*5.2.1 Frontal lobe epilepsy*

Frontal lobe epilepsy [FLE] is the second most common focal epilepsy. Seizures with origin in the frontal lobe tend to occur preferentially during sleep and have prominent motor features, often recognized by family members or friends, **Table 1**. There are two very distinct epileptic syndromes that characterized frontal lobe seizure. They are known as nocturnal frontal lobe epilepsy and supplementary sensorimotor area epilepsy.

Nocturnal frontal lobe epilepsy (NFLE) predominates in male, typically with onset in infancy through adolescence, and is familial in 6-40% of the cases [30–32]. It is characterized by paroxysmal arousals with brief hypermotor features, motor attacks with complex dystonic and dyskinetic movements, and/or episodic nocturnal wandering that mimics the NREM parasomnia called sleepwalking. NFLE usually presents with multiple attacks per night. Video-EEG polysomnography is necessary for definitive diagnosis. Approximately 50% of the cases have normal ictal or interictal EEGs. NFLE usually respond to carbamazepine, but cases of medically intractable NFLE have been well established [30–33].

Supplementary sensorimotor area (SSMA) epilepsy is another unique subtype of frontal lobe epilepsy. Seizures characteristically begin with somatosensory auras progressing to a "fencing" posture with the arm contralateral to seizure


#### **Table 1.**

*General features of frontal lobe seizures.*

focus relatively extended and ipsilateral arm abducted and flexed; speech arrest or vocalization and flailing or trashing limb movements.

### *5.2.2 Autosomal dominant nocturnal frontal lobe epilepsy*

The autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) shares the same characteristics as NFLE described above, but is associated with genetically heterogenous mutations in the nicotinic acetylcholine receptor complex, which is inherited in an autosomal dominant pattern [33]. There are four known loci for ADNFLE, three with known causative agents. These genes, CHRNA4, CHRNB2, and CHRNA2, encode various nicotinic acetylcholine receptor α and β subunits [34].

ADNFLE is often misdiagnosed as nightmares. Attacks often occur in clusters and typically first manifest in childhood.

#### *5.2.3 Benign focal epilepsy of childhood*

This is the most common type of epilepsy within the pediatric sleep-related epilepsy spectrum and accounts for 15-25% of all childhood epilepsies [35]. Benign Rolandic' s epilepsy or benign focal epilepsy of childhood with centrotemporal spikes is a simple partial seizure disorder with hypersalivation, hemifacial and/or hand focal motor-clonic activity that might secondarily spread with generalized tonic-clonic seizures. Seizures often occur exclusively during sleep in three-quarters of patients [36, 37]. The mean age of onset is 7 (3 to 13 years), with recovery by mid-adolescence. Normally, the children affected have normal development with infrequent seizure, but occasionally treatment is necessary. EEG shows high voltage spike and wave discharges over the ipsilateral centrotemporal regions but may occur bilaterally. The discharges increase in frequency, voltage, field, and complexity during sleep. Sleep usually enhances central-midtemporal epileptic discharges, especially in first third of the night, during N3, but also during REM sleep [38]. Treatment is usually successful with AEDs that are effective in partial epilepsy such as carbamazepine, oxcarbazepine, or levetiracetam.

#### *5.2.4 Laundau – Kleffner syndrome electrical status epilepticus of sleep*

Laundau-Kleffner syndrome (LKS) is a rare childhood disorder characterized by loss of language comprehension and verbal expression in association with electroencephalographic finding of status epilepticus during sleep [ESES]. This syndrome is associated with subacute progressive language regression. At some point during this syndrome, there is a dramatic activation of IEA during sleep called ESES that consist of generalized spike-wave complexes at 2-2.5 Hz occurring for >85% of slow wave-sleep with or without clinical seizures. There is marked attenuation of the spikes during REM sleep and wakefulness EEG. With the onset of ESES, there is usually an associated cognitive decline with a speech disorder [39]. Seizures may manifest as nocturnal focal motor or generalized tonic-clonic seizures. LKS most commonly presents in children 2-10 years of age. There is usually remission of the seizures and epileptiform discharges by age of 15, however some patients can develop an autistic regression [40]. Corticosteroid and IVIG are effective and can be considered for treatment of both clinical and EEG changes [41–43]. AEDs including valproate, ethosuximide, clonazepam, clobazam, vigabatrin and felbamate are also effective. In refractory cases, epilepsy surgery including temporal lobectomy in lesional and non-lesional cases have been associated with improvement in language and refractory seizures [44, 45].

**43**

*Sleep Disorders and Epilepsy*

*DOI: http://dx.doi.org/10.5772/intechopen.93989*

underlying primary sleep disorder.

Crowded upper airways [53].

studies [55–59].

10.2%–28.2% [48, 60].

**7. Sleep deprivation**

significant impact on quality of life [50].

