Atheromatous Emboli to Central Nervous System

Soloway, Henry B.; Aronson, Stanley M

doi:10.1001/archneur.1964.00460240089012

Cited by 76 publications

(30 citation statements)

References 9 publications

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“…Debris from the surface of an atherosclerotic plaque and from plaque ulcers may break off and become emboli. 48 In one study, 49 atheromatous intracranial emboli were found in all of 16 patients examined at post mortem. The lumen of 71 vessels containing atheromatous emboli was measured; the minimum was 17 and the maximum was 585 pm, and 31 were in the range 51-100 fim.…”

Section: Pathogenesis (Cause) Of Lacune(s) Hypertensionmentioning

confidence: 93%

The fallacy of the lacune hypothesis.

Millikan

Futrell

1990

Stroke

153

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We review the definition, pathogenesis, natural history, and prognosis and describe the first experimental model of lacunes. Defined pathologically or radiologically, lacunes are small cerebral infarcts which become cystic and are caused by occlusion of small arteries. The clinical definition of lacune is confused. The word "lacune" means a small stroke. While the immediate mortality rate from a small stroke is low, many patients are unable to return to work and the long-term prognosis is guarded. Photochemical damage to the carotid artery of rats produces microemboli to the brain, resulting in cavitary lesions resembling lacunes in humans. The "lacune hypothesis" is a fallacy because small cerebral infarcts are not caused solely by a combination of hypertension and small vessel disease, and the various "lacunar syndromes" are simply small strokes which should be investigated as such. (Stroke 1990;21:1251-1257) T he "lacune hypothesis" states that lacunes are caused by a combination of hypertension and characteristic vascular lesions involving single perforating brain arteries.

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Section: Pathogenesis (Cause) Of Lacune(s) Hypertensionmentioning

confidence: 93%

The fallacy of the lacune hypothesis.

Millikan

Futrell

1990

Stroke

153

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“…Cholesterol emboli are often large enough to occlude the penetrating arterioles of the cerebral cortex. 55 Brain imaging typically reveals small ischemic lesions and border zone infarcts. 56 Transcranial Doppler (TCD) ultrasonography, which was first described in 1982, can be used to detect microemboli in the cerebral circulation.…”

Section: Central Nervous Systemmentioning

confidence: 99%

Cholesterol Embolization Syndrome

2010

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“…18 In a mainly aqueous medium, such as is found in the center of a plaque, they form liposomes. 1 ' These structures are well characterized, 10 consisting of bilayers of phospholipid molecules oriented with hydrophilic poles at each surface, organized concentrically into multilamellar spheres; layers of water alternate with, and separate, the lipid layers. In the presence of cholesterol and its esters, liposomes have the capacity to incorporate, into the lipid bilayers, molecules of the former up to about 33% weight for weight of phospholipid.…”

Section: Smentioning

confidence: 99%

Differential contributions of major lipid components of atheroma to outcome of cerebral atheroembolism. A study in an animal model.

Rail¹,

Steiner²,

Fc³

1981

Stroke

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SUMMARY Cerebral atfaeroembolism, in which mainly lipid emboli are released from rupturing atheromatoas plaques, may occur without apparent effect, or result in cerebral ischemia and Infarction. The reasons behind these unpredictable consequences were sought in the interactions, in vitro and in an animal model, between the main lipid components of advanced plaques. Pure preparations of representative Upids were each harmless when embolized into the cerebral circulation. In contrast, combinations in proportions similar to those in advanced human plaques caused infarction, whether these were synthetic mixtures or extracts from plaques of the entire lipid fraction. The most important physical interaction between the lipids was aggregation of crystals by oils. Between cholesterol and the mainly liquid esters, this created in vitro a range of glutinous aggregates. Trigiyceride lowered the melting point of esters, increasing their oillness, and reduced the cohesiveness of aggregates in the face of operative mechanical forces through a fall in viscosity. Pftospholipid, acting principally as an emulsifying agent, promoted dispersion of the oQ, secondarily freeing die crystals from its aggregating effect. In the plaque, the balance of these factors will determine the size and number of particles likely to embolize, and, therefore, the clinical outcome should the plaque rupture. Stroke, Vol 12, No 4, 1981"CEREBRAL ATHEROEMBOLISM" is the term used for the release into the blood stream of mainly lipid emboli following rupture of advanced atheromatous plaques in vessels supplying the brain. Recognition of its clinical importance*'' hinges upon the argument that it is common. The precise prevalence is difficult to determine, 4 partly because it may occur without neurological sequelae* and remain unrecognized during life, and partly because difficulties in histological technique may prevent cerebral atheroemboli being found during postmortem examination.'1 ' In one autopsy study of unselected patients,* atheromatous lesions were found in one or more of the major arteries to the brain in all patients over 50 years of age, and over two-thirds harbored advanced lesions. In patients with abdominal aortic atherosclerosis, distal atheroemboli were found postmortem in 12% of those with advanced disease.' Although minor variations in plaque constitution may be expected, there is no reason to suppose that the process of atheroembolism is subject to major regional differences once severe atheromatous disease is established locally.Cerebral atheroembolism can be clinically silent," but a number of published patient reports (e.g., Refs. 2, 4, 10, 11) demonstrate that cerebral ischemia, with or without infarction, may result. The nature of atheroemboli, and their behavior in the cerebral circulation, need to be better defined before their effects on the brain can be understood.Chemical analysis of atheroemboli after release is seldom feasible, but the pultaceous contents of advanced atheromatous plaques from which they might arise have bee...

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Atheromatous Emboli to Central Nervous System

Cited by 76 publications

References 9 publications

The fallacy of the lacune hypothesis.

The fallacy of the lacune hypothesis.

Cholesterol Embolization Syndrome

Differential contributions of major lipid components of atheroma to outcome of cerebral atheroembolism. A study in an animal model.

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