Key result
Early AESD shows elevated Glx and decreased NAA, suggesting excitotoxic neuronal damage drives pathogenesis.
Why the study?
Excitotoxic neuronal damage in acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) was not well understood.
Does MR spectroscopy predict neurologic outcomes in patients with acute encephalopathy with biphasic seizures and late reduced diffusion?
Case Report (n=21)
Does MR spectroscopy predict neurologic outcomes in patients with acute encephalopathy with biphasic seizures and late reduced diffusion?
MR spectroscopy findings suggest excitotoxic neuronal damage plays a role in AESD pathogenesis and may predict neurologic outcomes.
MRS changes in AESD are hypothesis-generating; leaves open whether they predict outcomes or alter management.
Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is a recently described clinicoradiologic syndrome. MR spectroscopy in 3 patients with AESD revealed decreased N-acetylaspartate (NAA) and elevated glutamine/glutamate complex (Glx) during the week of presentation. Afterward, Glx normalized, whereas NAA remained low in 2 patients with neurologic sequelae but nearly normalized in the third patient without neurologic sequelae. These findings support the hypothesis that excitotoxic neuronal damage plays an important role in the pathogenesis of AESD and suggest that MR spectroscopy might be predictive of outcome.
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Takanashi et al. (2008) conducted a case report in Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) (n=21). Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) vs. Prolonged febrile seizures and healthy controls was evaluated on Brain metabolite concentrations (Glx and NAA) measured by MR spectroscopy. Patients with AESD exhibited elevated glutamine/glutamate complex (Glx) and decreased N-acetylaspartate (NAA) during the first week of presentation, suggesting excitotoxic neuronal damage plays a role in its pathogenesis.