Shearwood McClelland III, AB1, Steven S Chin, MD, PhD2, David J Adams, MD3, Stanley R Resor Jr., MD3, Jeffrey N Bruce, MD1, Guy M McKhann II, MD1 and Robert R Goodman, MD, PhD1. 1Neurological Surgery, Columbia College of Physicians and Surgeons ; 2Neuropathology and 3Neurology, Columbia College of Physicians and Surgeons, New York, NY, United States, 10032 .


RATIONALE: Patients with focal seizures often have MRI abnormalities in the brain region of their presumed seizure focus. Neoplasms, vascular malformations, ischemic infarctions, hemorrhages, inflammatory processes, demyelinating diseases, and other specific pathologic entities have been diagnosed by biopsies of such MRI abnormalities. Three patients with this presentation had brain lesion biopsies with a leading presumptive diagnosis of glial neoplasm and were in contrast found to have indistinct histopathology.


METHODS: Patient 1 was a 55yo man with new onset of right focal sensorimotor seizures corresponding with a left central region MRI lesion with high signal on T2 and mild enhancement. Patient 2 was a 38yo woman with a remote history of focal onset seizures and normal MRI, with seizure control for five years on antiepileptic medication before presenting with new onset of frequent left sensorimotor seizures. MRI showed a sharply defined increased T2 signal right parietal lesion with no definite gadolinium enhancement. Patient 3 was a 52yo right language-dominant man with new onset unprovoked seizure and an increased T2 signal throughout his right hippocampus and possible gadolinium enhancement in the anterior hippocampus. In each patient, preoperative clinical suspicion was for neoplasm or inflammatory process.


RESULTS: Open biopsy two months after seizure onset in patient 1 revealed vascular abnormalities and other findings suggestive of subacute/chronic venous infarction. Several weeks after seizure onset, craniotomy in patient 2 and stereotactic needle biopsy in patient 3 revealed mild gliosis and perivascular hemosiderin deposition, not permitting a specific diagnosis. Postoperatively, patients 1 and 3 had normalization of their MRI and no further seizures, while Patient 2 has had some brief sensory seizures and has not yet had MRI.


CONCLUSION: We describe three patients who had brain biopsies of striking focal increased T2 signal MRI abnormalities associated with new onset seizures. Pathologic findings contradicted our preoperative suspicions. The findings in Patient 1 suggested venous infarction. Patients 2 and 3 had similar clinical and MRI findings. Pathologic findings were subtle but similar to patient 1 and also suggest the possibility of subacute venous infarctions. Our experience indicates that patients with new onset seizures may have an associated discrete intra-axial MRI lesion that is not a neoplasm. To our knowledge, this is the first report of focal seizure-associated MRI lesions with biopsy findings suggestive of venous infarction. Our experience does not allow us to determine if the MRI and tissue abnormalities preceded, or were caused by, the seizures.