An Examination of Nocturnal Frontal Lobe Epilepsy
Abstract & commentary
Source: Provini F, et al. Nocturnal frontal lobe epilepsy, A clinical and polygraphic overview of 100 consecutive cases. Brain 1999;122:1017-1031.
Provini and colleagues identify three different patterns of nocturnal frontal lobe epilepsy (NFLE) in 100 cases, many of which in the past have been diagnosed simply as sleep disorders. All attacks occurred during non-REM sleep. All were thought to be derived from deep frontal lobe loci and most have benefited from antiepileptic drugs. All were identified by detailed clinical and audio-video EEG sleep studies. Most subjects had onsets in infancy or adolescence, but overall onsets ranged from 1 to 64 years. Males dominated 7 to 3.
One syndrome labeled as nocturnal paroxysmal dystonia (NPD) consisted of recurrent, sudden dystonic-dyskinetic attacks interrupting sleep and lasting for less than two minutes. Abnormal EEG records were often obtainable by placing special sphenoidal or zygomatic electrodes. Paroxysmal arousal (PA) attacks consisted of stereotypic behavioral activity lasting less than 20 seconds. Suggesting their epileptic origins, abnormal EEGs accompanied the attacks and antiepileptic drugs suppressed them. Some patients were susceptible to both NPD and PA attacks. The third pattern was characterized by episodic nocturnal wanderings (ENW) by Pedley and Guilleminault (Ann Neurol 1977;2:30-35) and consisted of somnambulic agitation. A major factor in classifying all three of these syndromes as being epileptic is that a number of individual patients show more than one pattern and a few have suffered all three.
Genetic patterns indicated that 39 (39%) of their 100 patients had at least one first-degree relative with a primary parasomnia. Twenty-five percent had a family history of epilepsy, several with multiple sufferers. Onset age for seizures ranged from 1 to 64 years (mean 14 ± 10). Overall the 100 patients reported 20 ± 11 seizures monthly, of which 1-20 occurred at night. Specific triggering factors were uncertain and 28% of patients had more than one nighttime seizure pattern. Altogether, 72% of patients were unaware of their nocturnal attacks; 34% had occasional attacks during wakefulness. Neurological examinations were normal in 92%, two had mental handicaps, and the remainder were trivial. Imaging results included various potential epileptogenic abnormalities in 14%. Videosomnographics, however, revealed classic motor seizures in 93%, plus seven with only one episode, but who, nevertheless, expressed classic EEG abnormalities. Other evidence of video-EEG associations are detailed in the parent article in Brain.
All in all, findings included the following video-EEG patterns: patients with PA, 9; with NPD, 51; and with ENW, 40. PA patients all were otherwise normal; three accepted carbamazepine, of which two became seizurefree and one reduced by 75%. Of the NPD group, 24% had a structural brain injury. Of these, 24% became seizurefree with antiepileptics and another 31% had a 50% reduction of attacks. Of the ENW group, carbamazepine halted seizures in five and reduced seizures in at least half of the other 35.
Provini et al conclude that NFLE’s relation to sleep often relates to a mesio frontal epileptic focus that activates during NREM sleep. Also, k complexo may sometimes cluster to trigger the epileptic focus. The table, adapted from Provini et al’s article, lists epileptic and nonepileptic differences that divide relatively benign parasomnias from those of NFLE. (See Table 1.)
| Table 1-Clinical Criteria for Parasomnia and NFLE | ||
| Parasomnia | NFLE | |
| Onset age | < 10 years | 14 ± 10 years |
| Family history | ± 79% | 39% |
| Frequency/month | 0-4 | ± 25% |
| Future | Ceases ± 7 years | Increases ± 20 yrs |
| Length of attack | Up to 30 minutes | 2-180 secs |
| Movement | Physiologic | Violent, consistent |
| Precipitators | Sleep-deprived; fever; | ± 0 |
| Stress; alcohol/drugs | ||
| Sleep stage onset | 3-4 REM | 2 NREM in ± 60% |
Commentary
This is an important paper for the therapy programs of both epileptologists and sleep center physicians. The cohort emphasizes patients whose nocturnal behaviors consisted of more complicated activity than most uncomplicated somnambulism. The relatively few persons who had only frequently repeated, stereotypic motor arousals were designated as PA. Since these overlapped the other syndromes in certain patients and they improved with anticoagulants suggests a frontal lobe epileptic focus. Your editor suspects that the Tinuper-Lugaresi-Montagna laboratory ordinarily does not study many children with uncomplicated somnambulism. Otherwise, the contribution provides considerable interest in how to treat unusual adolescent-mature somnambulism or young children with complicated sleep behavior. —fp
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