Glycaemic Imbalances in Seizures and Epilepsy of Paediatric Age: A Literature Review

Abstract

Cerebral excitability and systemic metabolic balance are closely interconnected. Energy supply to neurons depends critically on glucose, whose fluctuations can promote immediate hyperexcitability resulting in acute symptomatic seizures. On the other hand, chronic disorders of sugar metabolism (e.g., diabetes mellitus) are often associated with long-term epilepsy. In this paper, we aim to review the existing knowledge on the association between acute and chronic glycaemic imbalances (hyper- and hypoglycaemia) with seizures and epilepsy, especially in the developing brain, focusing on clinical and instrumental features in order to optimize the care of children and adolescents and prevent the development of chronic neurological conditions in young patients.

Keywords: diabetes mellitus; epilepsy; hyperglycaemia; hypoglycaemia; hypoglycaemic seizures; paediatric age.

Figure 1

Flow chart summarizing the main themes of the review and the potential mechanisms implicated in the pathophysiology of epilepsy in the context of hypo- and hyperglycaemia.

Figure 2

Evolving brain injury in brain MRI from perinatal hypoglycaemia. Symptomatic hypoglycaemia was detected on day 4, postnatally. A posterior brain lesion pattern is reported here, with predominant parietal and occipital lobe involvement. From the left to the right side of the images, brain MR axial images of the same patient are shown at 6, 40 days, and 12 months of age. In detail, (a) DWI (left) and T2W (right) images showing abnormal signal intensities and oedema in the parietal and occipital regions; (b) T1W (left) and T2W (right) images showing the evolution of hypoglycaemia-related abnormalities to brain poromalacia in the same parietal and occipital regions; (c) T2W (left) and T1W (right) images depict chronic brain abnormalities with parietal and occipital white and grey matter volume reduction and local signal tissue abnormalities, in particular involving occipital cortical areas.

Figure 3

Brain MRI and EEG in focal symptomatic epilepsy in perinatal hypoglycaemia. Axial FLAIR 1.5T brain MRI (left) depicts bilateral symmetrical hyperintensity of the occipital white matter in a 12-year-old child who suffered recurrent convulsive seizures during neonatal hypoglycaemia and still exhibits drug-resistant focal impaired awareness seizures with staring, sialorrhea and left eye/head deviation. EEG recording (10–20 International System) (right) display sharp waves in a burst over the posterior brain areas, predominating on the left parieto–occipital region (arrow).

Figure 4

Example of comorbidity between young-onset diabetes mellitus and idiopathic generalized epilepsy. EEG recording (10–20 International System) of a 10-year-old boy affected by MODY (inherited CGK mutation) referred for recurrent episodes of unresponsiveness. The exam displays diffuse rhythmic 3.5 Hz spike-and-wave discharges, compatible with childhood absence epilepsy.