- Neurocognitive deficits commonly occur in Rolandic epilepsy, but it's unknown how the pathology of epilepsy disrupts cognition in this disease
- This study investigated relationships between the absence of sleep spindles—characteristic sigma band oscillations on EEG during sleep—and performance on neurocognitive tasks
- Spindle rate was decreased in the inferior Rolandic cortex (the site of seizures) in children with active Rolandic epilepsy, and spindle deficits were also apparent in parts of the prefrontal, insula, temporal and parietal cortices
- Adding regional estimates of spindle rates to focal rates was better than focal rates alone at predicting cognitive performance
- Sleep spindle deficits in Rolandic epilepsy reflect regional disruption to the thalamocortical circuit; they are a mechanistic explanation for the cognitive symptoms of the disease and may be a useful biomarker in therapeutic trials
Rolandic epilepsy, the most common form of childhood epileptic encephalopathy, is characterized by seizures in the inferior Rolandic (sensorimotor) cortex during non–rapid eye movement (NREM) sleep. Affected children also have a broad range of neurocognitive deficits, which can be subtle to severe. Fortunately, both sets of symptoms spontaneously resolve by adolescence.
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Why the cognitive deficits occur is still unknown, but growing evidence suggests the involvement of the thalamus, which synchronizes and regulates sleep. Massachusetts General Hospital researchers recently reported in the Journal of Neuroscience that children with Rolandic epilepsy showed a focal absence of sleep spindles (characteristic sigma band oscillations on EEG) during NREM sleep.
Building on that research, Elizabeth R. Spencer, a graduate researcher in the Department of Neurology at Mass General, Catherine J. Chu, MD, MA, MMSc, director of Neonatal and Pediatric Continuous Electroencephalography Monitoring in that department, and colleagues now report, in NeuroImage: Clinical, that sleep spindle deficits occur in several areas of cortex besides the inferior Rolandic cortices where seizures occur. This regional thalamocortical circuit dysfunction potentially explains the wide range of cognitive deficits observed in children with Rolandic epilepsy—and it may represent a therapeutic target.
The researchers studied three groups of children: eight with active Rolandic epilepsy, 10 with resolved Rolandic epilepsy (no seizures for at least 12 months), and eight control subjects. The three groups were similar in age and sex, and the two epilepsy groups were similar regarding the use of antiepileptic medication.
Each subject completed tests of fine motor dexterity, processing speed, global intellectual function, and phonological awareness, the hallmark cognitive challenges in Rolandic epilepsy. They underwent high-density EEG and high-resolution MRI, and the researchers compared how cognitive performance related to rates of sleep spindles in each cortical region.
The key findings were that:
- In children with active Rolandic epilepsy compared with controls, the sleep spindle rate was reduced in the inferior Rolandic cortex; there was no detectable difference in spindle rate between controls and children with resolved epilepsy
- Spindle deficits in children with the active disease also occurred in parts of the prefrontal, insula, temporal, and parietal cortices
- Both focal and regional estimates of spindle rates predicted cognitive deficits, but combining them tended to improve the prediction of global cognitive function, and the combination significantly improved the prediction of motor performance
A Sensitive Biomarker
Rolandic epilepsy has been considered a focal epilepsy, but a regional model of dysfunction better explains the cognitive symptoms of the disease. Along with treating seizures, future therapeutic trials in Rolandic epilepsy could have the goal of improving sleep, signaled by increasing sleep spindle production, with the hope of improving cognition.
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