**6. Comorbid sleep disorders in epilepsy**

Many patients with epilepsy complain of excessive daytime sleepiness (EDS), with reported prevalence as high as 16.9%–28% [46–48]. In fact, EDS is the most common complaint of subjects referred to sleep disorder centers. EDS in epileptic patients may result from nocturnal seizures, sedative effects of antiepileptic drugs, poor sleep hygiene, and co-morbid primary sleep disorders [49]. EDS in these patients is often mistakenly attributed to AED adverse effect rather than to an

More than 50% of the epileptics suffer from insomnia up to certain extent, as a result of adverse effects of AEDs, substance abuse, nocturnal seizures, and comorbid anxiety and depression. and out of these 43% has poor seizure control and

Co-morbid primary sleep disorder should be sought and treated, but the exact incidence of primary sleep disorders in patients with epilepsy remains uncertain. Obstructive sleep apnea (OSA) is the most common cause of sleep-disordered

Polytherapy AEDs in patients with drug-resistant epilepsy are at increased risk of obesity as compared to monotherapy. Anti-seizure drugs including valproic acid, pregabalin, perampanel, gabapentin and vigabatrin are associated with weight gain, therefore, can potentially worsen or increase the risk of OSA [54]. Adults who developed epilepsy later in life or had worsening seizure control, had a higher apnea–hypopnea index (AHI) and Epworth Sleepiness Scale (ESS) score compared with those who were seizure-free or had an improvement in seizure control [52]. Nasal continuous positive airway pressure (CPAP) therapy demonstrated seizure reduction in patients with OSA and refractory epilepsy in several observational

Restless legs syndrome (RLS), which is defined as the urge to move the legs that improve or partially relieves with activity, worsen with inactivity and is

Sleep deprivation is one of the most potent triggers of epileptic seizures and epileptiform discharges in patients with generalized epilepsy, triggering seizures in

Back in the 1960s and 1970s a series of articles suggested that sleep deprivation was a facilitator of interictal epileptiform discharges, and therefore a promoter of seizures. Lack of adequate sleep causes dysregulation of the hypothalamic pituitary function with release of stress hormones such a cortisol and noradrenaline, which leads to worsening of seizure control [62]. In a recent study, more than 97% of patients with epilepsy reported at least one factor that provokes seizures, and the top three were sleep deprivation, stress, and fatigue [61]. In many cases alcohol

Sleep deprivation is often used in epilepsy monitoring units to increase the frequency of seizures. In addition, interictal epileptiform discharges are also more

worse at night, is common feature in epileptics with a prevalence of

up to 25% of patients suffering from epilepsy [61].

consumption was also a common trigger.

apparent after sleep deprivation.

breathing and may exacerbate seizure burden in as many as 33% of patients with medically intractable epilepsy undergoing pre-surgical planning [51, 52]. Predisposing factors for OSA are older age, male, obesity, dental mal-occlusion and *Updates in Sleep Neurology and Obstructive Sleep Apnea*

and typically first manifest in childhood.

as carbamazepine, oxcarbazepine, or levetiracetam.

*5.2.4 Laundau – Kleffner syndrome electrical status epilepticus of sleep*

Laundau-Kleffner syndrome (LKS) is a rare childhood disorder characterized by loss of language comprehension and verbal expression in association with electroencephalographic finding of status epilepticus during sleep [ESES]. This syndrome is associated with subacute progressive language regression. At some point during this syndrome, there is a dramatic activation of IEA during sleep called ESES that consist of generalized spike-wave complexes at 2-2.5 Hz occurring for >85% of slow wave-sleep with or without clinical seizures. There is marked attenuation of the spikes during REM sleep and wakefulness EEG. With the onset of ESES, there is usually an associated cognitive decline with a speech disorder [39]. Seizures may manifest as nocturnal focal motor or generalized tonic-clonic seizures. LKS most commonly presents in children 2-10 years of age. There is usually remission of the seizures and epileptiform discharges by age of 15, however some patients can develop an autistic regression [40]. Corticosteroid and IVIG are effective and can be considered for treatment of both clinical and EEG changes [41–43]. AEDs including valproate, ethosuximide, clonazepam, clobazam, vigabatrin and felbamate are also effective. In refractory cases, epilepsy surgery including temporal lobectomy in lesional and non-lesional cases have been associated with improvement in language

*5.2.3 Benign focal epilepsy of childhood*

vocalization and flailing or trashing limb movements.

*5.2.2 Autosomal dominant nocturnal frontal lobe epilepsy*

focus relatively extended and ipsilateral arm abducted and flexed; speech arrest or

The autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) shares the same characteristics as NFLE described above, but is associated with genetically heterogenous mutations in the nicotinic acetylcholine receptor complex, which is inherited in an autosomal dominant pattern [33]. There are four known loci for ADNFLE, three with known causative agents. These genes, CHRNA4, CHRNB2, and CHRNA2, encode various nicotinic acetylcholine receptor α and β subunits [34]. ADNFLE is often misdiagnosed as nightmares. Attacks often occur in clusters

This is the most common type of epilepsy within the pediatric sleep-related epilepsy spectrum and accounts for 15-25% of all childhood epilepsies [35]. Benign Rolandic' s epilepsy or benign focal epilepsy of childhood with centrotemporal spikes is a simple partial seizure disorder with hypersalivation, hemifacial and/or hand focal motor-clonic activity that might secondarily spread with generalized tonic-clonic seizures. Seizures often occur exclusively during sleep in three-quarters of patients [36, 37]. The mean age of onset is 7 (3 to 13 years), with recovery by mid-adolescence. Normally, the children affected have normal development with infrequent seizure, but occasionally treatment is necessary. EEG shows high voltage spike and wave discharges over the ipsilateral centrotemporal regions but may occur bilaterally. The discharges increase in frequency, voltage, field, and complexity during sleep. Sleep usually enhances central-midtemporal epileptic discharges, especially in first third of the night, during N3, but also during REM sleep [38]. Treatment is usually successful with AEDs that are effective in partial epilepsy such

**42**

and refractory seizures [44, 45].
