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Increased Intracranial Pressure ll: Pathophysiology01:29

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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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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...
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A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
Traumatic Brain Injury l: Introduction01:28

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DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
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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...
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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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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
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Traumatic dural sinus thrombosis causing persistent headache in a child.

Bhavana Lakhkar1, Bhushan Lakhkar, Brij Raj Singh

  • 1Datta Meghe Institute of Medical Sciences, Sawangi (Meghe), Wardha, India.

Journal of Emergencies, Trauma, and Shock
|February 19, 2010
PubMed
Summary
This summary is machine-generated.

Dural venous sinus thrombosis (DVST) is a recognized complication of mild head injury. This case report details a pediatric patient successfully treated for DVST after a minor fall, highlighting effective management strategies.

Keywords:
Head injurylateral sinussigmoid sinussinus thrombosis

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Area of Science:

  • Neurology
  • Pediatric Neurology
  • Vascular Neurology

Background:

  • Dural venous sinus thrombosis (DVST) is an uncommon but increasingly recognized neurological emergency.
  • Mild head trauma is a potential trigger for DVST, particularly in pediatric populations.
  • Early diagnosis and prompt management are crucial for favorable outcomes in DVST.

Observation:

  • A 9-year-old male child presented with progressive headache and vomiting after a minor fall.
  • Initial nonenhancing computed tomography (CT) raised suspicion for DVST.
  • Magnetic resonance venography (MRV) confirmed the diagnosis of dural venous sinus thrombosis.

Findings:

  • The pediatric patient with DVST was managed with a multi-modal approach.
  • Treatment included intravenous fluids, anticoagulation (heparin and oral coumarin), antiedema therapy (mannitol), and antiepileptics (phenytoin).
  • The child achieved a good clinical outcome following this therapeutic regimen.

Implications:

  • This case underscores the importance of considering DVST in children presenting with neurological symptoms after head trauma.
  • Aggressive management including anticoagulation and supportive care can lead to positive outcomes in pediatric DVST.
  • Further research into the specific mechanisms and optimal treatment protocols for pediatric DVST is warranted.