Related Experiment Video
Updated: May 12, 2026
10:13
Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
Temporary recovery after resuscitation: delayed postanoxic encephalopathy.
Stephan Goedee1, Gerarda A M van der Nat, Gerwin Roks
1Department of Neurology, St Elisabeth Hospital, Tilburg, The Netherlands. stephangoedee@gmail.com
BMJ Case Reports
|April 18, 2013
Summary
Delayed postanoxic encephalopathy, a rare condition following anoxic insult, involves a recovery period before neurological decline. This summary covers a case report and literature review on this poorly understood neurological disorder.
Area of Science:
- Neuroscience
- Neurology
- Critical Care Medicine
Background:
- Delayed postanoxic encephalopathy (DPE) is an infrequent neurological complication.
- It is characterized by a distinct lucid interval after an initial anoxic insult.
Observation:
- Patients exhibit a period of apparent recovery lasting days to weeks.
- Subsequent neurological deterioration may manifest as altered behavior, motor deficits, or decreased consciousness.
- Some individuals may experience a secondary recovery phase.
Findings:
- The pathogenesis of DPE remains largely unknown.
- Prognosis is generally considered poor, with outcomes ranging from severe disability to death.
- Current treatment strategies are primarily symptomatic and lack robust evidence.
Implications:
- This case report and literature review highlight the diagnostic and therapeutic challenges posed by DPE.
- Further research into the underlying mechanisms is crucial for developing effective treatments.
- Understanding DPE is vital for improving patient outcomes after hypoxic-ischemic events.
Related Concept Videos
01:29Hepatic 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...
01:25Secondary 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...
01:15Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
01:25Cardiopulmonary Resuscitation IV: Pharmacological Management
Pharmacologic intervention is crucial in treating cardiac arrest patients during ACLS or Advanced Cardiovascular Life Support. The ACLS algorithms guide the administration of specific drugs based on the patient's cardiac arrest rhythm, which includes pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), asystole, and pulseless electrical activity (PEA).EpinephrineIndication: Epinephrine is the first-line drug for all cardiac arrest rhythms.Mechanism of Action: Epinephrine...
01:21Acute Respiratory Failure-II
Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include: