Related Experiment Video

Updated: Jul 17, 2026

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

A case of cerebral amyloid angiopathy

Richard Felwick1, Khaled Amar

  • 1Department of Medicine for the Elderly, Royal Bournemouth Hospital, Castle Lane East, Bournemouth, UK.

Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
|January 31, 2007
PubMed

Insights

Cerebral amyloid angiopathy (CAA) is a condition causing amyloid buildup in brain blood vessels. Early diagnosis in patients with recurrent lobar hemorrhages and cognitive issues is crucial for managing bleeding risks.

Area of Science:

  • Neurology
  • Pathology
  • Vascular Biology

Background:

  • Cerebral amyloid angiopathy (CAA) involves amyloid protein deposition in cerebral blood vessels.
  • CAA is linked to recurrent lobar hemorrhages and cognitive impairment.
  • Underdiagnosis of CAA is a significant clinical concern.

Observation:

  • An 84-year-old patient presented with recurrent collapses and cognitive decline.
  • Brain CT revealed multiple lobar hemorrhages.
  • The patient met diagnostic criteria for probable CAA.

Findings:

  • CAA diagnosis requires considering multiple lobar hemorrhages, especially with cognitive impairment.
  • Exclusion of other causes like trauma or coagulopathy is essential.
  • The Boston criteria can aid in diagnosing probable CAA.

Implications:

  • Recognizing CAA is vital for patient management.
  • Accurate diagnosis guides strategies to reduce future hemorrhage risk.
  • Timely intervention can mitigate the progression of CAA-related neurological deficits.
Abstract

More Related Videos

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia09:35

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia

Published on: November 15, 2024

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...
Hemorrhagic Stroke l: Introduction01:17

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...
Dementia l: Introduction01:22

Dementia l: Introduction

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...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic 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...
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...