The etiology of cerebral abnormalities after focal status epilepticus
(SE) is unknown. Possible causes include hypoxia and the excessive rel
ease of excitatory amino acids. Magnetic resonance imaging (MRI) of a
21-year-old patient with ''cryptogenic'' continuous motor seizures sho
wed swelling and signal hyperintensity of the contralateral parietotem
poral cortex, the thalamus, and the ipsilateral cerebellum on T-2-weig
hted images. These regions are connected by glutamatergic pathways. Pr
oton magnetic resonance spectroscopy (MRS) of the cortical lesion yiel
ded a signal peak at the resonance frequency of 2.29 ppm, suggesting a
focal increase of glutamate or its degradation product glutamine. At
3-month follow-up, structural alterations had disappeared, but the N-a
cetyl-aspartate/choline ratio was still reduced in the previously abno
rmal area, These findings are the first to demonstrate the contributio
n of MRS to pathophysiologic studies of focal SE in humans and, in com
bination with the pattern of imaging abnormalities, support a major ro
le of glutamate for seizure-related brain damage.