Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD)

Infectious diseases

General description

Acute Encephalopathy with Biphasic Seizures and Late Reduced Diffusion (AESD) is characterized by an initial presentation of status epilepticus, followed by a temporary resolution of symptoms. However, after several days, the individual experiences a recurrence of status epilepticus accompanied by unconsciousness. This biphasic pattern of seizures, with a transient period of improvement before a second phase of neurological deterioration, is a hallmark of AESD.

Seizures and brain damage triggered by infections, such as influenza, are significant complications that can arise from the body's response to the infection.

Bright tree appearance

  • Cerebrum
    Frontal lobe
    Cerebral white matter
    Subcortical white matter
    U-fiber
  • Cerebrum
    Parietal lobe
    Cerebral white matter
    Subcortical white matter
    U-fiber
Symmetric
Bilateral
Linear
T2WI
Hyperintensity
FLAIR
Hyperintensity
DWI
Hyperintensity
ADC
Hypointensity

T2WI and FLAIR reveal linear hyperintensity involving the subcortical U-fibers, predominantly affecting the frontal and parietal lobes bilaterally, often accompanied by diffusion restriction. Diffuse subcortical white matter diffusion restriction is observed; however, the precentral and postcentral gyri remain spared, a phenomenon referred to as central sparing.

Basal ganglia and thalamus lesion

  • Caudate nucleus
  • Subthalamic nucleus
  • Thalamus
Asymmetric
Unilateral
Bilateral
T2WI
Hyperintensity
FLAIR
Hyperintensity
DWI
Hyperintensity

In AESD, MRI occasionally reveals asymmetric T2WI and FLAIR hyperintensities in the caudate nucleus, substantia nigra, and thalamus, accompanied by DWI hyperintensity without ADC hypointensity. Unlike Acute necrotizing encephalopathy (ANE), AESD does not exhibit hemorrhagic changes in the thalamus.