SUMMARYObjective: Thalamic injury has been implicated in the development of continuous spike-wave during slow-wave sleep (CSWS) in children with epilepsy. We studied thalamic abnormalities in children with CSWS using F-18-fluorodeoxyglucose (FDG)-positron emission tomography (PET) imaging. Methods: Twenty-three patients (12 male; mean age 9 years) with CSWS and normal thalami on brain magnetic resonance imaging (MRI) underwent FDG-PET. Thalamic glucose metabolism, represented by standardized uptake value normalized to whole brain (nSUV, RT for right thalamus and LT for left thalamus), and its asymmetry-absolute asymmetry index (AAI): |(RT-LT)|*100/ [(RT+LT)/2]-was calculated. These values were compared with those from 10 normal healthy controls (five female; mean age 11.1 years). Results: Thalamic glucose metabolism was abnormal in 18 patients (78.3%). Thalamic nSUV was decreased (n = 6) or increased (n = 1) bilaterally in seven children without any asymmetry. Abnormal thalamic symmetry [AAI = 3.7-31.5% (0.8-3.3% in controls)] was seen in 11 children. Of these, six children had a unilateral thalamic metabolic abnormality (increased metabolism, n = 3 and decreased metabolism, n = 3), whereas 5 of 14 children had abnormal asymmetry index with bilaterally normal (n = 4) or increased (n = 1) thalamic metabolism. No clear association of thalamic metabolic abnormalities was seen with the stage of evolution of CSWS (prodromal, acute, or residual) or with the cortical FDG abnormalities. Significance: Functional thalamic abnormalities, both unilateral and bilateral, are frequently seen in patients with CSWS. FDG-PET is a sensitive and quantifiable modality to detect these changes. KEY WORDS: Continuous spike-wave during slow-wave sleep, Electrical status epilepticus in sleep, Thalamus, F-18-fluorodeoxyglucose positron emission tomography.The association between epilepsy and sleep is well recognized, and activation of epileptiform discharges during non-rapid eye movement (non-REM) sleep is frequently seen.1-3 Continuous spike-wave during slow-wave sleep (CSWS) represents an extreme form of sleep-potentiation of epileptiform activity, manifesting on electroencephalography (EEG) with electrical status epilepticus in sleep (ESES).4,5 CSWS is defined as an age-related epileptic encephalopathy that is characterized by a combination of epilepsy, neuropsychological impairment, and typical EEG findings with a diffuse pattern of spike-waves in ≥85% of slow-wave sleep.6-8 CSWS occurs during early childhood,