Cerebellar and brainstem variant of posterior reversible encephalopathy syndrome

Posterior reversible encephalopathy syndrome (PRES) represents a clinical and radiographic finding that comprises many aetiologies. Clinically, it is characterized by headache, impaired variable mental status, visual disturbances and seizures with a reversible course as the main cause is solved. The underlying pathophysiology seems to be a breakdown in cerebral autoregulation and endothelial dysfunction. Neuroimaging is essential for the diagnosis and typically consists of symmetrical white-matter oedema in the posterior regions of the cerebral hemispheres. The diffusion-weighted images (DWI) sequences play an important role in differential diagnosis and prognosis evaluation. Differential diagnosis must be made with illdefined lesions situated in the white matter of the posterior fossa structures of the brain. Isolated posterior fossa lesions are uncommon and represent a variant of PRES. McKinney et al. [1], evaluated fluid attenuated inversion recovery (FLAIR) images of 124 patients with PRES to determine the incidence of this uncommon variant, which they refer to as the ‘‘central variant’’; the authors found that 4 % of patients with PRES had magnetic resonance imaging (MRI) findings consistent with the central variant that is, either brainstem, cerebellum or basal ganglia involvement and a lack of cortical or subcortical oedema of the cerebrum. The imagistic hallmark of PRES is reversibility once aetiological factors have been controlled [1–5]. We present a rare case of cerebellar and brainstem variant of PRES as the inaugural manifestation of an end-stage chronic renal disease. A 42-year-old male patient with no significant past medical history was admitted to the emergency department with complains of occipital headache, nausea, vomiting and dysequilibrium. The clinical examination was relevant only for elevated blood pressure values (190/110 mmHg). The neurological examination revealed globally brisk deep-tendon reflexes, ataxic gait and mild bilateral dysmetria. Upon admission, laboratory analysis revealed elevated blood urea nitrogen (194.7 mg/dl) and elevated serum creatinine 9.68 mg/dl. Autoimmune and infectious markers were negative. Cerebral computer tomography (CT) showed multiple white-matter hypodensities in both cerebellar hemispheres and the brainstem (Fig. 1). MRI showed confluent areas of hypersignal on T2 and FLAIR-weighted images situated in the cerebellar white matter as well as in the pons and midbrain (Fig. 2). Supratentorially, MRI revealed lacunar infarctions and leukoaraiosis (Fig. 2). No contrast was administered due to renal involvement. DWI showed slight hypointensity corresponding to the hyperintense lesions seen on T2 and FLAIR sequences. R. Bălasa S. Maier Z. Bajko Department of Neurology, University of Medicine and Pharmacy Târgu Mures, Târgu Mures, Romania