(mfg1-2, mesial frontal gyrus contacts sfg, superior frontal gyrus pcl, paracentral lobule Mc, motor cortex SSc, somatosensory cortex pcg, posterior cingulate gyrus PC1-4, precuneus contacts EKG, electrocardiogram EOG, electro-oculogram EMG, electromyogram). The SOZ initiates a low voltage fast rhythmic epileptiform discharge (asterisk) that progressively evolves, reaching other contacts outside the SOZ at the end of the epoch. (D) Seizure: a hypermotor seizure occurs in NREM sleep approximately 1 minute after the end of the PA. Meanwhile, the motor cortex (Mc), the somatosensory cortex (SSc) and the SOZ shift from delta rhythms to wake-like beta activity. Following arousal, the lateral portion of the frontal lobe (sfg, mfg1, mfg2) produces high voltage sleep-like slow waves, which are also detectable in the centro-parietal regions on scalp EEG. (C) Paroxysmal arousal (PA): example of the observed “dissociated” pattern of co-existent sleep-like slow waves and fast wake-like activity on stereo-EEG. Stereo-EEG contacts outside the lesional area and scalp EEG show periodic K-complexes, bursts of slow waves and sleep spindles. (B) NREM sleep: the SOZ produces the typical pseudo-rhythmic low voltage fast discharges (“brushes”) that are intermingled with spindle-like activity. , Of note, this activity is not transferred to the scalp EEG recording over the SOZ. (A) Wakefulness: the seizure onset zone (SOZ) exhibits the typical wake interictal activity of type II focal cortical dysplasia (FCD) consisting of sub-continuous rhythmic or sub-rhythmic spike- and polyspike-and-waves. © 2015 American Academy of Sleep Medicine.Įach EEG segment represents a 30-second epoch.

Hypermotor seizure nocturnal frontal lobe epilepsy parietal lobe epilepsy paroxysmal arousal sleep. A stereo-EEG investigation confirmed the extra-frontal seizure onset of the HMS and highlighted the interrelationship between unstable sleep and seizure precipitation. Although many aspects of DOA have been clarified in the last two decades there is still a lack of objective and quantitative diagnostic criteria for DOA. The presence of an infrequent feeling of levitation before the HMS was key to suspecting a subtle focal cortical dysplasia in the right precuneus region. Furthermore, adult DOA need to be differentiated from other sleep disorders such as Sleep-related Hypermotor Epilepsy or REM Sleep Behavior Disorder. Here we report an unusual case of a patient presenting with a seven-year history of drug-resistant sleep related HMS arising from the mesial parietal region. Nevertheless, in recent years, reports have showed that the seizure onset zone (SOZ) need not be of frontal origin to generate HMS. Hypermotor seizures (HMS) represent a classic manifestation of this syndrome, associated with a perturbation of the ventromesial frontal cortex and anterior cingulate gyrus regions. Nocturnal frontal lobe epilepsy (NFLE) is a syndrome characterized by the occurrence of sleep related seizures of variable complexity and duration.

Sleep related hypermotor epilepsy