Abstract
Continuous spikes during slow wave sleep (CSWS) syndrome is an age-related and self-limited severe epileptic encephalopathy characterized by electrical status epilepticus in sleep (ESES) on electroencephalogram(EEG), seizures, and developmental regression in, at least, two domains of development
Highlights
Continuous spikes during slow wave sleep (CSWS) syndrome is an age-related and self-limited severe epileptic encephalopathy characterized by electrical status epilepticus in sleep (ESES) on electroencephalogram(EEG), seizures, and developmental regression in, at least, two domains of development [1]
The interactions between neurotransmitters, hormones, and cytokines can explain the occurrence of CSWS syndrome
The expression of many neurotransmitter receptors including GABAA as well as ion channels such as voltage dependent potassium and calcium channels, hormones such as GHreleasing hormone (GHRH), cortisol, melatonin, and cytokines such as IL-6, IL1 beta and tumor necrosis factor (TNF) are regulated by circadian rhythm
Summary
Continuous spikes during slow wave sleep (CSWS) syndrome is an age-related and self-limited severe epileptic encephalopathy characterized by electrical status epilepticus in sleep (ESES) on electroencephalogram(EEG), seizures, and developmental regression in, at least, two domains of development [1]. Several anti-epileptic drugs work through GABAA receptor to enhance sleep. We hypothesize that one of the mechanisms of steroids in CSWS syndrome is attributed by its action on GABAA receptor.
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