Frequency and pathogenesis of silent subcortical brain infarction in acute first-ever ischemic stroke

Tomohide Adachi1, Shotai Kobayashi, Shuhei Yamaguchi

  • 1Department of Internal Medicine III, Shimane Medical University, Izumo.

Abstract

Insights

Silent subcortical brain lesions are more common in lacunar infarction than other stroke types. These lesions are linked to small-vessel vasculopathy, the likely cause of lacunar infarction.

Area of Science:

  • Neurology
  • Radiology
  • Cerebrovascular Disease

Background:

  • Silent subcortical brain lesions are frequently observed in ischemic stroke patients.
  • Limited data exists on the association between these lesions and specific stroke subtypes.
  • Understanding this relationship is crucial for stroke subtyping and pathogenesis research.

Purpose of the Study:

  • To determine the incidence of MRI-detected silent subcortical brain lesions in first-ever ischemic stroke patients.
  • To analyze the relationship between these lesions and stroke subtypes (lacunar, atherothrombotic, cardioembolic).
  • To discuss the potential pathogenesis of silent subcortical lesions.

Main Methods:

  • 171 patients with acute first-ever ischemic stroke were evaluated.
  • Patients were classified into lacunar, atherothrombotic, and cardioembolic infarction groups.
  • MRI was used to assess silent subcortical brain infarction (SSBI), enlarged perivascular spaces (EPS), and white matter lesions.

Main Results:

  • Silent subcortical brain infarction (SSBI) was significantly more frequent in lacunar infarction (81.5%) compared to atherothrombotic (44.4%) and cardioembolic (42.1%) groups.
  • High-grade enlarged perivascular spaces (EPS) (grade 2+) were also more prevalent in lacunar infarction (63.3%) versus atherothrombotic (24.2%) and cardioembolic (0%) groups.
  • Scheltens' score for silent subcortical lesions was notably higher in the lacunar infarction group.

Conclusions:

  • Silent subcortical ischemic brain lesions occur more frequently in lacunar infarction than in atherosclerotic or cardioembolic infarction.
  • The findings suggest a common pathogenesis for silent subcortical lesions and lacunar infarction, likely related to small-vessel vasculopathy.
  • This highlights the importance of small-vessel disease in the development of silent subcortical lesions in stroke patients.

Related Concept Videos

Stroke: Introduction and Types01:29

Stroke: Introduction and Types

A stroke is an acute neurological event caused by the sudden disruption of cerebral blood flow, leading to rapid loss of neuronal function. Neurons depend on continuous oxygen and glucose supply, so even brief interruptions can cause irreversible injury within minutes. Strokes are classified into ischemic and hemorrhagic types.Ischemic StrokeIschemic strokes are most common and occur due to arterial occlusion, depriving brain tissue of oxygen and nutrients. This leads to energy failure, ionic...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...