ABSTRACT
Posterior reversible encephalopathy (PRES) is a condition characterized by T2 and FLAIR hyperintensities in magnetic resonance imaging (MRI) studies, localized preferentially in the occipital-parietal white matter regions. Pathological MRI images located in midbrain, pons, medulla and spinal cord, that could be asymptomatic, were recently included in this entity. These images are interpreted as vasogenic edema, which is caused by arterial hypertension or eclampsia, neurotoxicity related to immunosuppressive agents or chemotherapy, among other causes. We report a 25 years old asymptomatic male with AIDS, with normal blood pressure who after initiating highly active antiretroviral therapy (HAART) reported vertigo. The MRI showed a central pontine T2 hyperintensity with diffusion restriction, which was interpreted as a central pontine myelinolysis (CPM), but the lack of motor symptoms made improbable a real demyelination of the pons. The follow-up MRI revealed complete regression of the images. To our knowledge, this case could be the second report of a reversible leucopathy of the pons in a patient with AIDS, were the MRI images also simulated a CPM. This report extends the knowledge around the variability of the pathogenic interpretation of CPM images and their association with HAART.
Subject(s)
Humans , Male , Adult , Acquired Immunodeficiency Syndrome/complications , Antiretroviral Therapy, Highly Active/adverse effects , Posterior Leukoencephalopathy Syndrome/chemically induced , Magnetic Resonance Imaging , Acquired Immunodeficiency Syndrome/drug therapy , Posterior Leukoencephalopathy Syndrome/diagnostic imagingABSTRACT
Reversible posterior leukoencephalopathy syndrome (PLS) is characterized by headache, clouding of sensorium, visual disturbances and seizures. It is associated to hypertension, renal disease or immunosuppressive therapy. We report three males, aged 9, 12 and 16 years and one female, aged 5 years wih PLS associated to immunosuppressive therapy. All had seizures and three had headache and clouding of sensorium. One case was associated to an hypertensive emergency, one to liver failure and one to high tacrolimus levels. Magnetic resonance imaging showed lesions in the white matter in two patients and in the gray matter in the other two. The lapse between the start of immunosuppressive treatment and neurological symptoms ranged from 4 days to 6 months. All received antiepileptic drugs and immunosuppresive therapy was changed or decreased, with complete clinical recovery.