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Related Concept Videos

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.
Regulation of Stroke Volume01:27

Regulation of Stroke Volume

The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
Cardiac Output II: Effect of Stroke Volume on Cardiac Output01:22

Cardiac Output II: Effect of Stroke Volume on Cardiac Output

Cardiac output (CO), the amount of blood the heart pumps per minute, is a parameter in cardiovascular physiology determined by stroke volume and heart rate. Stroke volume, the amount of blood pushed from one of the ventricles per heartbeat, is influenced by preload, afterload, and contractility.
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...
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...
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 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...

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Related Experiment Video

Updated: Jul 7, 2026

Gathering Self-Initiated Rat Behavioral Data to Characterize Post-Stroke Deficits
05:08

Gathering Self-Initiated Rat Behavioral Data to Characterize Post-Stroke Deficits

Published on: March 15, 2024

Body composition after stroke.

Berna Celik1, Kadriye Ones, Nurhan Ince

  • 1Department of Physical Medicine and Rehabilitation, Istanbul 70. Yil Physical Medicine and Rehabilitation Teaching Hospital, Istanbul, Turkey. celikbe@hotmail.com

International Journal of Rehabilitation Research. Internationale Zeitschrift Fur Rehabilitationsforschung. Revue Internationale De Recherches De Readaptation
|February 16, 2008
PubMed
Summary

Stroke patients experience significant loss of lean tissue mass and bone mineral content, particularly on the paretic leg. This loss worsens over time but may be mitigated by spasticity.

Related Experiment Videos

Last Updated: Jul 7, 2026

Gathering Self-Initiated Rat Behavioral Data to Characterize Post-Stroke Deficits
05:08

Gathering Self-Initiated Rat Behavioral Data to Characterize Post-Stroke Deficits

Published on: March 15, 2024

Area of Science:

  • Rehabilitation Medicine
  • Neuroscience
  • Orthopedics

Background:

  • Stroke frequently leads to long-term motor deficits and changes in body composition.
  • Understanding the impact of stroke on lean tissue mass, fat tissue mass, and bone mineral content is crucial for effective rehabilitation.

Purpose of the Study:

  • To compare body composition (lean mass, fat mass, bone mineral content) between paretic and nonaffected legs in stroke survivors.
  • To investigate the influence of time since stroke, spasticity, and motor recovery on body composition within the first year post-stroke.

Main Methods:

  • Dual-energy X-ray absorptiometry (DXA) was used to assess body composition in both lower extremities of 35 stroke patients.
  • Physical examinations included Brunnstrom motor recovery and modified Ashworth spasticity scales.

Main Results:

  • Paretic legs showed significantly lower lean tissue mass and bone mineral content compared to nonaffected legs.
  • Lean tissue mass and bone mineral content correlated negatively with time since stroke (<1 year).
  • Moderate to high spasticity was associated with higher lean tissue mass and bone mineral content.

Conclusions:

  • Stroke significantly reduces lean tissue mass and bone mineral content, especially in the paretic limb.
  • The loss of these components progresses with time post-stroke.
  • Spasticity may play a protective role in preserving lean tissue mass and bone mineral content.