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Related Concept Videos

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...
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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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...
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Alzheimer's Disease: Overview

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The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...

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Related Experiment Video

Updated: May 7, 2026

Visualization of Amyloid &#946; Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
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Cerebral amyloid angiopathy.

M Tzimou1, A Anastasiou, Z Katsarou

  • 12nd Propedeutic Department of Internal Medicine, Hippokration General Hospital; Thessaloniki, Greece - a.pyrpasopoulou@doctors.org.uk.

The Neuroradiology Journal
|September 14, 2013
PubMed
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This case report highlights cerebral amyloid angiopathy in an elderly patient presenting with stroke-like symptoms. Early diagnosis is crucial as antiplatelet drugs may increase microbleed risk in these individuals.

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Published on: May 23, 2016

Area of Science:

  • Neurology
  • Neuroradiology
  • Geriatrics

Background:

  • Cerebral amyloid angiopathy (CAA) is a common cause of non-traumatic intracerebral hemorrhage in the elderly.
  • CAA is associated with cognitive decline and dementia.
  • Acute cerebrovascular events can mimic other neurological conditions.

Purpose of the Study:

  • To describe a case of an elderly patient with CAA and dementia presenting with acute cerebrovascular symptoms.
  • To emphasize the importance of accurate diagnosis in managing patients with CAA.
  • To highlight the potential risks associated with antiplatelet therapy in this population.

Main Methods:

  • Case report of an elderly patient.
  • Clinical presentation review.
  • Computed tomography (CT) and magnetic resonance imaging (MRI) analysis.
  • Review of diagnostic criteria for CAA.

Main Results:

  • Patient presented with symptoms suggestive of an acute cerebrovascular event.
  • CT scan indicated a possible ischemic event.
  • MRI revealed diffuse parenchymal lesions and hemosiderin deposits, confirming CAA.
  • The patient had associated dementia.

Conclusions:

  • Accurate diagnosis of cerebral amyloid angiopathy is critical in elderly patients with cerebrovascular events.
  • Antiplatelet therapy, including aspirin, may be associated with an increased risk of microbleeding in patients with CAA.
  • Careful consideration of anticoagulation and antiplatelet strategies is necessary in this patient group.