Chapter 11

Epilepsy is a condition of recurrent unprovoked seizures, whereas a seizure is a paroxysmal event as a result of sudden excessive discharge of cerebral cortical neurons. There is a reciprocal relationship between sleep and epilepsy: Sleep triggers seizures, and seizures disrupt sleep architecture. The estimated frequency of nocturnal seizures varies between 7.5% and 45%, reflecting the heterogeneity of such seizures. Some types of epileptiform syndromes are prone to recur exclusively or frequently during sleep. Examples of predominantly sleep (nocturnal) seizures include the following: benign partial epilepsy of childhood with centrotemporal spikes or occipital paroxysms; nocturnal frontal lobe epilepsy (this includes nocturnal paroxysmal dystonia, paroxysmal arousals, and episodic nocturnal wanderings); autosomal dominant nocturnal frontal lobe epilepsy; juvenile myoclonic epilepsy; generalized tonic-clonic seizures on awakening; nocturnal temporal lobe epilepsy (a subgroup of partial complex seizure of temporal lobe origin); tonic seizure (as a component of Lennox-Gastaut syndrome); epilepsy with continuous spike and waves during non–rapid eye movement (NREM) sleep (CSWS); and Landau-Kleffner syndrome, probably a variant of CSWS.

The spectrum of nocturnal frontal lobe epilepsy includes four major manifestations characterized by stereotyped motor behavior arising out of NREM sleep lasting usually for less than a minute with brief postictal confusion and occurring often in clusters (see Video Vignette 14):

Ictal electroencephalograms (EEGs) are normal in more than 50% of patients, and EEGs may not show epileptiform spikes or sharp waves in the frontocentral region. About 25% to 30% are drug resistant but may show good response after surgical treatment. The most common histological abnormality is Taylor-type focal cortical dysplasia. An interesting observation is a history of high frequency of arousal parasomnias in the patients and their relatives.

Most interictal epileptiform discharges are triggered during NREM stages 1 and 2 but occasionally in stage 3 sleep. In epileptic patients NREM sleep acts as a convulsant, causing excessive synchronization and activation of seizure in an already hyperexcitable cortex. In contrast, rapid eye movement (REM) sleep generally behaves like an anticonvulsant because of inhibition of thalamocortical synchronizing mechanism and tonic reduction of interhemispheric impulse transmission through the corpus callosum. Overnight polysomnography (PSG) using multiple channels of EEG recording combined with simultaneous video recording is the single most important test for evaluating nocturnal seizure. For recognition of epileptiform patterns in the EEG and CSWS see Chapter 2. In this section of the atlas we provide several case vignettes along with overnight EEG and PSG segments showing characteristic patterns (Figs. 11.1 to 11.21).