Pathologic changes associated with intracranial hypotension and meningeal enhancement on MRI

Related Experiment Video

Updated: Nov 8, 2026

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
09:04

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging

Published on: June 8, 2017

D C Good1, M Ghobrial

  • 1Department of Neurology, Southern Illinois University School of Medicine, Springfield.

Neurology
|December 1, 1993
PubMed

Insights

Intracranial hypotension causes postural headaches. MRI shows meningeal enhancement, and biopsy reveals fibrocollagenous proliferation, explaining the syndrome's pathology.

Area of Science:

  • Neurology
  • Pathology
  • Radiology

Background:

  • Intracranial hypotension is a condition characterized by low cerebrospinal fluid pressure.
  • Postural headache is a primary symptom, often worsening when upright.

Observation:

  • A patient presented with a 6-week history of postural headaches.
  • Magnetic resonance imaging (MRI) demonstrated diffuse meningeal enhancement after gadolinium contrast.
  • Cerebrospinal fluid (CSF) analysis was not detailed in the abstract.

Findings:

  • The MRI findings were typical for intracranial hypotension syndrome.
  • Leptomeningeal biopsy revealed significant fibrocollagenous proliferation.
  • No inflammatory cells were observed in the leptomeningeal biopsy.

Implications:

  • The observed pathological changes correlate with the clinical and radiological findings of intracranial hypotension.
  • This suggests that fibrocollagenous proliferation in the leptomeninges may be an early response to intracranial hypotension.
  • Understanding these early pathological changes can aid in diagnosing and managing this condition.

Related Concept Videos

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...
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...
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...
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...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial 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...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...