Long-term radiosurgery effects in the treatment of temporal lobe epilepsy

Case report

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Epilepsy surgery is an effective treatment for medically resistant temporal lobe epilepsy (TLE). To minimize complication rates and potentially improve neuropsychology outcomes, stereotactic radiosurgery (SRS) has been explored as an alternative. Two pilot trials have demonstrated the effectiveness of SRS for the treatment of medically resistant TLE, with seizure-free outcomes for approximately 65% of patients at last follow-up. Despite encouraging results, no conclusive long-term outcomes are available for SRS. This article discusses a single patient who presented with recurrent seizures, worsening headaches, and persistent abnormal MRI findings 7 years and 8 months after SRS.

This 29-year-old woman with a history of medically refractory complex partial seizures since childhood was referred for evaluation. Medical management had failed in this patient. The workup was compatible with left mesial temporal lobe onset, with MRI findings suggestive of mesial temporal sclerosis. In 2003, at the age of 23 years, she underwent Gamma Knife surgery (GKS) targeting the left temporal mesial area with a dose of 24 Gy at the 50% marginal isodose line. After GKS, the patient's seizures decreased in frequency over several months, but auras were persistent. Nine months after treatment, she developed worsening headaches. A follow-up MRI study demonstrated a thick, irregular, enhancing lesion in the medial part of the temporal lobe. She was placed on corticosteroids, with resolution of her headaches.

Her seizures and headaches recurred in March 2010. An MRI study showed a 2.2-cm, ill-defined, enhancing cystic lesion in the left mesial temporal lobe with T2 and FLAIR hyperintensity, which was presumably radiation induced. At that time, the patient opted for left temporal lobe resection to control her seizures. Histological examination showed moderately severe, remote, longstanding sclerosis at the level of the hippocampus. A vascular lesion was identified, and it was most consistent with radiation-induced capillary hemangioma. The entorhinal region was severely damaged, with hemorrhage, necrosis, neuronal loss, astrogliosis, and hemosiderin deposition. There was evidence of radiation vasculopathy.

Radiation-induced lesions after SRS for the treatment of epilepsy are not well documented. Although GKS is a promising technique for the treatment of medically resistant TLE, the ideal candidate is not yet well defined. The selection of the appropriate technical parameters to obtain a desirable functional effect without histological damage to the surrounding neural tissue remains a challenge. This case illustrates the need for long-term follow-up when radiosurgery is used for epilepsy.

Abbreviations used in this paper:GFAP = glial fibrillary acidic protein; GKS = Gamma Knife surgery; SRS = stereotactic radiosurgery; TLE = temporal lobe epilepsy.

Article Information

Address correspondence to: Fernando L. Vale, M.D., Department of Neurosurgery, University of South Florida, 2 Tampa General Circle, 7th Floor, Tampa, Florida 33606. email: fvale@health.usf.edu.

Please include this information when citing this paper: published online July 27, 2012; DOI: 10.3171/2012.6.JNS111905.

© AANS, except where prohibited by US copyright law.

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Figures

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    Screen shot showing radiosurgery planning, with axial T1-weighted MRI studies targeting the left mesial structures (amygdala and hippocampus).

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    Preoperative MRI studies (post-GKS treatment). A: Axial T2-weighted image. B: Axial image obtained using the FLAIR technique. C: Contrast-enhanced axial T1-weighted image. D and E: Coronal cuts (contrast enhanced). F: Sagittal view. Notice degree of abnormal signal and heterogeneous enhancement along the temporal lobe.

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    Photographs showing intraoperative views of the surgical site. A and B: The temporal horn has been exposed and the vascular lesion is noted at the head of the hippocampus. C and D: A surgical specimen.

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    Postoperative MRI studies. A and B: Contrast-enhanced coronal T1-weighted images. C and D: Contrast-enhanced axial T1-weighted images. Imaging findings documented complete resection of the mesial structures.

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    Photomicrographs showing sections of the lesion. A: Hippocampal, dentate gyrus, and CA1–CA4 regions. B: Astrogliosis of CA4, CA2, and CA1 regions. C: The CA4 region, with profound loss of pyramidal cell neurons. D: The CA3 region, with profound loss of pyramidal cell neurons, and a portion of CA2, with a few pyramidal cell neurons. H & E (A, C, and D) and GFAP (B) staining; original magnification × 2 (A and B) and × 10 (C and D).

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    Photomicrographs showing sections of the lesion. A–C: Matching brain sections with different staining methods. A: Vascular lesion consistent with capillary hemangioma. B: Vascular lesion lacking intervening brain parenchyma. C: Special vascular stain demonstrating capillary–small vessel walls without collagen, fibrosis, or gliosis. D: Close-up demonstrating dilated vascular lumen, back-to-back vessels separated by only thin capillary walls (arrowheads). H & E (A), GFAP (B), and Movat pentachrome (C and D) staining; original magnification × 2 (A–C) and × 20 (D).

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    Photomicrograph of a section of the specimen showing radiation injury of entorhinal cortex (inferolateral to the hippocampal formation). Intervening injured brain with gliosis is evident: hyalinized, damaged blood vessels (arrows), and hemorrhage and hemosiderin (arrowheads). H & E, original magnification × 2.

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    Photomicrographs showing radiation-induced changes in the vasculature in sections of the lesion. A: The internal elastic layer is split in radiation-damaged vessels (arrowheads). B: Inflammatory cells in the vessel wall (arrowhead) and clefts in homogenized vessel wall (arrow). C: Homogenized vessel wall (arrow), inflammatory cells in the vessel wall (arrowhead), and clefting in the vessel wall (double arrowheads). D: Serum extravasation (arrowhead) and red blood cell extravasation (arrow). E: Serum extravasation (arrowhead) and capillary endothelial cell (arrow). Movat pentachrome (A) and H & E (B–E) staining; original magnification × 20 (A–D) and × 40 (E).

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