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Related Concept Videos

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...
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...
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...
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...

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Related Experiment Video

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A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats
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Microbleeds and post-stroke emotional lability.

W K Tang1, Y K Chen, J Y Lu

  • 1Department of Psychiatry, Shatin Hospital, Shatin, NT, Hong Kong SAR, China. tangwk@cuhk.edu.hk

Journal of Neurology, Neurosurgery, and Psychiatry
|June 23, 2009
PubMed
Summary
This summary is machine-generated.

Microbleeds (MBs) in the thalamus are linked to post-stroke emotional lability (PSEL). This finding suggests thalamic MBs may contribute to PSEL development in stroke survivors.

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Area of Science:

  • Neuroimaging
  • Neurology
  • Psychiatry

Background:

  • Post-stroke emotional lability (PSEL) is a common psychiatric condition.
  • The role of microbleeds (MBs) in PSEL development is not well understood.
  • Lesions in various brain areas are implicated in PSEL pathophysiology.

Purpose of the Study:

  • To investigate the association between microbleeds (MBs) and post-stroke emotional lability (PSEL).
  • To determine if the location and number of MBs correlate with PSEL.
  • To identify potential predictors of PSEL in stroke patients.

Main Methods:

  • A cohort of 519 Chinese patients with acute ischemic stroke was studied.
  • Post-stroke emotional lability (PSEL) was assessed 3 months after stroke using Kim's criteria.
  • Microbleeds (MBs) were identified and quantified using Magnetic Resonance Imaging (MRI).

Main Results:

  • 14.3% of patients developed PSEL.
  • Patients with PSEL had a higher prevalence of thalamic MBs (16.2% vs 6.5%).
  • Thalamic microbleeds were an independent predictor of PSEL (OR=4.7, p=0.002).

Conclusions:

  • Microbleeds in the thalamus may contribute to the development of post-stroke emotional lability (PSEL).
  • Further research is needed to explore the role of MBs in PSEL and other psychiatric conditions post-stroke.