Presentation
Recurrent seizure
Patient Data
Cortical thickening and blurring of grey-white matter junction with abnormal architecture of subcortical layer in left parietal cortex. T2 and FLAIR hyper-intensity of subcortical white matter with transmantle sign and subtle T2 and FLAIR hyper-intensity of grey matter is seen. There is no overt abnormal sulcal or gyral pattern. There is no diffusion restriction. Cavum verge noted.
Case Discussion
Focal cortical dysplasia is malformation of cortical development, which is most common cause of medically refractory epilepsy in the pediatric population and the second/third most common etiology of medically intractable seizures in adults. Both genetic and acquired factors are involved in the pathogenesis of cortical dysplasia. Three types of cortical dysplasia are generally recognized and they are: Type I focal cortical dysplasia with mild symptomatic expression and late onset, is more often seen in adults, with changes present in the temporal lobe; Type II of cortical dysplasia usually seen in children with severe clinical symptoms, more extensive changes occur outside the temporal lobe with predilection for the frontal lobes; and new type III is one of the above dysplasias with associated another principal lesion as hippocampal sclerosis, tumor, vascular malformation or acquired pathology during early life.
EEG of this patient shows low voltage activities over frontal region; photic stimulation and hyperventilation induce no additional abnormality with definite abnormal activity: Normal awake record.
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