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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...
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...
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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic 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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...

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Related Experiment Video

Updated: Jul 8, 2026

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
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A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia

Published on: November 15, 2024

Insulin-related decrease in cerebral glucose despite normoglycemia in aneurysmal subarachnoid hemorrhage.

Florian Schlenk1, Daniela Graetz, Alexandra Nagel

  • 1Department of Neurosurgery, Charité Campus Virchow Medical Center, Augustenburger Platz, 13353 Berlin, Germany.

Critical Care (London, England)
|January 26, 2008
PubMed
Summary

Insulin treatment for hyperglycaemia in subarachnoid hemorrhage (SAH) patients lowered cerebral glucose levels, indicating increased utilization. This intensive glucose control may require careful monitoring to avoid metabolic complications in SAH patients.

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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

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Last Updated: Jul 8, 2026

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
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Published on: November 15, 2024

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
09:14

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Published on: June 18, 2021

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
10:34

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

Area of Science:

  • Neuroscience
  • Intensive Care Medicine
  • Endocrinology

Background:

  • Hyperglycaemia post-aneurysmal subarachnoid hemorrhage (SAH) is linked to poor outcomes.
  • Effective glucose control strategies are crucial for neurological recovery in SAH patients.

Purpose of the Study:

  • To investigate the impact of insulin therapy for glucose control on cerebral metabolism in SAH patients.
  • To assess cerebral glucose utilization and potential metabolic derangements during insulin treatment.

Main Methods:

  • Prospective study of 31 SAH patients in intensive care.
  • Microdialysis catheter inserted into the affected cerebral territory.
  • Intravenous insulin administered to maintain blood glucose < 140 mg/dl, with hourly microdialysate analysis for 12 hours.

Main Results:

  • Insulin treatment was required in 24 patients; higher SAH grade and age were risk factors.
  • Insulin stabilized blood glucose but significantly decreased cerebral glucose levels, suggesting increased utilization.
  • No evidence of ischemia; however, glycerol levels trended higher, possibly indicating cellular distress or tissue damage.

Conclusions:

  • Intensive glycaemic control with insulin in SAH patients reduces cerebral glucose but may increase glycerol.
  • Higher SAH grade predicts the need for insulin therapy.
  • Further research is needed to optimize insulin strategies and prevent metabolic crises in SAH patients.