Related Experiment Video

Updated: Jul 13, 2026

Semi-quantitative Assessment Using [18F]FDG Tracer in Patients with Severe Brain Injury
09:58

Semi-quantitative Assessment Using [18F]FDG Tracer in Patients with Severe Brain Injury

Published on: November 9, 2018

Bilateral basal ganglia lesions after hypoglycemic coma in a 6-year-old child

Cengiz Kara1, Omer Faruk Aydin, Belma Aslan

  • 1Department of Pediatric Endocrinology, Dr. Sami Ulus Children's Hospital, Ankara, Turkey.

Journal of Child Neurology
|July 11, 2007
PubMed

Insights

Childhood hypoglycemia can cause brain damage, including cerebral and cerebellar atrophy and putaminal lesions, as seen in a 6-year-old girl. This case highlights the long-term neurological effects of severe hypoglycemia in children.

Area of Science:

  • Neurology
  • Pediatrics
  • Neuroradiology

Background:

  • Neonatal hypoglycemia's effects on brain development are established.
  • The neurological consequences of hypoglycemia during childhood remain less understood.
  • This study focuses on a pediatric case to elucidate these effects.

Observation:

  • A 6-year-old girl presented with seizures attributed to hypoglycemia.
  • She had a history of a hypoglycemic coma approximately one year prior.
  • The patient was managed for presumed epilepsy over a year.

Findings:

  • Brain MRI revealed generalized cerebral and cerebellar atrophy.
  • Bilateral, symmetrical hyperintense lesions were observed in the putamina.
  • The patient was diagnosed with hyperinsulinism-induced hypoglycemia.

Implications:

  • Childhood hypoglycemia can lead to significant, persistent brain structural changes.
  • Imaging findings like putaminal lesions may serve as biomarkers for hypoglycemia-induced brain injury.
  • Early diagnosis and management of hyperinsulinism are crucial to prevent long-term neurological sequelae.

More Related Videos

Full-Endoscopic Surgery for Hypothalamic Hamartoma Resection02:22

Full-Endoscopic Surgery for Hypothalamic Hamartoma Resection

Published on: April 12, 2024

Frontal Disconnection for Treating Mild Malformation of Cortical Development with Oligodendroglial Hyperplasia in Epilepsy (MOGHE) in the Frontal Lobe06:04

Frontal Disconnection for Treating Mild Malformation of Cortical Development with Oligodendroglial Hyperplasia in Epilepsy (MOGHE) in the Frontal Lobe

Published on: August 16, 2024

Related Concept Videos

Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
Hypoglycemia01:26

Hypoglycemia

Hypoglycemia is a blood glucose level below 70 mg/dL. It commonly occurs in individuals using insulin or insulin-secreting drugs, but may also arise in non-diabetic conditions. People with type 1 diabetes are at the highest risk because they depend on exogenous insulin. People with type 2 diabetes are also at risk, especially when treated with insulin or medications such as sulfonylureas, which increase insulin release regardless of blood glucose levels. It develops when insulin levels exceed...
Hyperosmolar Hyperglycemic State01:21

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State, or HHS, is a serious and life-threatening complication of type 2 diabetes mellitus. It is characterized by three main features: severe hyperglycemia, profound dehydration, and elevated serum osmolality, all occurring without significant ketoacidosis.HHS typically develops in older adults or individuals with limited access to fluids. This may result from illness, cognitive impairment, or medications such as diuretics or corticosteroids. These factors reduce...
Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...