Relationship of sleep and epilepsy is complex and reciprocal. Sleep in epileptic patients is usually altered and this may lead to intractability. Moreover, it is confirmed that prolonged awakening has a negative impact on increased cortical excitability and susceptibility to seizures. In addition, sleep–wake cycle and its regulatory mechanisms can affect epilepsy. Putting these data in mind, we could hypothesize a relation between epilepsy and sleep disorders [8]. In patients with epilepsy, studies of sleep architecture have been a very fruitful area of clinical research [9]. Our study is the first Egyptian study, to our knowledge, to compare between sleep architecture in medically controlled and refractory epilepsy patients.
In this study, we aimed to characterize possible abnormalities in sleep architecture, quality, and distribution of primary sleep disorders in a group of patients with controlled epilepsy versus medically refractory ones. Interestingly, none of the enrolled patients had any seizures during the PSG recordings or the day before. This was a valuable coincidence, since it rules out the possibility of disturbed sleep being attributed directly to epileptic seizures.
Elwan and colleagues (2005) found that untreated epileptic patients had significant excessive daytime sleepiness compared to controls [10]. In the present study, we found that patients with refractory and medically controlled epilepsy reported frequent symptoms of sleep disturbance including insomnia, EDS, and snoring which comes in agreement with a couple of earlier studies [11, 12]. It was noted that the most frequent sleep disorder among refractory epilepsy patients was snoring followed by EDS. The high prevalence of EDS in the refractory epilepsy group could be attributed to the use of older AEDs and combination of AEDs [3].
However, the most encountered symptom in medically controlled patients was found to be insomnia. This finding was confirmed by the higher mean arousal index, higher limb movement index, and greater sleep fragmentation in the controlled epilepsy group. Vendrame and colleagues found that the prevalence of moderate and severe insomnia was 51% in their group of epileptic patients, with a stronger association in patients on higher number of AEDs. Also, it should be noted that the prevalence of chronic or severe insomnia in the general population has been estimated to approach 10% [13, 14].
In the present study, the architecture of sleep of medically refractory epilepsy patients was markedly disturbed with greater sleep fragmentation and instability on seizure-free nights compared with medically controlled subjects, and the efficiency of sleep was poorer among the patients with medically refractory epilepsy, which is in accordance with other former studies [11, 15]. These studies agreed that reduction and instability of REM sleep is most often reported, yet shorter total sleep time, lower sleep efficiency, more sleep fragmentation, longer sleep latency, and increased stage shifts and awakenings are also found.
In 40 pediatric-age-group patients, Kaleyias and colleagues reported that intractable epilepsy patients have longer sleep latency, poor sleep efficiency, along with higher arousal index as compared to medically controlled epilepsy [16]. Our findings regarding sleep efficiency, sleep onset latency, REM latency, and AHI are similar to those in the previously mentioned study, which is also in accordance with Zanzmera and colleagues’ study. The only major difference observed by us is the much shorter sleep latencies among our patients in both groups, while the intergroup difference noted was similar, which is again similar to the findings reported by Zanzmera and colleagues [15]. It could be attributed to the effect of AEDs, especially CBZ and VPA [17, 18].
The interesting finding in our study was that significantly less number of group I patients had PLMs as compared to group II patients. This finding is unlikely to be clinically significant as the index in both groups is quite low, and similar finding was reported before, in the study of Zanzmera and colleagues [15]. This difference could, however, be attributed to AEDs, specifically CBZ and VPA, which might decrease PLMs [17, 19].
It is known the AEDs affect sleep structure [20]. Prolonged CBZ and VPA therapy have restorative and normalizing effects on sleep pattern in idiopathic epilepsies, in addition to improving subjective daytime sleepiness. CBZ leads to an increase in the number of sleep stage shifts, a reduction in REM sleep, increased fragmentation of REM sleep, and a significant reduction in sleep latency. In addition, studies suggested that VPA increases the number of arousals, prolongs the light stages of sleep and NREM phase, and decreases the length of the REM phase [21].
In our study, we found that the number of subjects taking CBZ and VPA in group II was much greater than those in group I, which could contribute partially in the observed findings of NREM sleep prolongation and reduction in REM sleep. However, this does not justify the significant decrease in sleep latency in both groups.
