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Related Concept Videos

Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
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...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
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 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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

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Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
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Reversible obstructive hydrocephalus from hypertensive encephalopathy.

Abhay Kumar1, Salah G Keyrouz, Jon T Willie

  • 1Department of Neurology, Washington University School of Medicine, 660 S Euclid Ave, Campus Box 8111, St Louis, MO 63110, USA.

Neurocritical Care
|January 12, 2012
PubMed
Summary
This summary is machine-generated.

Hypertensive encephalopathy can cause posterior fossa edema and reversible hydrocephalus. Prompt blood pressure management is key, often avoiding the need for permanent cerebrospinal fluid (CSF) shunting.

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Area of Science:

  • Neurology
  • Nephrology
  • Radiology

Background:

  • Hypertensive encephalopathy can manifest as posterior fossa edema.
  • This edema rarely leads to hydrocephalus.
  • This study explores this reversible syndrome.

Observation:

  • Patients exhibited clinical and radiographic signs of obstructive hydrocephalus.
  • Two patients required temporary external cerebrospinal fluid (CSF) drainage.

Findings:

  • Aggressive management of elevated blood pressure led to the resolution of both edema and hydrocephalus.
  • Literature review identified 15 additional cases of reversible obstructive hydrocephalus in hypertensive encephalopathy.
  • Neurological recovery was achieved in all patients once blood pressure was controlled, with most avoiding permanent CSF shunting.

Implications:

  • Early recognition of hypertensive encephalopathy-induced hydrocephalus is crucial.
  • Focusing on blood pressure control is key to managing this reversible syndrome and preventing invasive CSF diversion procedures.