NFLE is characterised by onset during infancy or childhood with persistence in adulthood, family history of similar NFL seizures and nocturnal episodes simulating non-rapid eye movement (NREM) parasomnias (sleep terrors or sleepwalking), general absence of morphological substrates based on clinical history and brain imaging, motor dystonic–dyskinetic attacks emerging from NREM sleep, repetitive and stereotypical features in the same patient and similar features among different patients, normal ictal and interictal EEGs without clear-cut epileptic paroxysms in more than 50% of the cases and general benefit from some antiepileptic drugs (AEDs), but occasional resistance to AEDs in some severe forms.

The different types of NFLE seizures may cause severe sleep disruption affecting both the macrostructure and microstructure of sleep and resulting in poor sleep quality, daytime tiredness and sleepiness. The movements may also be so severe that injuries resulting from striking hard objects can occur. One-third to half of patients also have occasional attacks during the day, not necessarily of the same type as those occurring at night-time, as well as secondary generalised tonic–clonic seizures. Neurological examination is generally normal.^1–4

Arousal Disorders
NREM parasomnias (arousal disorders) include confusional arousals, sleep terrors and sleepwalking. All are characterised by a motor component, autonomic activation, emotional involvement, poor memory or fragmented recalls of the episode, long duration (one to 20 minutes) and occurrence on emergence from deep NREM sleep, typically in the first third of the night with impairment in the ability to awake fully from slow-wave sleep (SWS). They typically occur during the maturational age of life (childhood and adolescence), but may also persist in adulthood. Notwithstanding the sleep EEG characteristics of these arousal disorders as delta bursts or rhythmic delta activity preceding the episode, the slow-wave activity during the episodes and the polygraphic modification of heart rate, respiration and muscle tone, there is not, to date, a polysomnographic marker of these nocturnal phenomena.^5–7

NFLE should be differentiated from parasomnias, in particular from NREM parasomnias such as arousal disorders. The clinical/anamnestic features are quite similar; however, the older age of onset, the high frequency of the episodes and their short duration, the partial preservation of consciousness and the tendency of the syndrome to persist in adulthood differentiate NFLE from arousal disorders. The motor pattern during sleep and the semiology of the attacks (stereotypy, dyskinetic and dystonic component, abrupt and sudden onset, dancing or jumping features for the more complex seizures) may be helpful, although the definite boundaries between the two types of episodes are still not completely understood. Differentiating paroxysmal arousal (PA) from confusional arousal (CA) is difficult because of the lack of paroxysmal EEG discharges in PA, and requires videopolysomnography (video-PSG).^5,8

The features that differentiate REM parasomnias from NFLE include later age of onset, motor episodes during the night enacting behaviour related to a dream, less stereotypical behaviour, polysomnographic characteristics of REM without electromyogram (EMG) atonia and an increase in EMG activity of the limbs.^6,9 Other motor phenomena during sleep or sleep transitions, such as rhythmic movement disorder, hypnic myoclonus or physiological body movements, are easier to recognise. Nocturnal panic attacks are characterised by sudden awakening with complex autonomic activities and an unpleasant sensation of fear or imminent death, usually lasting longer than NFLE and, unlike in NFLE, not recurring. The presence of the same attacks during the day may also help to differentiate the syndrome from NFLE.^3,4