relating to the posterior cerebral artery supply. during the late course of PRES: demyelination and myelin pallor along with evidence of ischemia, anoxic neuronal damage, laminar necrosis, or older hemorrhage in the white matter and cortex 3.during the acute course of PRES: vasogenic edema, without inflammation, ischemia, or neuronal damage 3.ventriculoperitoneal shunt insertion/overshunting 12.bone marrow or stem cell transplantation.thrombocytopenic thrombotic purpura (TTP).endothelial dysfunction secondary to circulating endogenous or exogenous toxins.vasospasm theory results in local ischemia and hypoperfusion.high blood pressure (breakthrough theory) leads to loss of self-regulation, hyperperfusion with endothelial damage and vasogenic edema.The underlying mechanisms involved are not well understood but is thought to culminate in altered integrity of the blood-brain barrier. Three main precipitant theories have been proposed, that are not mutually exclusive 19: PathologyĪlthough posterior reversible encephalopathy syndrome is most commonly thought of occurring as secondary to marked hypertension, this does not appear to be a necessary or sufficient explanation, given the very large and heterogeneous clinical scenarios that precipitate the development of posterior reversible encephalopathy syndrome and the fact that hypertension is not present or does not reach the upper limits of self-regulation (140-160 mmHg) in 25% of patients. However, the presentation can be quite varied, and may include other neurological symptoms such as ataxia, focal neurological deficits, vertigo, or tinnitus 19. visual disturbance, including reversible cortical blindness 20.encephalopathy ( acute confusion or altered mental state or decreased level of consciousness).Common presenting clinical features include 16,19:
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