PARIETAL LOBE EPILEPSY - DIAGNOSTIC CONSIDERATIONS AND RESULTS OF SURGERY

Eleven patients, evaluated between 1983 and 1988, with parietal lobe seizure origin as determined by circumscribed lesion detection in all and successful surgery in 10, were retrospectively evaluated in terms of clinical seizure characteristics and electroencephalographic (EEG) findings. Seven of 11 patients reported auras prior to seizures. In 4 patients, auras were lateralized somatosensory sensations, but in 1 they were ipsilateral to the side of seizure origin, and in 2 they had only occurred many years previously when seizures began. Other auras were either nonspecific or suggested seizure origin outside of the parietal lobe. Observed seizures were of two types: asymmetrical tonic seizures with or without clonic activity and complex partial seizures with loss of contact and automatisms. Four patients had only the first type of seizure and an equal number had only the second type. Three patients had both types of seizures during different episodes. Scalp EEGs correctly localized the side and region of seizure onset in only 1 patient. Three additional patients with congruent parietal localization on scalp EEG had additional misleading EEG findings. All patients had lesions detected with neuroimaging, but in 5 this detection occurred after they had been initially evaluated. These 5 patients had intracranial EEG studies designed to localize the region of seizure origin, and correct seizure onset localization was achieved in 2. Of the other 3 patients, false localization occurred in 1, and 2 could not be localized. Four patients with known lesions and 2 of the patients in whom lesions were detected after initial intracranial evaluations were studied with subdural grid electrodes placed over the lesions. Seizures were recorded during monitoring in all 6 patients, but seizure origin was well localized in only 1. One patient with false localization had a temporal lobectomy, and 2 unlocalized patients had partial corpus callosotomies. Surgery was ineffective in all 3. Surgery aimed at lesion resection in 10 patients (including 2 who had had previous procedures) resulted in all 10 patients becoming seizure-free with minimal or no neurological deficits. We conclude that (1) a syndrome of parietal lobe epilepsy based on clinical and scalp EEG findings could not be defined in this series of 11 patients; (2) intracranial EEG findings are often not helpful and sometimes misleading, even when parietal lesions are known or suspected; (3) when circumscribed parietal lobe lesions are detected they are the cause of the patient's seizures regardless of seizure type and EEG findings; and (4) guided by the results of functional mapping, parietal lobe lesions can be safely resected with excellent surgical results.