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Between 1982 and 1991, 11 patients (4 male, 7 female) ranging in age from 16 to 42 years who had been diagnosed with idiopathic focal epilepsy resistant to medication, were treated with stereotactic radiosurgery. The preoperative symptomatic period was 3–24 years. The process of localizing epileptic focus was based on chronic electrocorticography with flexible electrodes introduced into the subarachnoid space through single burr holes, and left in place during a maximum of 7 days until a clinical seizure was recorded. In most cases the procedure had to be repeated until localization was clear. This process was aided by a computer-assisted automatic analysis procedure. Final confirmation of focus location was done with depth electrode recording in most cases. Stereotactic radiosurgery was performed with a ⁶⁰Co gamma source using 10 mm collimators, except in two cases in which a betatron was used. The estimated dose was 10–20 Gy at the isocenter. Four of the 11 patients (36%) were medication-and seizure-free after a mean follow-up of 102.5 months. Five patients (45%) presented a reduction of seizures of 98, 89, 86, 75 and 75%, respectively. Two patients did not respond to treatment. Seizure reduction began after a delay period of 2–12 months except in 2 patients and in most cases seizure rate decreased progressively during several months (range: 3–48) postoperatively until stabilization. No complications related to irradiation were recorded. Doses effective for epilepsy are much lower than those for producing cerebral lesions, so the mechanism is not destruction of the focus or the pathways spreading the epileptic activity. It may be an effect upon neurotransmitters involved in epilepsy mechanisms, or an indirect effect through changes in the glial cells or by local plasticity phenomena.

An experimental model of cobalt-induced epilepsy was performed on 15 cats. 3 months later, they were irradiated by means of a gamma source with a total target dose of 10 Gy. One month after irradiation all EEG recordings returned to normal, while a control group maintained the epileptiform traces. Histological study of the irradiated foci showed neuronal reafferentation. The action mechanism of ionizing radiation over epileptogenic foci in relation to this reafferentation and neuronal plasticity mechanisms is discussed.

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