Lobar intracerebral hemorrhage

1992 ◽  
Vol 76 (2) ◽  
pp. 231-238 ◽  
Author(s):  
Susumu Wakai ◽  
Nahomi Kumakura ◽  
Masakatsu Nagai
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Vascular Malformation ◽  
Cavernous Malformation ◽  
Ct Scans ◽  
Amyloid Angiopathy ◽  
Content Type ◽  
Negative Angiography ◽  
Cerebral Amyloid ◽  
Fine Print

✓ The authors operated consecutively on 50 patients with lobar intracerebral hemorrhage during a prospectively designed study period from January, 1986, to March, 1990. They investigated the correlations between the underlying causes and the clinicoradiographic features in 29 patients who showed no angiographic vascular abnormalities, in order to elucidate the operative indication for such cases. Patients with ruptured saccular aneurysm or trauma were not included in this study. There were 15 males and 14 females, ranging in age from 7 to 76 years (mean 52.4 years). Histological diagnoses of the surgical specimens were as follows: vascular malformation in nine cases (arteriovenous malformation (AVM) in six and cavernous malformation in three), microaneurysm in 11, cerebral amyloid angiopathy in six, and brain tumor in two; in the remaining case the cause was not verified histologically. The underlying cause was determined in 96.5% of cases. The mean patient age was lowest in the cavernous malformation group (27.0 years), followed by the AVM (45.8 years), microaneurysm (59.8 years), and cerebral amyloid angiopathy (70.0 years) groups. Four patients with vascular malformation (three AVM's and one cavernous malformation) had previous episodes of bleeding at the same site, whereas none of those with microaneurysms or cerebral amyloid angiopathy had such episodes. On computerized tomography (CT) scans, the round to oval hematoma was related to the presence of an AVM or cavernous malformation in contrast to microaneurysms and cerebral amyloid angiopathy. Upon infusion of contrast material, variable enhancement was seen in five (two AVM's and three cavernous malformations) of the nine vascular malformations while no enhancement was noted in any patient with microaneurysm or cerebral amyloid angiopathy at the acute stage. Subarachnoid extension of the hematoma was associated with cerebral amyloid angiopathy significantly more frequently than with AVM's (p < 0.05) and microaneurysms (p < 0.01). The results suggest that clinicoradiographic pictures in cases with negative angiography are quite different among the three major pathological categories; namely, vascular malformation (AVM and cavernous malformation), microaneurysm, and cerebral amyloid angiopathy. It is suggested that the underlying etiology of a given lobar intracerebral hemorrhage with negative angiography may be predicted by a combination of patient age, history of previous bleeding at the same site, hematoma shape, and subarachnoid extension of the hematoma on CT scans. Based upon these findings, the authors discuss operative indications for such cases.

Intracerebral hemorrhage due to cerebral amyloid angiopathy

1985 ◽  
Vol 63 (6) ◽  
pp. 965-969 ◽  
Author(s):  
Norbert Roosen ◽  
Jean-Jacques Martin ◽  
Christian De La Porte ◽  
Michel Van Vyve
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Clinicopathological Features ◽  
Amyloid Angiopathy ◽  
Correct Treatment ◽  
Content Type ◽  
Cerebral Amyloid ◽  
Occipital Lobes ◽  
The Relationship ◽  
Fine Print

✓ The case is presented of a 59-year-old man with cerebral amyloid angiopathy and three consecutive hemorrhages in the occipital lobes. The clinicopathological features and the relationship to Alzheimer's dementia are discussed. The correct treatment of intracerebral hemorrhage related to cerebral amyloid angiopathy is a matter of controversy.

