Agonal Nature of the Cerebral Ring Hemorrhages

Cammermeyer, Jan

doi:10.1001/archneurpsyc.1953.02320310060004

Cited by 12 publications

(2 citation statements)

References 29 publications

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“…CRHs have been reported in various conditions, including sepsis, DIC, cerebral malaria, acute hemorrhagic leukoencephalitis, viral encephalitis, cerebral vasospasm, barotrauma, fat and air embolisms, carbon monoxide poisoning, drug intoxications, thrombotic thrombocytopenic purpura, pernicious anemia, aplastic anemia, leukemia, and solid tumors. [1][2][3][4][5][6][7] CRHs are occasionally accompanied by a massive hematoma. 2,4,5,7 However, there are no known reports explaining the relationship between CRHs and a massive hematoma.…”

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confidence: 99%

“…Although the mechanisms underlying CRH development remain elusive, Cammermeyer hypothesized that preexisting minute necrosis, which was facilitated by microemboli, is a prerequisite for the CRH development; then, agonal hemodynamic stagnation increases the pressure of the venous and capillary vessels, resulting in blood leakage into the perivascular tissue. 1 Moreover, fibrin thrombi may be localized around affected lesions because of focal brain damage. 6 Mycotic aneurysm rupture, vasculitis, and hemorrhagic infarction have been reported as the major cause of intracranial hemorrhage; these abnormal conditions complicate IE.…”

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Cerebral ring hemorrhages and a massive hematoma in a patient with infective endocarditis

Kon

Nagawa²,

Nakata³

et al. 2020

Neuropathology

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Letter to the Editor Cerebral ring hemorrhages and a massive hematoma in a patient with infective endocarditis Dear Editor, Cerebral ring hemorrhages (CRHs) are rounded, ringshaped hemorrhages occurring around small vessels. 1-3 CRHs are observed in various conditions and typically develop in the white matter, with most of the center portion containing thrombi or amorphic structures. 1-3 An 82-year-old man presented with a fever. Due to his medical history of transcatheter aortic bioprosthetic valve implantation and percutaneous coronary intervention, he was prescribed oral prasugrel. Vital signs and laboratory data indicated sepsis and disseminated intravascular coagulation (DIC), and methicillin-resistant Staphylococcus aureus was detected in the blood. Systemic computed tomography (CT) did not reveal any infectious foci. Roth spots, Osler's nodes, and Janeway lesions were not observed, and vegetation in the cardiac valves was not seen on transthoracic echocardiography. However, because infective endocarditis (IE) was suspected, he was treated with administration of antibiotics, intravenous infusion of immunoglobulin and recombinant human soluble thrombomodulin, and platelet transfusion. Unfortunately, intracranial hemorrhage developed on day 44 (Fig. 1A), and the patient died two days later. Autopsy

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