Childhood absence epilepsy patients with cognitive impairment have decreased sleep spindle density
Wei Zhang1, Meiying Xin1, Ge Song2
1Department of Pediatric Neurology, The First Hospital of Jilin University, Changchun, China; Jilin Provincial Key Laboratory of Pediatric Neurology, Changchun, China.
Insights
Children with childhood absence epilepsy have reduced sleep spindle density and duration. This deficit is linked to cognitive impairment and may serve as a biomarker.
Area of Science:
- Neuroscience
- Pediatric Neurology
- Sleep Medicine
Background:
- Childhood absence epilepsy (CAE) is a common epilepsy syndrome in children.
- Sleep spindles (SSs) are transient electroencephalographic events during N2 sleep, crucial for cognitive functions.
- Cognitive impairment is a frequent comorbidity in CAE.
Purpose of the Study:
- To investigate differences in sleep spindle characteristics during N2 sleep between children with CAE and healthy controls.
- To examine sleep spindle alterations in children with CAE, comparing those with and without cognitive impairment.
Main Methods:
- Recruited 29 children with CAE (treatment-naive) and 30 age-matched controls.
- Collected medical history, conducted overnight video-EEG monitoring, and administered the Wechsler Intelligence Scale for Children-Fourth Edition.
- Compared anterior SS characteristics (density, frequency, duration, amplitude, cycle length, sleep stage distribution).
Main Results:
- Children with CAE showed significantly lower SS density and duration during N2 sleep compared to controls (P < 0.01).
- Reduced SS density was observed in CAE patients with cognitive impairment, with significantly lower density in the impaired group (P < 0.01).
- No significant differences were found in SS amplitude, frequency, cycle length, or sleep stage distribution.
Conclusions:
- Reduced SS density and duration are associated with the pathophysiology of CAE.
- Deficits in SS density correlate with cognitive impairment in children with CAE.
- SSs may serve as a predictive biomarker for cognitive impairment and a potential therapeutic target in CAE.
Objective:
To explore the differences in sleep spindle (SS) characteristics during stage N2 sleep between children with childhood absence epilepsy and healthy controls, and between children with childhood absence epilepsy with or without cognitive impairment.
Methods:
We recruited 29 children (14 females, 15 males, mean age: 8 (2.5) years) with childhood absence epilepsy who did not undergone antiseizure treatments previously and 30 age-matched controls (14 females, 16 males, mean age: 9 (3.0) years). For all patients, data on medical history were collected. Each child was monitored overnight by long-term video electroencephalography and was evaluated by the Wechsler Intelligence Scale for Children-Fourth Edition. Next, we compared anterior SS characteristics, including density, frequency, cycle length, duration, amplitude, and percentage of sleep stages.
Results:
The childhood absence epilepsy group exhibited lower spindle density and duration in the first 37.5 min of stage N2 sleep than the control group (P < 0.01). A decrease in spindle density could be observed in the childhood absence epilepsy group with aggravated cognition impairment. The spindle density was substantially lower in the cognitively impaired group than in the cognitively unimpaired group (P < 0.01). No significant differences were observed in SS amplitude, SS frequency, SS cycle length, and the distribution of sleep stages.
Conclusions:
Reduction in spindle density and duration is associated with the mechanisms underlying childhood absence epilepsy. The deficit in SS density is related with impaired cognition. This deficiency in SSs may be a useful predictive indicator of cognitive impairment in children with absence epilepsy, indicating that SSs may become a useful biomarker and potential adjuvant anti-seizure target for cognitive impairment caused by childhood absence epilepsy.
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