Focal Cortical Dysplasia Does Not Spread
Focal cortical dysplasia (FCD) is a static, congenital malformation of cortical development that does not spread or progress over time. 1 The lesion is present from birth due to disrupted cortical development during fetal brain formation, and the anatomical extent of the dysplastic tissue remains fixed throughout life. 1, 2
Nature of FCD as a Developmental Malformation
FCD represents a failure of normal cortical development during gestation, not a progressive or spreading disease process. 1, 3 The dysplastic cortex is formed during neuronal migration and differentiation phases of fetal development, making it a static structural abnormality. 2, 3
The epileptogenic zone in FCD corresponds to the histologically defined dysplastic tissue and does not expand beyond the original malformation. 4 Studies using stereoelectroencephalography demonstrate that the epileptogenic zone matches the anatomical boundaries of the dysplastic cortex in 82% of cases. 4
What May Appear as "Spreading" But Is Not
Seizure activity itself can cause secondary changes in surrounding brain tissue, including cortical swelling in acute phases and later focal volume loss or reduced myelination from repeated seizures. 1 These are consequences of seizure-related tissue damage, not expansion of the dysplasia itself. 1
MRI may show larger areas of abnormality than the actual dysplastic tissue, particularly on functional imaging like FDG-PET, which typically demonstrates hypometabolism extending beyond the structural lesion. 1, 2 This reflects the epileptogenic network and seizure-related metabolic changes, not spread of the malformation. 1
In young children with severe epilepsies and multilobar FCD Type I, the affected hemisphere may be significantly smaller (hypoplastic) compared to the contralateral side. 5 This represents the original extent of developmental compromise, not progressive spread. 5
Critical Clinical Implications
Complete surgical resection of the entire dysplastic cortex is required for seizure freedom, and incomplete resection results in poor outcomes. 4, 3 The main predictor of favorable surgical outcome is complete removal of both the epileptogenic zone and the dysplastic cortex (P<0.01). 4
The dysplastic tissue visible on MRI may be smaller than the actual seizure-generating region, particularly in FCD Type I. 2, 3 This reflects the difficulty in detecting subtle architectural abnormalities, not spread of disease. 1, 3
Bilateral focal metabolic abnormalities on FDG-PET indicate bilateral disease from the outset and serve as an independent predictor of seizure recurrence after hemispherotomy. 6 This represents bilateral developmental abnormalities, not spread from a unilateral focus. 6
Common Pitfalls to Avoid
Do not mistake seizure-related secondary brain changes for progression of the dysplasia itself. 1 Cortical swelling, volume loss, and metabolic changes reflect epileptic activity consequences, not malformation expansion. 1
Do not confuse the larger epileptogenic network seen on functional imaging with anatomical spread of dysplastic tissue. 1, 2 FDG-PET hypometabolism typically extends beyond structural MRI abnormalities but represents functional disturbance, not progressive pathology. 1
In multilobar FCD, particularly Type I in young children, the extensive involvement represents the original developmental insult, not progressive spread. 5, 3 These patients have compromised cortical development affecting large regions from the outset. 5