MR Findings of Seizure-Related Cerebral Cortical Lesions during Periictal Period

PURPOSE: This study investigated the MRI, MR angiography (MRA) and MR perfusion findings of seizure-related cerebral cortical lesions during the periictal period. MATERIALS AND METHODS: From a retrospective review of the institutional database between 2011 and 2014, a total of 21 patients were included in this study. Two radiologists assessed periictal MRI, including MRA and MR perfusion, in patients with seizure-related cortical lesions. The parameters examined include: location of cortical abnormality, multiplicity of the affected cortical region, cerebral vascular dilatation, perfusion abnormality and other parenchymal lesions. RESULTS: All patients showed T2 hyperintense cerebral cortical lesions with accompanying diffusion restriction, either unilateral (18/21, 85.7%) or bilateral (3/21, 14.3%). Of the 21 patients enrolled, 10 (47.6%) had concurrent T2 hyperintense thalamic lesions, and 10 (47.6%) showed hippocampal involvement. Of the 17 patients (81%) who underwent MRA, 13 (76.5%) showed vascular dilatation with increased flow signal in the cerebral arteries of the affected cortical regions. On MR perfusion, all 5 patients showed cortical hyperperfusion, corresponding to the region of cortical abnormalities. CONCLUSION: Seizure-related cerebral cortical lesions are characterized by T2 and diffusion hyperintensities, with corresponding cerebral hyperperfusion and vascular dilatation. These findings can be helpful for making an accurate diagnosis in patients with seizure.

MR Findings of Seizure-Related Cerebral Cortical Lesions during Periictal Period

PURPOSE: This study investigated the MRI, MR angiography (MRA) and MR perfusion findings of seizure-related cerebral cortical lesions during the periictal period. MATERIALS AND METHODS: From a retrospective review of the institutional database between 2011 and 2014, a total of 21 patients were included in this study. Two radiologists assessed periictal MRI, including MRA and MR perfusion, in patients with seizure-related cortical lesions. The parameters examined include: location of cortical abnormality, multiplicity of the affected cortical region, cerebral vascular dilatation, perfusion abnormality and other parenchymal lesions. RESULTS: All patients showed T2 hyperintense cerebral cortical lesions with accompanying diffusion restriction, either unilateral (18/21, 85.7%) or bilateral (3/21, 14.3%). Of the 21 patients enrolled, 10 (47.6%) had concurrent T2 hyperintense thalamic lesions, and 10 (47.6%) showed hippocampal involvement. Of the 17 patients (81%) who underwent MRA, 13 (76.5%) showed vascular dilatation with increased flow signal in the cerebral arteries of the affected cortical regions. On MR perfusion, all 5 patients showed cortical hyperperfusion, corresponding to the region of cortical abnormalities. CONCLUSION: Seizure-related cerebral cortical lesions are characterized by T2 and diffusion hyperintensities, with corresponding cerebral hyperperfusion and vascular dilatation. These findings can be helpful for making an accurate diagnosis in patients with seizure.

Encefalopatía hepática fulminante vinculada a hiperintensidad de la corteza cerebral en la resonancia magnética / Fulminant hepatic encephalopathy vinculated with hyperintensity of the cerebral cortex in magnetic resonance

Background: The presence of manganese deposits in basal ganglia is an expression of chronic liver damage in neuroimaging, whereas diffuse edema of the white matter and hyperintensity of the internal capsule are seen in MRI in acute decompensation. In fulminant encephalopathy, changes in intensity in the cerebral cortex have been described, suggesting different pathogenic aspects. Purpose: To describe and try to interpret hyperintensities images of the cerebral cortex in fulminant hepatic encephalopathy. Case report: A 42 years old woman, with history of hyperthyroidism treated with propylthiouracil developed abdominal pain, choluria and general malaise, without fever. At admission, she had jaundice, elevated liver enzymes, and hyperammronemia of 481 ug. She developed progressive impairment of consciousness falling into a non-reactive coma with intermediate size and poorly reactive pupils, absence of oculocephalic reflexes and diminished osteotendinous reflexes, with indifferent plantar reflexes. Brain CT showed brain edema without focal lesions. The MRI showed hyperintense signal abnormalities in the fronto-parietal cortex in T2 and FLAIR with restriction in difussion sequency. She became brain dead. Comment: These exceptional images on MRI are considered an expression of cytotoxic damage, consistent with high levels of ammonium in fulminant hepatic encephalopathy. The swelling of astrocytes and cortical neurons is caused by the accumulation of intracellular glutamine, highly osmophilic, and explains the restriction on the difussion and lower values in the ADC. Interstitial edema would be part of the chronic forms by acquisition of compensatory mechanisms capable of preventing the accumulation of glutamine.

Antecedentes: La presencia de depósitos de manganeso en los núcleos basales es una expresión neuroimagenológica de daño hepático crónico, así como el edema difuso de la substancia blanca y la hiperintensidad de la cápsula interna con RM en descompensaciones agudas. En encefalopatías fulminantes se ha visualizado cambio de intensidad en la corteza cerebral, sugiriendo aspectos patogénicos distintos. Propósito: Describir e intentar interpretar imágenes hiperintensas de la corteza cerebral en una encefalopatía hepática fulminante. Caso clínico: Mujer de 42 años, hipertiroidea en tratamiento con propiltiouracilo. Consultó por dolor abdominal, coluria y compromiso del estado general, sin fiebre. Ingresó con ictericia, enzimas hepática elevadas, e hiperamonemia de 481 ug. Desarrolló progresivo compromiso de conciencia cayendo en un coma no reactivo, con pupilas de tamaño intermedio pobremente reactivas, ausencia de reflejos oculocefálicos y reflejos osteotendíneos apagados, con reflejos plantares indiferentes. TAC de cerebro mostró edema cerebral, sin lesiones focales. La RM definió áreas hiperintensas en la corteza fronto-parietal en T2 y FLAIR, que presentaban incremento de señal en la difusión. Evolucionó hasta la muerte cerebral. Comentario: Estas imágenes excepcionales en la RMson consideradas expresión de daño citotóxico, en concordancia con los altos niveles de amonio de una encefalopatía hepática fulminante. El edema de astrocitos y neuronas corticales se origina por la acumulación de glutamina intracelular, altamente osmofílica, y explica la restricción en la difusión y valores menores en el ADC. El edema intersticial, sería atributo de las formas crónicas, debido a la adquisición de mecanismos compensatorios capaces de impedir la acumulación de glutaminas.