PMC5014750_01
EEG recording of a writing-induced reflex seizure (low- and high-frequency filters were set at 0.5 and 35 Hz, respectively): A) onset of writing; B) preictal repetitive polyspike and wave discharges over right centroparietal leads; C) transition to the low-voltage, fast activity pattern subsequently increasing in amplitude and decreasing in frequency; D) eye-blinking artifact; E) seizure offset.
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Electrically, repetitive preictal polyspike and wave discharges over the right centroparietal leads appeared within 3 s of writing, followed by low-voltage fast activity increasing in amplitude and decreasing in frequency maximum over right more than left centroparietal regions (Fig. 1, Video 1).
Preoperative axial T2-weighted (A) and FLAIR (B) images showing thickening and blurring of the gray-white matter junction within the depth of the right intraparietal sulcus (green mark on the corresponding cortical surface in (C)). Intraoperative images (D) after microsurgical resection of the corresponding epileptogenic focus, guided preoperatively by electrocorticography (not shown). Postoperative axial T2-weighted image (E) confirming excision of the focal cortical dysplasia.
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MRI revealed blurring and thickening of the gray-white matter junction consistent with focal cortical dysplasia located in the right inferior parietal lobule, within the depth of the intraparietal sulcus at the junction with the postcentral sulcus (Fig. 2A/B). Because the patient had previously failed 6 antiseizure drug trials (carbamazepine, valproate, lamotrigine, topiramate, clobazam, and vigabatrin) and deemed her seizures to be disabling, she underwent neurosurgical removal of the cortical dysplasia (Fig. 2D). Neuronavigation and electrocorticography were essential to guide the resection (Fig. 2C). The presumed cortical dysplasia was not seen on postoperative MRI (Fig. 2E).