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Updated: Jun 23, 2026

Inducing Post-Traumatic Epilepsy in a Mouse Model of Repetitive Diffuse Traumatic Brain Injury
Published on: February 10, 2020
Pathophysiology and long-term outcome of reversible tumor-like lesions induced by presenting status epilepticus
Nuno Canas1, Pedro Soares, Sofia Calado
1Department of Neurology, Hospital de Egas Moniz, 1349-019 Lisbon, Portugal. nunocanas@netcabo.pt
Background And Purpose:
Within the spectrum of reversible neuroimaging abnormalities induced by status epilepticus (SE) tumor-like lesions (TLL) have been rarely described. Their etiology, pathophysiology, and long-term outcome remain uncertain. These issues could be clarified by long-term magnetic resonance imaging (MRI) studies in TLL induced by presenting SE.
Methods:
Prospective multi-sequence MRI and clinical and electroencephalographic long-term (18 to 60 months) follow-up studies were performed in 3 patients with reversible TLL induced by presenting SE.
Results:
In the peri-ictal MRI, TLL are hypointense in T1-weighted, hyperintense in T2-weighted, and fluid-attenuated inversion recovery images with a marked subcortical component and sulci effacement. The diffusion and MR-spectroscopy studies disclosed intermixed areas of increased/decreased diffusivity associated with a lactate peak and a decreased N-acetylaspartate. At long-term follow-up, none of the patients had seizure recurrence or electroencephalographic epileptiform abnormalities; MRI showed residual focal atrophy and gliosis associated with neuronal loss/dysfunction.
Conclusions:
SE per se may induce TLL. MRI multi-sequence studies disclosed that they are mainly formed by focal vasogenic and cytotoxic edema resulting from the hypermetabolism associated with seizure activity. In spite of a clinical favorable long-term outcome, the demonstration of irreversible brain damage argues in favor of immediate treatment of SE.
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