Abstract
Abstract
Objective
Sleep deprivation (
SD
) triggers seizures in only a subset of patients with juvenile myoclonic epilepsy (
JME
). We compared sleep macro‐architecture between
SD
‐sensitive and
SD
‐insensitive
JME
patients and healthy controls.
Methods
Overnight polysomnography was done in healthy volunteers (
n
= 30), JME patients without SD‐triggered seizures (SD‐insensitive,
n
= 31), and JME patients reporting SD‐triggered seizures on a structured interview (SD‐sensitive,
n
= 68). Eleven participants with clinically diagnosed narcolepsy were excluded. We analyzed sleep continuity, stage distribution, rapid eye movement (REM)/non‐REM (NREM) stability, and cardiorespiratory indices.
Results
SD‐insensitive patients had lower sleep efficiency than controls but preserved stage N3 and REM. SD‐sensitive patients had significantly lower N3 than SD‐insensitive patients (
p
= .002) and reduced REM vs controls (
q
= .005). SD‐sensitive status independently predicted N3% after adjusting for sex and anti‐seizure medication class (
β
= −8.28,
p
= .013), and remained significant after further adjustment for generalized tonic–clonic seizure (GTCS) frequency (
β
= −7.35,
p
= .035). Valproate use was also independently associated with N3 reduction (
β
= −8.37,
p
= .007). Respiratory and cardiac indices did not differ.
Significance
SD‐sensitive JME shows a light NREM‐dominant sleep profile with decreased N3 vs SD‐insensitive patients along with decreased REM when compared to controls. These differences are associative (SD sensitivity was self‐reported; no experimental challenge). No polysomnography parameter independently predicted SD sensitivity. Prospective studies with controlled SD challenge are required to determine if lighter sleep is a vulnerability factor or a parallel correlate of seizure risk.