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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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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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Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

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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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Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

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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...
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Cerebral Edema l: Introduction01:19

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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...
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Cerebral Edema ll: Pathophysiology01:22

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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...
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Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

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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...
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Dynamic changes in glymphatic function in reversible cerebral vasoconstriction syndrome.

Chia-Hung Wu1,2, Yu Kuo1,2,3, Yu-Hsiang Ling2,4

  • 1Department of Radiology, Taipei Veterans General Hospital, No.201, Sec. 2, Shipai Rd., Taipei, Taiwan.

The Journal of Headache and Pain
|February 5, 2024
PubMed
Summary

Glymphatic function in reversible cerebral vasoconstriction syndrome (RCVS) improves over time, correlating with vascular changes and headache severity. This study reveals dynamic glymphatic changes in RCVS patients.

Keywords:
Diffusion-tensor imaging along the perivascular space (DTI-ALPS) indexGlymphaticsHealthy controls (HCs)Reversible cerebral vasoconstriction syndrome (RCVS)The six-item Headache Impact Test (HIT-6)Transcranial color-coded duplex sonography (TCCS)

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Area of Science:

  • Neurology
  • Neuroimaging
  • Cerebrovascular Diseases

Background:

  • The pathophysiology of reversible cerebral vasoconstriction syndrome (RCVS) is not fully understood.
  • The role of the glymphatic system in RCVS has not been previously investigated.

Purpose of the Study:

  • To investigate glymphatic dynamics in patients with RCVS.
  • To explore the clinical and vascular correlates of glymphatic dysfunction in RCVS.

Main Methods:

  • Prospective evaluation of glymphatic function using diffusion-tensor imaging along the perivascular space (DTI-ALPS) index in RCVS patients and healthy controls (HCs).
  • Clinical and vascular assessments including transcranial color-coded duplex sonography were performed.
  • Analysis of DTI-ALPS index trends, acute stage, and longitudinal changes, with correlations to clinical and vascular parameters.

Main Results:

  • Acute RCVS patients showed significantly lower DTI-ALPS index compared to HCs and patients in remission.
  • A continuous increasing trend of the DTI-ALPS index was observed after disease onset.
  • Lower DTI-ALPS index correlated with higher internal carotid artery resistance index and headache impact scores; higher DTI-ALPS index correlated with higher middle cerebral artery flow velocity during 50-100 days post-onset.

Conclusions:

  • Glymphatic function in RCVS exhibits dynamic evolution over time.
  • Glymphatic changes are temporally linked to vascular indices and headache-related disability.
  • Findings offer new insights into the interplay between glymphatic transport, vasomotor control, and pain in RCVS.