Related Experiment Video

Updated: Jul 11, 2026

Spinal Hernia Repair and Cauda Equina Repositioning After Lumbar Decompression under Three-Dimensional Microscopy: A Case Report and Literature Review
04:33

Spinal Hernia Repair and Cauda Equina Repositioning After Lumbar Decompression under Three-Dimensional Microscopy: A Case Report and Literature Review

Published on: November 8, 2024

Causes of late death due to hydrocephalus and meningomyeloceles

W A Maier

    Progress in Pediatric Surgery
    |January 1, 1979
    PubMed

    Keywords:
    hydrocephalus mortalitypostoperative follow-upneurosurgical outcomespediatric neurological care

    More Related Videos

    Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats04:12

    Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

    Published on: March 28, 2025

    Expansion Duroplasty For Severe Cervical Spinal Cord Swelling After Traumatic Injury: A Step-by-Step Surgical Protocol05:45

    Expansion Duroplasty For Severe Cervical Spinal Cord Swelling After Traumatic Injury: A Step-by-Step Surgical Protocol

    Published on: May 26, 2026

    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...
    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...
    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...
    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...
    Huntington Disease l: Introduction01:21

    Huntington Disease l: Introduction

    Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
    Secondary Spinal Cord Injury llI: Pathophysiology01:25

    Secondary Spinal Cord Injury llI: Pathophysiology

    Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...