FCDI* | FCDIa abundant microcolumns | FCDIb abnormal layering | FCDIc vertical and horizontal abnormalities | |
FCDII* | FCDIIa dysmorphic neurons | FCDIIb dysmorphic neurons and balloon cells | ||
FCDIII* | FCDIIIa cortical dyslamination associated with hippocampal sclerosis | FCDIIIb cortical dyslamination adjacent to brain tumor | FCDIIIc cortical dyslamination adjacent to vascular malformation | FCDIIId cortical dyslamination adjacent to lesion acquired during early life, eg, stroke |
White matter* | mMCD¶ with excessive heterotopic neurons* | mMCD with oligodendroglial hyperplasia in epilepsy (MOGHE)Δ | ||
No definite FCD on histopathology* | Abnormality of cortical organization remains ambiguous and histopathologic findings not compatible with FCDI, II or III◊ |
* The Task Force (TF) recommends applying immunohistochemical staining for the detection of architectural abnormalities and FCD subtypes, ie, antibodies directed against neuronal nuclear antigen (NeuN), neurofilaments, vimentin, microtubule associated protein 2 (MAP2), CD34, OLIG2, glial fibrillary acid protein (GFAP), or alpha B-crystallin. The diagnostic term of "not otherwise specified (NOS)" shall be used if the microscopic diagnosis is not based on appropriate immunohistochemical staining, eg, FCD type I (NOS).
¶ Mild malformations of cortical development (mMCD): not associated with any other principal lesion, such as hippocampal sclerosis, brain tumor, or vascular malformation.
Δ Although mild malformations of cortical development with oligodendroglial hyperplasia (MOGHE) is primarily a white matter abnormality, abnormal cortical folding can be seen on MRI, and the combination of the two is often interpreted as FCD.
◊ No definite FCD on histopathology: a descriptive report is recommended to highlight anatomic ambiguities in clinically suspected cases of FCD.
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