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Related Concept Videos

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...
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...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
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...
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...

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Effects of Blast-induced Neurotrauma on Pressurized Rodent Middle Cerebral Arteries
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EXPRESS: Does Post-Traumatic Cerebral Vasospasm Matter?

Jody L Manners1, Jaime Podell1,2, Nicolas Dorsey3

  • 1Program in Trauma, R Adams Cowley Shock Trauma Center, Baltimore Maryland.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|June 1, 2026
PubMed
Summary
This summary is machine-generated.

Traumatic brain injury (TBI) can lead to secondary injury like post-traumatic cerebral infarction (PTCI). This review explores PTCI causes, focusing on vasospasm, to improve TBI patient outcomes.

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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
10:41

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A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
08:12

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

Published on: July 28, 2018

Area of Science:

  • Neurology
  • Neurosurgery
  • Critical Care Medicine

Background:

  • Traumatic brain injury (TBI) involves primary and secondary insults that can impair cerebral function.
  • Secondary injury mechanisms include hypotension, hypoxia, edema, and ischemia, significantly impacting patient prognosis.
  • Post-traumatic cerebral infarction (PTCI) is an underrecognized complication that can exacerbate TBI outcomes.

Purpose of the Study:

  • To review the incidence, etiology, and consequences of PTCI following TBI.
  • To emphasize the role of vasospasm as a potential contributor to PTCI.
  • To discuss diagnostic challenges, therapeutic strategies, and future research directions for managing PTCI.

Main Methods:

  • Literature review of studies on TBI, PTCI, and vasospasm.
  • Analysis of evidence regarding the mechanisms linking TBI to cerebral infarction.
  • Examination of clinical data on vasospasm following TBI.

Main Results:

  • PTCI is a significant, potentially preventable cause of neurological deterioration after TBI.
  • Post-traumatic vasospasm is implicated in the development of PTCI, though its exact role is debated.
  • Current diagnostic and therapeutic approaches for PTCI and vasospasm require further refinement.

Conclusions:

  • PTCI represents a critical secondary injury after TBI that warrants greater clinical attention.
  • Understanding the relationship between vasospasm and PTCI is crucial for developing targeted interventions.
  • Further research is needed to optimize the diagnosis and management of PTCI to improve TBI patient outcomes.