Related Experiment Video
Updated: May 27, 2026
09:01
Minimally Invasive Endoscopic Intracerebral Hemorrhage Evacuation
Published on: October 15, 2021
[Intracranial complications from ENT infections]
1Service de radiologie I, hôpital de Hautepierre, CHRU de Strasbourg, avenue Molière, 67098 Strasbourg cedex, France. sophie.riehm@chru-strasbourg.fr
Journal De Radiologie
|November 22, 2011
Summary
Ear, nose, and throat (ENT) infections can spread to the brain and surrounding structures. Skull defects and inner ear anomalies increase the risk of these serious intracranial complications.
Area of Science:
- Otorhinolaryngology
- Neurology
- Infectious Diseases
Context:
- Sinonasal and temporal bone infections pose a risk for intracranial extension.
- Spread can occur via contiguous or hematogenous routes.
- Congenital/acquired skull defects and inner ear anomalies are predisposing factors.
Purpose:
- To outline the potential intracranial complications of ENT infections.
- To highlight the relationship between infection site and complication type.
- To identify risk factors for intracranial spread.
Summary:
- ENT infections can spread to the skull base, meninges, brain parenchyma, dural sinuses, cerebral veins, intracranial arteries, and cranial nerves.
- Specific infections correlate with distinct complications: ethmoid sinusitis with orbital issues, sphenoid sinusitis with cavernous sinus thrombophlebitis, mastoiditis with transverse sinus thrombophlebitis, and frontal sinusitis with superior sagittal sinus thrombophlebitis.
- All these pathways can ultimately lead to brain abscess formation.
Impact:
- Understanding these pathways is crucial for timely diagnosis and management of ENT infections.
- Recognizing predisposing factors allows for targeted preventive strategies.
- This knowledge aids in managing complex cases involving both ENT and neurological involvement.
Related Concept Videos
01:14Increased 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...
01:29Increased 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...
01:26Brain Abscess l: Introduction
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,...
01:26Bacterial Meningitis II: Pathophysiology
Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
01:19Cerebral 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...
01:22Cerebral 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...