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Published on: June 11, 2020
Symptomatic occipital lobe epilepsy following neonatal hypoglycemia
Roberto H Caraballo1, Diego Sakr, Marcela Mozzi
1Servicio de Neurología. Hospital de Niños "Prof. Dr. Juan P. Garrahan", Buenos Aires, Argentina.
Insights
Neonatal hypoglycemia can lead to posterior brain lesions and epilepsy, often occipital lobe epilepsy with a good prognosis. However, some cases develop severe epileptic encephalopathy, highlighting the need for MRI in assessing brain damage.
Area of Science:
- Neurology
- Pediatrics
- Neuroscience
Background:
- Neonatal hypoglycemia is a common condition in newborns.
- It can have long-term neurological consequences.
- Understanding these consequences is crucial for early intervention.
Purpose of the Study:
- To investigate the clinical, electrophysiologic, and neuroradiologic features of epilepsy secondary to neonatal hypoglycemia.
- To characterize the types of neonatal hypoglycemia and their association with epilepsy.
- To evaluate the outcomes and prognosis of epilepsy in affected children.
Main Methods:
- Retrospective study of 15 patients with epilepsy and neonatal hypoglycemia.
- Clinical evaluation, electroencephalogram (EEG), and neuroradiologic imaging (MRI) were performed.
- Patients were followed in an epilepsy clinic over a 13-year period.
Main Results:
- 12 patients had focal seizures and posterior EEG abnormalities, mostly with good outcomes.
- 2 patients presented with epileptic encephalopathy and refractory seizures.
- All but two patients had parieto-occipital lesions on imaging; 14 were mentally retarded, and 8 had visual disturbances.
Conclusions:
- Neonatal hypoglycemia is a significant cause of posterior cerebral lesions and symptomatic epilepsy, particularly occipital lobe epilepsy.
- While many cases have a good prognosis, some develop severe epileptic encephalopathy.
- MRI is essential for characterizing cerebral lesions following neonatal hypoglycemia.
Abstract:
This study reports on the clinical, electrophysiologic, and neuroradiologic aspects of patients with epilepsy secondary to neonatal hypoglycemia. Fifteen patients with epilepsy and/or posterior cerebral lesions, and neonatal hypoglycemia were studied in the epilepsy clinic between February 1990 and March 2003. The mean age was 12 years. The different types of neonatal hypoglycemia were as follows: four patients had transitional-adaptive, seven classic transient, two secondary-associated, and two severe recurrent hypoglycemia. As to epilepsy, we recognized a larger group of 12 patients characterized by focal seizures and posterior abnormalities on the electroencephalogram, the majority of whom had a good outcome, and a second group of two patients presenting electroclinical features of encephalopathy with refractory seizures. All patients except two manifested parieto-occipital lesions on neuroradiologic images. Neurologic examination was normal in one patient. Six patients had microcephaly; eight manifested visual disturbances. Fourteen patients were mentally retarded. One had a pervasive developmental disorder. This study indicates neonatal hypoglycemia may cause posterior cerebral lesions, abnormal findings at neurologic examination, and symptomatic epilepsy, most frequently occipital lobe epilepsy, usually with a good prognosis, and occasionally epileptic encephalopathy with refractory seizures. MRI studies are essential to define the characteristics of cerebral lesions after neonatal hypoglycemia.
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