We estimated equivalent current dipoles (ECDs) using dipole tracing method with realistic head model in patients with temporal lobe epilepsy and compared them to the epileptic focus identified by subdural electrode recording. The mean patient age was 43 years (range 17-67 years). Three patients were men and two patients were women. Three patients had mesial temporal lobe epilepsy and two patients had lateral temporal lobe epilepsy. The mean distance between the center of ECDs and the center of epileptic focus identified by subdural electrode recording was 14 mm (range 8-18 mm). In patients with mesial temporal lobe epilepsy, we estimated ECDs in temporal base rather than mesial temporal lobe. We though epileptic activiry spread from hippocamps to temporal basal cortex where we estimated ECDs. In patients with lateral temporal lobe epilepsy, ECDs showed activated lateral cortex precisely.

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We report two patients with anticonvulsant hypersensitivity syndrome associated with viral infections. Patient 1 is an 8-month-old girl with acute encephalitis/encephalopathy caused by HHV-6. Twenty-one days after administration of phenobarbital (PB), fever and rash developed. Pancytopenia, elevation of serum LDH and ferritin levels, and hemophagocytosis by macrophases were found. Steroid therapy was effective against all these symptoms. However, the symptoms recurred. Patient 2 is a 4-year-old boy. Carbamazepine (CBZ) was given against complex partial seizure. Eleven days after, fever, rash, and severe cough developed. At first, he was diagnosed as having measles, but he had skin lesions of toxic epidermal necrolysis. Steroid therapy was effective without recurrence. Aromatic antiepileptic drugs such as PB, CBZ, phenytoin, and primidone frequently cause hypersensitivity syndrome. The symptoms and signs include not only eruption and fever, but also lymphadenopathy, hepatitis, and blood abnormalities. Although the mechanism has not yet been clarified, hypercytokinemia caused by activation of T lymphocytes and immunologically reactive metabolites of drugs are thought to play a major role. Systemic corticosteroid therapy was effective according to our experience. It is important to note viral infection being a facilitating factor of drug hypersensitivity syndrome during drug therapy of epileptic patients.

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We reported a case of 56 year-old right-handed man who presented reversible low T1-weighted, high T2-weighted and FLAIR signal intensity lesion over the left anterior temporal lobe with hippocampal atrophy on the same side. His epileptic symptoms were characterized by focal seizures such as twitching of the right facial muscles, vocal arrest, tonic convulsion or atonic attacks of the right limbs. He also presented disturbance of recent memory. Electroencephalogram revealed focal spike activities restricted to the left sphenoidal lead. The abnormal signal lesion on MRI disappeared almost completely in three months after the beginning of medication leaving a marked atrophy of the left hippocampus with the recent memory disturbance remaining unchanged. Several reports mention that reversible abnormal signal lesion on MRI often occurs after status epileptics. Our patient indicates that less frequent focal seizures and/or paroxysmal electrical discharges can also cause this lesion.

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