The incidence of primary sleep disorders in the epileptic population is unknown. The literature contains mostly retrospective studies in which patients with epilepsy and suspected sleep disorders are included. Consequently, the reported incidence of sleep disorders is likely to be overestimated. Prospective studies are required to determine how these figures compare with those of the general population.
In the largest retrospective study, 63 adults with epilepsy were referred for PSG for EDS and suspected OSAS (27), suspected OSAS without EDS (22), spells and EDS or suspected OSAS (10), nocturnal spells (2), or EDS alone (2) (Malow et al., 1997). Multiple sleep latency tests (MSLTs) were performed in 33 cases. Sleep disorders were suspected in 79% of patients. Obstructive sleep apnea syndrome was diagnosed in 71%. The disorder was considered mild in 14, moderate in 21, and severe in 10 patients, including 7 females. Other diagnoses included nocturnal seizures (4), mild OSAS and narcolepsy (1), and insufficient sleep syndrome with probable idiopathic hypersomnia (1). In 13 cases, the diagnosis was uncertain. These included six subjects with PLMS with 20 or greater leg movements per hour generally not causing arousal. Of the subjects who had MSLTs, the average mean sleep latency was 6.8 min, suggesting a moderate degree of daytime sleepiness. Treatment of OSAS with continuous positive airway pressure (CPAP) or with bilevel positive airway pressure (BIPAP) was prescribed in 28 cases. However, only 54% were still using the device at the time of last follow-up. Seizure control improved with CPAP in five of nine patients having seizures before treatment. In two cases, EDS improved despite higher doses of AEDs or the administration of new AEDs. Treatment with CPAP was discontinued in 12 patients due to poor tolerance (9) and lack of efficacy (3).
Other studies have confirmed a high incidence of primary sleep disorders in subjects with epilepsy and sleep complaints. Of 43 adults admitted for video EEG monitoring (28 with confirmed epilepsy), abbreviated sleep studies were performed to evaluate for suspected OSAS (24); PLMS or nocturnal spells (9); and EDS, cataplexy, or both (10) (Bromfield et al., 1997). OSAS was confirmed in 12 cases (8 with epileptic and 4 with nonepileptic seizures). The disorder was mild in five, moderate in three, severe in two, and restricted to rapid eye movement (REM) sleep in two cases. Hypersomnia without cataplexy was diagnosed in two subjects, and one patient was found to have PLMS. Despite limited follow-up, daytime sleepiness improved with treatment of the sleep disorder in most cases. However, seizure frequency was not significantly affected.
Of 22 patients with epilepsy who underwent PSG for evaluation of EDS with or without snoring, sleep disorders were identified in 18 (72%) (Marsilio et al., 1997). Of these 22 patients, 12 had OSAS, with a mean apnea-hypopnea index (number of respiratory events per hour) of 23. Upper airway resistance syndrome (UARS), a disorder characterized by abnormal increases in resistance of the upper airway in sleep that produce arousal, oxygen desaturation, and EDS, was found in four subjects (Guilleminault et al., 1993). Two patients were diagnosed with PLMS; however, the disorder was of questionable clinical significance in one because leg jerks typically did not disrupt sleep.
Several authors have reported an improvement in seizure frequency following treatment of OSAS (Devinsky et al, 1994; Vaughn et al., 1996; Koh et al., 1997; Barthlen et al., 1998; Wyler and Weymuller, 1981). Seven adults with focal epilepsy and moderate to severe OSAS were treated with CPAP alone (3), CPAP with weight reduction (1), CPAP with pharmacotherapy (1), pharmacotherapy alone (1), and tracheostomy with supplemental oxygen and acetazolamide (1) (Devinsky et al., 1994). Treatment reduced seizure frequency and severity in six cases. However, noncompliance was an issue in three of five patients in whom CPAP was prescribed.
In another series, four of ten patients with OSAS experienced a dramatic improvement in seizures (three patients were rendered seizure free) with CPAP or positional therapy (Vaughn et al., 1996). Seizures occurred exclusively on awakening or in sleep in three of the four patients experiencing the greatest reduction in seizures. A typical body habitus of OSAS was present in only two of these patients. Seizure frequency was reduced in three others after AED adjustments and treatment of the sleep disorder. Three subjects, with seizures unrelated to the sleep-wake cycle, experienced less than a 50% seizure reduction. There was no correlation between severity of OSAS and seizure frequency.
The impact of treatment for OS AS on seizures was reported in 10 epileptic children treated with tonsillectomy (8), tracheostomy (1), and CPAP (1) (Koh et al., 1997). Seizure frequency improved in six cases. After one year of treatment, the mean seizure frequency decreased from 1 or 2 per month to one seizure every 4 months.
Very little is known of the incidence of PLMS and RLS in patients with epilepsy. In one report, three of six patients with untreated epilepsy had PLMS, but the disorder produced sleep disruption in only one case (Newell and Drake, 1994). Restless legs syndrome was described in two subjects taking methsux-imide and phenytoin (PHT), respectively (Drake, 1988). In the first case, symptoms resolved after methosuximide was replaced by valproic acid (VPA). Symptoms improved when PHT was replaced by CBZ in a male with a hemiparesis following subarachnoid hemorrhage. No evidence of neuropathy was found in either case.
Daytime sleepiness was assessed in 30 adults with epilepsy using the MSLT (Drake et al., 1994). Of those, 23 subjects reported intermittent tiredness or difficulty sleeping and 20 described feelings of depression and irritability. Another 20 subjects reported feeling sleepy during some of the naps. A mean sleep latency of greater than 8 min was considered normal. The mean sleep latency was greater than 8 min in 10, between 5 and 8 min in 7, and less than 5 min in 3 of the 20 subjects reporting sleepiness. Of the patients who denied feeling sleepy during the test, two failed to sleep during the MSLT, 7 had a mean sleep latency greater than 8 min, and one had a mean sleep latency between 5 and 8 min. The mean sleep latency of the entire cohort was 8.4 min, which is suggestive of mild to moderate hypersomnia, using 10 min as a cutoff by conventional scoring standards (Carskadon et al., 1986). Pathological hypersomnia (mean sleep latency less than 5 min) was found in 10% of cases. Patients who had seizures or were sleep deprived the previous night were excluded. However, the presence of chronic sleep deprivation, concomitant sleep disorders and the remote effects of AEDs were not investigated.
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