Department of Neurology, Kyoto University School of Medicine, Shogoin, Sakyo-ku, Kyoto, 606, Japan.
We performed long-term video/ EEG monitoring and a single photon emission computed tomographic (SPECT) study to clarify generating mechanism of bilateral tonic motor seizures resembling seizures generated by the supplementary motor area (SMA), in patients with bilateral parietal lesions.
We describe 2 patients (age 24 and 32 years), with bilateral parietal lesions. Clinically, seizures were preceded by lightning sensation in the body, followed by asymmetric tonic posturing of both hands and thrashing movements of the feet, lasting for less than 1 min.
Ictal rhythmic (7-15 Hz) activity at the vertex was observed on the EEG in 1 patient. Interictal SPECT in 2 patients showed decreased blood flow in both parietal areas, consistent with bilateral parietal abnormalities on T2- and T1-weighted MRIs. Ictal SPECT in 1 patient showed increased blood flow in the right parietal and frontopolar areas.
The present 2 patients had clinically asymmetric tonic seizures, most likely resulting from spreading of the ictal activity from the parietal lesions via the superior longitudinal fasciculus to the SMA. Bilateral, homologous lesions in the parietal area might cause disinhibition on the unilateral epileptogenic side.
Tonic seizures belong to generalized seizures in the ILAE seizure classification of 1981 , but clinically tonic seizures involving bilateral body parts are also seen in frontal lobe epilepsy, in which either asymmetric body involvement or focal EEG pattern can correctly lead us to a diagnosis of focal (frontal) epilepsy rather than generalized epilepsy . The supplementary motor area (SMA) is one of the eloquent frontal areas which provokes asymmetric tonic posturing involving mainly the proximal parts of the extremities and trunk, and speech arrest and vocalization appear without loss of awareness . We recently saw two patients whose seizure semiology was essentially consistent with SMA seizures, but both patients had bilateral parietal to parieto-occipital lesions, associated with other common clinical features. We hypothesize that the bilateral homologous parietal lesions may cause disinhibition of ictal activity, which can easily spread into the frontal lobe, generating seizures of frontal lobe origin as the symptomatogenic zone, distant from the epileptogenic zone.