Epilepsy is characterized by frequent and unpredictable disruptions of brain functions resulting in “epileptic seizures.” Epilepsy has a great impact on the quality of life through increased incidence of injury and death, unemployment rates, lower monthly incomes, higher household costs and high absenteeism at work and schools (Jennum et al., 2017; Trinka et al., 2018; Wibecan et al., 2018). An epileptic seizure is considered as a transient episode of signs or symptoms, including transitory confusion, staring speech, irrepressible jerking movements, loss of consciousness, psychic symptoms such as fear and anxiety, due to the abnormal synchronous neuronal activity of the brain. The International League Against Epilepsy (ILAE) published a recent clinical definition of epilepsy in which a patient with any of the following conditions is considered to be an epileptic i.e., (i) two or more unprovoked seizures within more than 24 h apart; (ii) one unprovoked seizure and a probability of further seizures similar to the general recurrence risk, occurring over the next 10 years; (iii) definite diagnosis of an epilepsy syndrome (Fisher et al., 2014). Genesis of epilepsy is attributed to various predispositions that include neurological, perceptive, psychological, and social factors, which could either stimulate or worsen the syndrome. In early 2017, the point prevalence of active epilepsy was found to be 6.38/1,000 individuals, while the lifetime prevalence was 7.60/1,000 persons. Meanwhile, the annual cumulative incidence of epilepsy was 67.77/100,000 persons and the incidence rate was 61.44/100,000 person-years. The active annual prevalence, prevalence during lifetime and the incidence of epilepsy were found to be higher in the developing countries (Fiest et al., 2017).
A systematic review revealed that epilepsies of unknown etiology had the highest prevalence compared to the epilepsies of known origin (Fiest et al., 2017). These were due to known underlying factors that cause seizures such as brain damage (Sizemore et al., 2018), metabolic diseases (Tumiene et al., 2018), infections (Bartolini et al., 2018), hemorrhagic stroke (Zhao et al., 2018), and gene mutations (Leonardi et al., 2018). These precipitating factors tilt the balance between excitatory and inhibitory neurotransmissions which has been established in different types of epilepsy. Physical and psychological comorbidities are usually accompanied with epilepsy, such as depression (Jamal-Omidi et al., 2018), sleep disorders (Castro et al., 2018), and body injuries (Mahler et al., 2018). Advanced cases may suffer from memory loss (Reyes et al., 2018), behavioral disorders (Jalihal et al., 2018), and disturbance of autonomic functions (Fialho et al., 2018). The rate of sudden death in epileptic patients was reported to be three times higher than non-epileptic individuals (Kothare and Trevathan, 2018; Pati et al., 2018).
Sleep deprivation is very common among the epileptic patients and lack of sleep could worsen the seizure expressions (Neto et al., 2016). In animal models, sleep deprivation was shown to heighten the propensity to seizures (McDermott et al., 2003). Sleep deprivation has been correlated with decline in various aspects of brain functional connectivity (Nilsonne et al., 2017). Generally, sleep deprivation is secondary to other factors such as illness, emotional or psychological stress, and alcohol use. Hence, lack of sleep alone may not be sufficient to cause seizures (Razavi and Fisher, 2017). A large body of literature on the effects of epilepsy on sleep and/or sleep-deprivation on the epileptic state has been collated (St Louis, 2011; Unterberger et al., 2015).
Sleep-related epilepsy represents nocturnal seizures that manifest solely during the sleep state (Tchopev et al., 2018). Approximately 12% epileptic patients are affected by sleep-related epilepsy with the majority suffering from focal epilepsy (Derry and Duncan, 2013; Losurdo et al., 2014). In a recent case report, focal epilepsies were anatomically linked to epileptogenic origins at the right frontal lobe, using white matter tractography MRI (Tchopev et al., 2018). In a separate study, ambulatory electroencephalogram (EEG) measurement in outpatient setting reported frontal lobe seizures to manifest more readily between 12 a.m. and 12 p.m., particularly around 6:30 a.m., whereas temporal lobe seizures expressed more frequently between 12 p.m. and 12 a.m., specifically around 8:50 p.m. (Pavlova et al., 2012). In addition to seizure onset, few seizures seem to propagate more readily during sleep, based on anatomical locus. Medial temporal lobe regions were shown more likely to manifest spike production or propagation during NREM sleep stage compared to other brain regions (Lambert et al., 2018). Sleep-related epilepsy is often misdiagnosed as sleep disorders (Tinuper and Bisulli, 2017), especially in cases where the seizures manifest exclusively during sleep. Over the past decade, the discovery of numerous pre-disposing genes and availability of advanced diagnostic tools have shed more light in understanding the nature of sleep-related epilepsy.
In the present review, we discuss sleep-related epilepsy with particular emphasis on three of the most frequently implicated epilepsies during the sleep state which include sleep related hypermotor epilepsy (SHE), benign partial epilepsy with centrotemporal spikes (BECTS), and Panayiotopoulos Syndrome (PS).[…]