Introduction Neonatal hypoglycemia is a relatively common event with a variable clinical presentation, ranging from asymptomatic forms to refractory status epilepticus. It may present as a primary problem or appear in the context of other conditions, such as prematurity or severe systemic disorders (sepsis, hypoxic ischemic encephalopathy, ...), making it difficult to separate its effects on the CNS from those due to the underlying disorder. Aim: To describe the EEG features in term-newborns with primary hypoglycemia admitted to our neonatal unit between 10/2016 and 10/2017. Methods Retrospective review of clinical records of patients fulfilling the following: Inclusion criteria – Term newborns (Gestational age ⩾ 37 weeks). – Hypoglycemia (plasma glucose ⩽ 40 mg/dL or ⩽ 47 mg/dL if symptomatic: CNS dysfunction; dysautonomia). Exclusion criteria – Any antecedent disorder that may explain CNS dysfunction (Primary: e.g. genetic epileptic encephalopathy; Secondary: e.g. cardiorespiratory arrest). Results We identified 3 patients: 1. Female, presenting with irritability and tremor 48 h. after birth, with plasma glucose of 18 mg/dL, treated with oral glucose with good response. She presented recurrent asymptomatic hypoglycemia, with disproportionately high levels of insulin and C-peptide, and was treated with Cortisone and Diazoxide. Genetic tests confirmed congenital hyperinsulinism (ABCC8-mutation). MR and EEG were normal. At follow-up, 7 months old, she had a normal psychomotor development. 2. Male, presenting with hypoactivity, diaphoresis, and apnea 12 h. after birth, with plasma glucose of 15 mg/dL, metabolic acidosis and high lactate, improving rapidly on i.v. Glucose. His mother had insulin-treated gestational diabetes. He developed focal seizures evolving into status epilepticus, requiring treatment with PB, LEV, MDZ and Lidocaine to achieve control (48 h. after onset). MR showed extensive bilateral cortico-subcortical lesions, predominantly parieto-occipital. Initial EEG showed a discontinuous pattern and 8 focal temporal seizures. Control EEG showed persistent discontinuous pattern (silent periods up to 2 min) and absent cortical reactivity. He died aged 4 days. 3. Male, presenting with hypoactivity with plasma glucose of 16 mg/dL, rapidly improving with i.v. Glucose. He developed focal motor seizures evolving into status epilepticus, requiring PB, LEV and MDZ to achieve control (clinically after 24 h, but seizures persisted on CFM 12 h longer). MR showed bilateral cortico-subcortical lesions, predominantly parieto-occipital. Initial EEG showed normal background with left centro-temporal interictal epileptiform activity. Control EEG showed focal slowing over the same regions. He was discharged on LEV 23 days after onset, with axial hypertonia and brisk reflexes. Conclusion Neonatal hypoglycemia may present with refractory seizures, which can aggravate CNS damage and impair outcome. EEG monitoring is necessary to identify subclinical seizures and correlates with prognosis.