Paradoxical embolisation and cerebral white matter lesions in dementia

N Purandare1, R C Oude Voshaar, C McCollum

  • 1University of Manchester, Division of Psychiatry, Education and Research Centre, Wythenshawe Hospital, Wythenshawe, Manchester M23 9LT, UK.

Insights

Patent foramen ovale (PFO) is linked to white matter hyperintensities in Alzheimer's disease. Spontaneous cerebral emboli show a negative correlation with white matter changes in vascular dementia, suggesting different underlying mechanisms.

Area of Science:

  • Neurology
  • Neuroimaging
  • Cerebrovascular Disease

Background:

  • Alzheimer's disease (AD) and vascular dementia (VaD) are major causes of cognitive decline.
  • White matter hyperintensities (WMH) are common findings on cerebral MRI in dementia patients.
  • The role of patent foramen ovale (PFO) and spontaneous cerebral emboli (SCE) in dementia pathogenesis is under investigation.

Purpose of the Study:

  • To investigate the association between SCE, PFO, and WMH in patients with AD and VaD.
  • To explore the potential contribution of PFO and SCE to the development of WMH in different dementia subtypes.

Main Methods:

  • SCE detection using transcranial Doppler of the middle cerebral artery.
  • PFO identification via ultrasound contrast agent and assessment of venous-to-arterial circulation shunt (v-aCS).
  • WMH (DWMH and PVH) quantification using Schelten's scale on cerebral MRI.

Main Results:

  • In AD, both deep white matter hyperintensities (DWMH) and periventricular hyperintensities (PVH) were significantly associated with PFO after adjusting for cardiovascular risk factors.
  • No significant relationship between SCE and WMH was observed in AD.
  • In VaD, a significant negative correlation was found between the severity of DWMH and SCE.

Conclusions:

  • A significant venous-to-arterial shunt (PFO) is associated with more severe DWMH in Alzheimer's disease, potentially contributing to its etiology.
  • The negative correlation between SCE and DWMH in vascular dementia supports the hypothesis that VaD may result from predominantly embolic ischemic injury.

Related Concept Videos

Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
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...
Dementia01:30

Dementia

Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual.
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...
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...