The angiographically occult cerebrovascular malformation

1978 ◽  
Vol 48 (2) ◽  
pp. 292-296 ◽  
Author(s):  
James B. Golden ◽  
Richard A. Kramer
Keyword(s):  
Intracerebral Hemorrhage ◽  
Ct Scan ◽  
Vascular Malformation ◽  
Ct Scans ◽  
Cerebral Lesions ◽  
Content Type ◽  
Surgical Exploration ◽  
Diagnostic Possibility ◽  
Cerebrovascular Malformation ◽  
Fine Print

✓ Three cases presenting with hemiparesis, headache, or seizures gave no history suggestive of subarachnoid or intracerebral hemorrhage. Carotid arteriograms were performed, and in each case failed to demonstrate a vascular malformation. In all three cases cerebral lesions were shown by either computerized tomographic (CT) scan, radionuclide scan, or both. Surgical exploration and biopsy revealed a vascular malformation in each case. The CT scans in two of the cases showed dense lesions that could suggest vascular malformation as a diagnostic possibility.

Cerebral amyloid angiopathy presenting as multiple intracranial lesions on magnetic resonance imaging

1991 ◽  
Vol 75 (3) ◽  
pp. 458-460 ◽  
Author(s):  
Deepak Awasthi ◽  
Rand M. Voorhies ◽  
John Eick ◽  
William T. Mitchell
Keyword(s):  
Magnetic Resonance ◽  
Mr Imaging ◽  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Spontaneous Intracerebral Hemorrhage ◽  
Normotensive Patient ◽  
Content Type ◽  
Imaging Characteristics ◽  
Cerebral Amyloid

✓ Cerebral amyloid angiopathy is recognized as an important cause of spontaneous intracerebral hemorrhage in the elderly normotensive patient. Magnetic resonance (MR) imaging characteristics of this disease entity are rarely mentioned in the literature. The MR imaging findings of an elderly normotensive patient presenting with an acute spontaneous intracerebral hemorrhage secondary to amyloid angiopathy are reported and a brief review of amyloidosis is presented.

Cerebral amyloid angiopathy with multiple intracerebral hemorrhages

1982 ◽  
Vol 57 (2) ◽  
pp. 286-289 ◽  
Author(s):  
Kenneth L. Tyler ◽  
Charles E. Poletti ◽  
Roberto C. Heros
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Neurological Disorders ◽  
Brain Parenchyma ◽  
Amyloid Angiopathy ◽  
Content Type ◽  
Intracerebral Hemorrhages ◽  
Cerebral Amyloid ◽  
Unclear Etiology ◽  
Adjacent Brain

✓ Cerebral amyloid angiopathy (CAA) has been associated with atypical dementia and a variety of other neurological disorders. Intracerebral hemorrhage is the most striking manifestation of CAA. A 63-year-old patient is described who sustained four intracerebral hemorrhages although he had no predisposing factors other than CAA. The neurological and pathological features of CAA are reviewed, with particular emphasis on the problem of CAA-associated intracerebral hemorrhage. On the basis of the experience with this case, it is recommended that adjacent brain parenchyma be biopsied in all patients undergoing evacuation of intracerebral hematomas of unclear etiology.

Matrix metalloproteinase—9 concentration after spontaneous intracerebral hemorrhage

2003 ◽  
Vol 99 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Sònia Abilleira ◽  
Joan Montaner ◽  
Carlos A. Molina ◽  
Jasone Monasterio ◽  
José Castillo ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neurological Diseases ◽  
Neurological Status ◽  
Acute Stage ◽  
Ct Scans ◽  
Enzyme Linked Immunosorbent Assay ◽  
Content Type ◽  
Blood Brain Barrier Disruption ◽  
Brain Barrier Disruption ◽  
Fine Print

