Related Experiment Video
Updated: May 24, 2026
04:12
Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
Published on: March 28, 2025
Acute hydrocephalus following cerebellar infarct
1Walsall Manor Hospital, Moat Road, Walsall WS29PS, UK.
BMJ Case Reports
|February 23, 2012
Summary
Subtle hydrocephalus after cerebellar infarct can rapidly worsen consciousness. Early recognition of these subtle computed tomography (CT) signs and prompt neurosurgical intervention are critical for patient survival and recovery.
Area of Science:
- Neurology
- Neurosurgery
- Radiology
Background:
- Cerebellar infarcts can lead to neurological deterioration.
- Hydrocephalus is a potential complication of cerebellar infarcts.
- Subtle imaging findings of hydrocephalus can be challenging to detect.
Purpose of the Study:
- To highlight the importance of recognizing subtle signs of hydrocephalus on computed tomography (CT) scans in patients with acute cerebellar infarct.
- To emphasize the critical role of timely neurosurgical intervention in managing this complication.
Main Methods:
- Case report of a 59-year-old male patient.
- Clinical assessment including Glasgow Coma Scale (GCS) scoring.
- Serial computed tomography (CT) brain imaging.
- Neurosurgical intervention.
Main Results:
- Patient presented with acute cerebellar infarct and subsequent deterioration of consciousness (GCS 5).
- Repeat CT scan revealed subtle signs of hydrocephalus.
- Neurosurgical intervention led to patient recovery.
Conclusions:
- Subtle CT findings of hydrocephalus in the context of cerebellar infarct require vigilant recognition.
- Prompt neurosurgical management is essential for improving outcomes and potentially saving lives in such cases.
Related Concept Videos
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...
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...
01:14Increased 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...
01:21Cytotoxic 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...
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,...