Specific Imaging Findings

The cortex involved is expanded and bright on T2 and FLAIR sequences. DWI shows high signal and on ADC maps values may be normal to slightly low. Mesial temporal lobes are typically affected but other parts of the brain may also be involved. Contrast enhancement is rare but has been described. Findings generally disappear from 2 weeks to 2 months after the ictus and the affected regions return to normal or become atrophic. MR spectroscopy may show normal choline, low n-acetyl aspartate (NAA) and lactate. Lactate tends to disappear within the first few days after the ictus. PET studies show increased fluoro-deoxyglucose uptake in corresponding sites. The abnormality may be localized in the splenium of the corpus callosum, also showing reduced diffusion. Occasionally the white matter can be diffusely affected, with T2 hyperintensity and reduced diffusion in a pattern similar to diffuse anoxia. In these patients, MR spectroscopy may show high glutamine and glutamate and low NAA. Patients with persistent low NAA after the first week have worse prognosis. This syndrome is called acute encephalopathy with biphasic seizures and late reduced diffusion (AESD).

Pertinent Clinical Information

Most patients have prolonged seizures which may be partial or generalized. The imaging findings are seen in the first 3 days that follow the seizure episode and thereafter tend to slowly normalize. Patients tend to be children, but these MRI findings may be seen at any age. These imaging abnormalities tend to correspond with sites of electroencephalographic ictal activity and increased radionuclide uptake on PET studies. Patients with AESD have a typical clinical course: a prolonged (> 30 min duration) usually febrile seizure followed by secondary seizures (generally clusters of partial complex ones) a few days later and encephalopathy. Infection and associated pathologic changes are considered responsible for AESD.