Abstracts

Rationale: To describe the diagnosis and treatment of patients who were found to have seizures arising from the cerebellum. Methods: The records of two patients with cerebellar lesions who underwent continuous video-EEG monitoring with depth electrodes in place were reviewed. Results: The first patient was an 8-year-old male who began having seizures at age 3 years. He was found to have a lesion in the right cerebellar peduncle, which was biopsied and found to be gliosis. However, he continued to have seizures despite multiple medications. During his Phase I evaluation in the epilepsy monitoring unit (EMU), he had seizures with secondary generalization that had maximum involvement of the right body with motor activity followed by right leg weakness. SPECT showed decreased metabolism in the area of the abnormality. It was thought that he would benefit from a Phase II evaluation with intracranial electrodes in the lesion and repeat biopsy at that time. Video-EEG monitoring was performed using scalp electrodes and depth electrodes within the lesion. His secondarily generalized tonic-clonic seizures began from a right cerebellar depth electrode. Biopsy from the time of placement of the depth electrodes confirmed that the lesion was gliosis. Medication controlled his seizures, so his parents opted not to pursue surgery. The second patient was a 3-year-old male who underwent partial resection of a juvenile pilocytic astrocytoma at an outside hospital. At the time of presentation, he was having as many as 25 myoclonic-tonic seizures per hour, which did not respond to treatment. He underwent a Phase I evaluation in the EMU, and it was felt that his seizures were likely of cerebellar origin. He had generalized EEG changes at the time of his seizures and was noted to have an apparent deep inspiration in a myoclonic-tonic manner. He was readmitted for Phase II epilepsy surgery evaluation, including placement of 2 cerebellar depth electrodes. He then underwent continuous video-EEG monitoring. Myoclonic-tonic seizures were again recorded. The onset was first seen in one of the depth electrodes in the cerebellum and then changes were seen on the scalp recording. He returned to the operating for resection of the lesion. Electrocorticography performed in the cerebellar lesion cavity following resection showed the absence of epileptiform discharges. Intraoperative MRI showed a gross total resection of the complete lesion. Pathology findings were consistent with pilocytic astrocytoma. Medication changes were made post-operatively. Currently, he is seizure-free on one medication. Conclusions: In patients with cerebellar structural lesions and seizures, one should consider a causative relationship. Surface EEG may not be helpful. However, continuous video-EEG monitoring using simultaneous scalp recording and intracranial monitoring with depth electrodes within a cerebellar lesion can determine whether seizures arise from the lesion. If seizures are intractable, resection of epileptogenic cerebellar lesions should be considered, and complete resection should be pursued whenever possible.