Several important characteristics of sleep associated with epilepsy are reviewd. 1) All night sleep analysis revealed that short episodes of awakening and sleep stage shift often increased and REM sleep is often decreased in epileptic patients. 2) Both generalized tonic-clonic seizure and complex partial seizure cause reduction of REM sleep. 3) Ten to thirty percent of epileptic patients are classified into so-called sleep epilepsy. About a half of them are pure sleep epilepsy, having seizures exclusively in sleep. One-third of pure sleep epileptic patients achieves a seizure-free outcome and an another one-third develops seizures also in wakefulness during their clinical courses. 4) Generalized tonic-clonic seizures of idiopathic generalized epilepsy occur predominantly during Non-REM sleep and never occur during REM sleep. Complex partial seizures occur predominantly during Non-REM sleep and rarely during REM sleep. Some complex partial seizures tend to occur in a transitional period between Non-REM and REM sleep. 5) In the majority of epileptic patients, interictal spiking rate increases during Non-REM sleep and decreases during REM sleep. 6) Nocturnal paroxysmal dystonia is described as parasomnia in the International Classification of Sleep Disorders. However, its epileptic nature has recently been cralified in many studies. Definition of nocturnal paroxysmal dystonia need careful re-examination.

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The objective of the present study is to describe characteristics of seven females with subependymal heterotopia and epilepsy. They consisted of four patients with temporal lobe epilepsy (TLE), two with West syndrome, and one with frontal lobe epilepsy (FLE). Subependymal heterotopia needs to be recognized as one of the causes of West syndrome. The age at seizure onset ranged from 6 months to 20 years. In patients from references and our patients, the plot of the number of patients versus the age at seizure onset showed two peaks. The first peak corresponded to below 3 years of age and the second peak to 16-18 years of age. Three patients (1 with TLE, 2 with West syndrome) had complete remission, three (1 with FLE, 2 with TLE) had a monthly seizure, and another patient with TLE had a weekly seizure. Four of these seven patients had mild mental retardation. Brain perfusion single-photon emission tomography was performed in four of these seven patients, revealing linear perfusion in the subependymal lesions similar to that in the cortex. Magnetoencephalography was carried out in two patients; however, dipoles were not detected in the subependymal lesions.

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The author presents here two boys who had been diagnosed as having epilepsies without cardiac disorders until potentially fatal cardiac symptoms developed. A boy aged 9 years and 10 months visited the neurological outpatient clinics following four episodes of nausea and loss of consciousness over the previous 7 months. These attacks were diagnosed as localization-related epilepsy and were controlled by carbamazepine for 11 months. At the age of 10 years and 9 months, he was brought to the emergency room because of a surffering look and a seizure like episode during exercise. His pulse could not be found, and cardiopulmonary resuscitation attempts were ineffective. Retrospective examination of the boy's electrocardiogram showed no abnormalities at the age of 6 years and 8 months, but prolonged QTc and inverted T waves at the age of 9 years and 5 months. Therefore, the cause of his sudden death was suspected to be due to previously undiagnosed cardiac disorder such as hypertrophic cardiomyopathy. The second patient, a 6-year-old boy, had a 3-year history of myoclonic jerks and loss of consciousness. As ictal electroencephalography (EEG) showed diffuse polyspikes and wave complexes, he was diagnosed as having epilepsy with myoclonic and absence seizures and treated with valproic acid and clonazepam. After the age of 5 years and 9 months, he sometimes developed shortness of breath and facial pallor to be precipitated by swimming or running, but these attacks were thought to be epileptic seizures. At the age of 6 years and 3 months, he was admitted to a branch hospital because of worsening of shortness of breath and cyanosis, and was diagnosed as having primary pulmonary hypertension. Cardiac disorders should be considered in patients with epilepsy, particularly when their attacks are precipitated by exercise.

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Sixty-seven epileptic patients were classified into the following 3 groups according to the diffuse alpha EEG pattern.; group A: patients with typical diffuse slow alpha pattern (A type), group B: patients with irregular diffuse alpha pattern (B type), and group C: patients with alpha waves sometimes spread diffusely (C type). The mean age of the group A was highter than that of the group B and C. The A type of EEG pattern seemed related to aging and medication. The incidence of epileptic discharges was less in the group A than in the group B, and clinical seizure was well controlled in the former. These findings seem to suggest that the A type EEG reflects slight dysfunction of brain as has been already described. On the other hand, nearly half of the patients in the group B still have seizures. It is suggested that epileptogenic and organic background may be factors for the appearance of the B type. The C type of EEG pattern means presumably early stage of the A or B type. It is necessary to clarify the meaning of the B type.

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