REVERSIBLE POSTERIOR LEUKOENCEPHALOPATHY SYNDROME

REVERSIBLE POSTERIOR LEUKOENCEPHALOPATHY SYNDROME

Received 19 May 2010, accepted 15 June 2010 | Dimitri Renard, Pierre Labauge, Rik Vandenberghe
Reversible posterior leukoencephalopathy syndrome (RPLS) is characterized by subacute onset of neurological symptoms such as headache, decreased alertness, vomiting, seizures, and visuo-perceptual disturbances, accompanied by bilateral white matter lesions in the posterior brain regions on brain imaging. The most common associated conditions are arterial hypertension and the use of immunosuppressive or cytotoxic treatments. MRI findings, particularly T2, FLAIR, and ADC-weighted images, reveal hyperintensities in periaqueductal white matter, with potential involvement of other regions. The underlying pathophysiology is likely vasogenic edema, influenced by factors such as cerebral autoregulation failure, endothelial dysfunction, disrupted blood-brain barrier, vasospasm, and direct toxic effects of drugs. Treatment involves discontinuing the causal drug, managing hypertension, and providing antiepileptic therapy. Early treatment is crucial for clinical recovery and regression of radiological abnormalities. However, delayed diagnosis and treatment can lead to irreversible brain damage, often associated with cerebral infarction or hemorrhage.Reversible posterior leukoencephalopathy syndrome (RPLS) is characterized by subacute onset of neurological symptoms such as headache, decreased alertness, vomiting, seizures, and visuo-perceptual disturbances, accompanied by bilateral white matter lesions in the posterior brain regions on brain imaging. The most common associated conditions are arterial hypertension and the use of immunosuppressive or cytotoxic treatments. MRI findings, particularly T2, FLAIR, and ADC-weighted images, reveal hyperintensities in periaqueductal white matter, with potential involvement of other regions. The underlying pathophysiology is likely vasogenic edema, influenced by factors such as cerebral autoregulation failure, endothelial dysfunction, disrupted blood-brain barrier, vasospasm, and direct toxic effects of drugs. Treatment involves discontinuing the causal drug, managing hypertension, and providing antiepileptic therapy. Early treatment is crucial for clinical recovery and regression of radiological abnormalities. However, delayed diagnosis and treatment can lead to irreversible brain damage, often associated with cerebral infarction or hemorrhage.
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