Neuroimaging features in subacute encephalopathy with seizures in alcoholics (SESA syndrome). (August 2016)

• Record Type: Journal Article
• Authors: Drake-Pérez, Marta; Marco de Lucas, Enrique; Lyo, John; Fernández-Torre, José L.
• Is Part Of: Seizure. Volume 40(2016)
• Page Start: 102
• Page End: 107
• Publication Date: 2016-08
• Subjects: SESA subacute encephalopathy with seizures in alcoholics -- EEG electroencephalography -- NCSE nonconvulsive status epilepticus -- PLDs periodic lateralized discharges -- MRI magnetic resonance imaging -- SE status epilepticus; SESA syndrome -- Nonconvulsive status epilepticus -- Periodic lateralized discharges -- Neuroimaging -- Alcohol abuse; Epilepsy -- Periodicals; Epilepsy -- Periodicals; Seizures -- Periodicals; Épilepsie -- Périodiques; Electronic journals; Electronic journals; 616.853
• DOI: 10.1016/j.seizure.2016.06.009
• Languages: English
• ISSNs: 1059-1311

Abstract

Highlights: SESA syndrome should be included among the alcohol-related encephalopathies. It presents with acute confusional state, PLDs, transient neurologic deficits and seizures. MRI features include temporal atrophy, chronic vascular lesions and findings similar to SE. Abstract: Purpose: To describe the neuroimaging findings in subacute encephalopathy with seizures in alcoholics (SESA syndrome). Methods: We reviewed all cases reported previously, as well as 4 patients diagnosed in our center. We included a total of 8 patients. All subjects had clinical and EEG findings compatible with SESA syndrome and at least one MRI study that did not show other underlying condition that could be responsible for the clinical presentation. Results: Initial MRI studies revealed the following features: cortical–subcortical areas of increased T2/FLAIR signal and restricted diffusion (6 patients), hyperperfusion (3 patients), atrophy (5 patients), chronic microvascular ischemic changes (4 patients). Follow-up MRI was performed in half of the patients, all showing a resolution of the hyperintense lesions, but developing focal atrophic changes in 75%. Conclusions: SESA syndrome should be included among the alcohol-related encephalopathies. Its radiological features include transient cortical–subcortical T2-hyperintense areas with restricted diffusion (overlapping the typical findings in status epilepticus) observed in a patient with atrophy and chronic multifocal vascular lesions.