Related Experiment Video

Updated: Jun 2, 2026

Electromagnetic Source Imaging in Presurgical Evaluation of Children with Drug-Resistant Epilepsy
09:57

Electromagnetic Source Imaging in Presurgical Evaluation of Children with Drug-Resistant Epilepsy

Published on: September 20, 2024

Postoperative encephalopathy with choreoathetosis

Allison Przekop1, Chalmer McClure, Stephen Ashwal

  • 1Division of Pediatric Neurology, Department of Pediatrics, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.

Handbook of Clinical Neurology
|April 19, 2011
PubMed

Insights

Survival rates for children with congenital heart defects (CHD) have improved due to advanced surgical techniques. However, this progress is linked to an increase in neurological complications like postpump chorea.

Area of Science:

  • Pediatric Cardiology
  • Pediatric Neurology
  • Cardiovascular Surgery

Background:

  • Improved survival in children with congenital heart defects (CHD) since the 1980s is attributed to surgical advancements like cardiopulmonary bypass and deep hypothermia.
  • A rise in survival has paralleled an increase in postoperative neurological complications.
  • Postpump chorea, a form of postoperative encephalopathy with choreoathetosis, is a significant and devastating neurological complication following pediatric cardiac surgery.

Purpose of the Study:

  • To explore the etiology and pathophysiology of postpump chorea.
  • To identify factors contributing to the development of choreoathetoid movements post-cardiac surgery.
  • To understand the varying long-term neurological outcomes in children affected by postpump chorea.

Main Methods:

  • Review of existing literature on postpump chorea and associated neurological complications in pediatric cardiac surgery.
  • Analysis of potential contributing factors including deep hypothermia, circulatory arrest, cardiopulmonary bypass, and blood gas variability.
  • Examination of the relationship between age at surgery and the severity of postpump chorea.

Main Results:

  • The exact cause and mechanisms of postpump chorea remain unknown.
  • Factors implicated include deep hypothermia, cardiopulmonary bypass, and fluctuations in cerebral blood flow due to pH and PaCO2 variations.
  • The severity and duration of choreoathetoid movements, and long-term outcomes, differ between mild and severe forms of encephalopathy. Older children may be at higher risk for the severe, persistent form.

Conclusions:

  • Postpump chorea is a serious neurological complication following pediatric cardiac surgery, with unknown etiology.
  • Management and understanding of risk factors like hypothermia and patient age are crucial for improving outcomes.
  • Further research is needed to elucidate the pathophysiology and develop targeted interventions for postpump chorea.

More Related Videos

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

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...