Abstract
Malow BA, Passaro E, Milling C, Minecan DN, Levy K
Neurology 2002;59:1371–137
Purpose
To determine whether acute sleep deprivation facilitates seizures during inpatient monitoring in a controlled protocol.
Methods
Eighty-four patients with medically refractory partial epilepsy undergoing inpatient monitoring were assigned in consecutive blocks to either sleep deprivation every other night or to normal sleep. In both groups, subjects were requested to stay awake during the day, from 6 am to 10 pm. In the sleep-deprivation group, patients also stayed awake between 10 pm and 6 am every other night beginning with day 2. Patients were removed from sleep deprivation if they had two or more secondarily generalized seizures within 24 hours. Patients were removed from the normal sleep group and were sleep deprived if they did not have a complex partial or secondarily generalized seizure by day 6 of monitoring. In these patients removed from sleep deprivation or from normal sleep, data were analyzed up to and including the day of removal from the protocol.
Results
The sleep deprivation and normal sleep subjects did not differ in age, sex, seizure localization, or percentage dosage reduction in antiepileptic drugs from baseline at days 1 to 3 of monitoring. Protocol duration was 6.5 ± 2.4 days (mean ± SD) for the sleep-deprivation group and 5.8 ± 2.0 days for the normal sleep group. Seizures per day for complex partial, secondarily generalized, and combined complex partial and secondarily generalized, calculated from admission until end of protocol, did not differ significantly between the two groups.
Conclusions
Acute sleep deprivation did not affect seizure frequency during inpatient monitoring in our patients with intractable complex partial seizures with secondary generalization.
Commentary
Malow et al. used a very systematic approach to the question of whether sleep deprivation increases seizures. Patients were in a controlled setting (an EMU), and were randomized to receive every-other-night sleep deprivation (more severe than used in many EMUs), or normal sleep nightly. In both groups, anticonvulsant drugs were tapered by using the same, standard protocol. The groups were similar in age, sex, seizure type, and time in the protocol; baseline seizure frequency was higher in the sleep-deprivation group, although this was not statistically significant. They found a virtually identical seizure frequency in the two groups.
The results are highly suggestive that sleep deprivation does not increase seizure frequency in this patient group, which consisted of patients with intractable localization-related epilepsy. There are several caveats to this conclusion. First, it may be that the hospitalized setting somehow changed the influence of sleep deprivation, whether by relief from other stresses of day-to-day living, medication taper, or other factors. This seems unlikely. Second, the study was by necessity un-blinded; it could be that the intervention of being in the study somehow altered the expectations of one or both groups, and therefore the seizure rate. This also seems very unlikely. Finally, the study was relatively short (average, 6 days), so more prolonged sleep deprivation could exacerbate seizures.
In some ways, this may be analogous to the belief that psychological stress increases the incidence of seizures. This is another widespread belief among patients and physicians; however, in a single study of a stressful event (SCUD missile attacks on Israel), there was no apparent increase in the frequency of seizures (5). Again, there may be other types of stressors or other conditions in which stress increases seizures, suggesting that this also is not a simple relation.
It is well known that other epilepsy syndromes, such as juvenile myoclonic epilepsy and awakening grand mal, are exacerbated by sleep deprivation. It also may be true that individual patients with localization-related epilepsy could be sensitive to the effects of sleep deprivation, but this effect could not be seen in a series of patients.
This study is important because it suggests that the routine practice of sleep deprivation in EMUs is not helpful in reducing hospital stays. More important, it highlights the gaps in our existing knowledge about the relation between sleep and epilepsy. In addition to the effects of sleep and sleep deprivation on seizures, several other, potentially important areas exist in which questions have incomplete answers. How frequently do various sleep disorders coexist with epilepsy? How prevalent is drowsiness in the epilepsy population (6), and how much of this arises from the disease itself, from seizures, from concurrent sleep disorders, or from medication? What are the effects of individual anticonvulsants on sleep (7–13), and (perhaps more important) are these clinically significant? Further research in this area is clearly warranted, and this study is an excellent first step toward understanding one aspect of the complicated sleep/epilepsy relation.