Virtual Conference
Sevil Jalilova

Sevil Jalilova

New Clinic. Bone Marrow Transplantation, Azerbaijan

Title: Posterior reversible encephalopathy syndrome during chemotherapy for acute lymphoblastic leukemia. Our clinical observations


Posterior reversible encephalopathy syndrome (PRES) is a clinical-neuroradiological syndrome with several known causes of hypertensive encephalopathy, eclampsia, and the use of cytotoxic, also immunosuppressive drugs. PRES is characterized by neuroimaging findings of reversible vasogenic subcortical edema without infarction. Hypertension and renal insufficiency are the most common etiological causes of PRES, and its pathophysiology is based on hyperperfusion. Its pathogenesis is still not fully known, there are several theories (1). Rather, two opposing hypotheses are cited; thus, the current more popular theory suggests that severe hypertension exceeds the autoregulatory threshold and causes severe cerebral edema, while another theory suggests that hypertension causes cerebral autoregulatory vasoconstriction, ischemia, and eventually cerebral edema (2). The clinical syndrome of PRES typically includes headache, encephalopathy, visual symptoms, and seizures. The clinical presentation is often nonspecific, and therefore the diagnosis of PRES is based on clinically documented recovery and repeated neuroimaging with pathological magnetic resonance imaging (MRI) consistent with PRES. The diagnosis has important therapeutic and prognostic implications, as reversal of clinical and radiological abnormalities depends on early control of arterial blood pressure (A/T) and/or discontinuation of causative drugs (3). PRES is usually symmetrically localized, observed in the occipital and parietal lobes, and typically characterized by vasogenic edema in the subcortical white matter (4). Although PRES is more common in adults, it has also been reported in some cases in children. Thus, PRES was observed in the pediatric group more often during the use of chemotherapy protocols used in acute leukemia. Its pathogenesis mainly involves impaired cerebral autoregulation leading to vasogenic edema of the parieto-occipital white matter, although involvement of the frontal and temporal lobes as well as the posterior fossa has also been described (5). Diagnosis of PRES is carried out by neurological examination and, most importantly, radiological examination method. Vasculopathy can be seen on MRI or angiography, and the vasculopathic changes seen are usually reversible. Cerebral vasoconstriction, diffuse or focal vasospasm, and a posterior bead pattern are more common. Sometimes cerebral hemangiomas in the form of hematoma in the parenchyma, hemorrhages smaller than 5 mm, subarachnoid hemorrhages are found in 5-19% of cases. Even in cases of severe edema, cerebral herniation may occur (6).