Related Experiment Video

Updated: Aug 11, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

[Cerebrovascular disease in the tropics]

O H del Brutto1

  • 1Departamento de Ciencias Neurológicas, Hospital-Clínica Kennedy, Guayaquil, Ecuador.

Revista De Neurologia
|January 11, 2002
PubMed

Insights

Cerebrovascular disease (CVD) in the tropics stems from various infectious and non-infectious conditions, leading to strokes. Early diagnosis and treatment are crucial to prevent severe brain damage and recurrent strokes.

Area of Science:

  • Neurology
  • Tropical Medicine
  • Vascular Diseases

Context:

  • Cerebrovascular disease (CVD) presents unique challenges in tropical regions.
  • A diverse range of infectious and non-infectious etiologies contribute to CVD in the tropics.

Purpose:

  • To review the clinical manifestations, diagnosis, and therapeutic strategies for tropical diseases causing CVD.
  • To highlight the importance of timely intervention in managing CVD in tropical settings.

Summary:

  • Prevalent causes of tropical CVD include sickle cell disease, Takayasu arteritis, cysticercosis, infective endocarditis, Chagas disease, viral hemorrhagic fevers, gnathostomiasis, leptospirosis, snake bites, cerebral malaria, puerperal venous thrombosis, and tuberculosis.
  • These conditions can result in cerebral infarcts or hemorrhages, often due to vascular damage from angiitis or bleeding disorders.
  • Neurological presentation can be complex, with cerebrovascular complications sometimes only identified via neuroimaging or autopsy.

Impact:

  • Prompt diagnosis and therapy are essential to mitigate the severity of brain damage.
  • Effective management strategies can help prevent recurrent strokes in patients with tropical CVD.
Abstract

More Related Videos

Quantification of Cerebral Vascular Architecture using Two-photon Microscopy in a Mouse Model of HIV-induced Neuroinflammation10:04

Quantification of Cerebral Vascular Architecture using Two-photon Microscopy in a Mouse Model of HIV-induced Neuroinflammation

Published on: January 12, 2016

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging09:04

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

Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
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...