Status epilepticus and cortical laminar necrosis

Case contributed by Dr Bruno Lorensini

Presentation

Patient with a history of convulsive focal seizures. Presented with focal motor seizures on the right just before the first MRI. No recent history of trauma

Patient Data

Age: 1
Gender: Female

MRI Brain (first exam)

Modality: MRI

Hyperintense areas on T2-weighted and FLAIR sequences in the right parietal gray matter, with mild impairment of subcortical white substance in these topographies (especially in right and left postcentral gyrus). In these areas there is restrict diffusion in specific sequence.

There is no evidence of other supratentorial or infratentorial parenchymal changes, intra or extra-axial lesions.


Laterals, third and fourth ventricles with topography, shape and normal size.

MRI Brain - 20 days later

Modality: MRI

Cortical involvement of both cerebral hemispheres, particularly in the insula and frontoparietal regions, with increased signal on T2-weighted sequences in cortical gray matter.

On T1-weighted sequences, there are areas of high signal in the cortical region of the right fronto-parietal transition (pre and post-central gyrus this side), and the gradient echo sequence is hypointense in these topographies, suggesting bleeding.

There is a mild enhancement of cortical vessels in the affected areas after the use of intravenous contrast.

There is restriction in DWI sequence.

No evidence of changes in the brainstem and cerebellar hemispheres.

All the findings are suggestive of bilateral cortical laminar necrosis, affecting the insula and frontal-parietal transitions, probably related to the vulnerability of intra-cortical border areas by anoxia, ischemia or depletion of glucose.

Case Discussion

The mechanisms that induce epileptic activity and make it durable, leading to status epilepticus (SE), are poorly known. Many mechanisms can lead to permanent brain damage as a result of SE.

It is known that status epilepticus increases the cerebral metabolic demand for glucose and oxygen and, as a result, a compensatory increase in cerebral blood flow occurs. When this blood inflow is not sufficient, adenosine triphosphate depletion and lactate accumulation occur and leads to hypermetabolic neural necrosis. 

Generally, all the radiological cortical signal changes observed with focal SE seem to be reversible. However, like in this case, a group of patients may display permanent brain damage after SE, with radiological changes suggestive of cortical laminar necrosis (CLN)

This patient had focal SE involving the posterior quadrant of the hemisphere, as previous cases reported in the literature 1.

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Case Information

rID: 39011
Case created: 15th Aug 2015
Last edited: 14th Sep 2015
Inclusion in quiz mode: Included

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