Object. Matrix metalloproteinases (MMPs) are overexpressed in the presence of some neurological diseases in which blood—brain barrier disruption exists. The authors investigated the MMP-9 concentration in patients after acute intracerebral hemorrhage (ICH) and its relation to perihematomal edema (PHE). Methods. Concentrations of MMP-9 and related proteins were determined in plasma by performing an enzyme-linked immunosorbent assay of samples drawn after hospital admission (< 24 hours after stroke) from 57 patients with ICH. The diagnosis of ICH was made on the basis of findings on computerized tomography (CT) scans. The volumes of ICH and PHE were measured on baseline and follow-up CT scans at the same time that the patient's neurological status was assessed using the Canadian Stroke Scale and the Glasgow Coma Scale. Increased expression of MMP-9 was found among patients with ICH. In cases of deep ICH, MMP-9 was significantly associated with PHE volume (r = 0.53; p = 0.01) and neurological worsening (237.4 compared with 111.3 ng/ml MMP-9; p = 0.04). A logistic regression model focusing on the study of absolute PHE volume showed ICH volume as an independent predictor (odds ratio [OR] 3.37; 95% confidence interval [CI] 1.1–10.3; p = 0.03). A second analysis of relative PHE volume (absolute PHE volume/ICH volume) in patients with deep ICH demonstrated that the only factor related to it was MMP-9 concentration (OR 11.6; 95% CI 1.5–89.1; p = 0.018). Conclusions. Expression of MMP-9 is raised after acute spontaneous ICH. Among patients with deep ICH this increase is associated with PHE and the development of neurological worsening within the acute stage.

Clinical and neuropathologic analysis of intracerebral hemorrhage in patients with cerebral amyloid angiopathy

2019 ◽  
Vol 176 ◽  
pp. 110-115
Author(s):  
Taro Yanagawa ◽  
Masaki Takao ◽  
Masami Yasuda ◽  
Tomoya Kamide ◽  
Hiroki Sato ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Abstract 36: The Boston Criteria V2.0 for Cerebral Amyloid Angiopathy: Updated Criteria and Multicenter MRI-Neuropathology Validation

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Andreas Charidimou ◽  
Gregoire Boulouis ◽  
Matthew Frosch ◽  
Jean-Claude Baron ◽  
Marco Pasi ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Diagnostic Accuracy ◽  
Cerebral Amyloid Angiopathy ◽  
Brain Mri ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Validation Sample ◽  
Temporal Validation ◽  
Cerebral Amyloid

Introduction: The Boston criteria are used worldwide for in vivo diagnosis of cerebral amyloid angiopathy (CAA). Given substantial advances in CAA research, we aimed to update the Boston criteria and externally validate their diagnostic accuracy across the spectrum of CAA-related presentations and across international sites. Methods: As part of an International CAA Association multicenter study, we identified patients age 50 or older with potential CAA-related clinical presentations (spontaneous intracerebral hemorrhage, cognitive impairment, or transient focal neurological episodes), available brain MRI, and histopathologic assessment for the diagnosis of CAA. We derived Boston criteria v2.0 by selecting MRI features to optimize diagnostic specificity and sensitivity in a pre-specified derivation sample (Boston cases 1994 to 2012, n=159), then externally validated in pre-specified temporal (Boston cases 2012-2018, n=59) and geographical (non-Boston cases 2004-2018; n=123) validation samples and compared their diagnostic accuracy to the currently used modified Boston criteria. Results: Based on exploratory analyses in the derivation sample, we derived provisional criteria for probable CAA requiring presence of at least 2 strictly lobar hemorrhagic lesions (intracerebral hemorrhage, cerebral microbleed, or cortical superficial siderosis focus) or at least 1 strictly lobar hemorrhagic lesion and 1 white matter characteristic (severe degree of visible perivascular spaces in centrum semiovale or white matter hyperintensities multispot pattern). Sensitivity/specificity of the criteria were 74.8/84.6% in the derivation sample, 92.5/89.5% in the temporal validation sample, 80.2/81.5% in the geographic validation sample, and 74.5/95.0% in cases across all samples with autopsy as the diagnostic gold standard. The v2.0 criteria for probable CAA had superior accuracy to the currently modified Boston criteria (p<0.005) in the autopsied cases. Conclusion: The Boston criteria v.2.0 incorporate emerging MRI markers of CAA to enhance sensitivity without compromising their high specificity. Validation of the criteria across independent patient settings firmly supports their adoption into clinical practice and research.

Familial Cerebral Cavernous Malformation Mimicking Cerebral Amyloid Angiopathy

2021 ◽  
pp. 10.1212/CPJ.0000000000001055
Author(s):  
Mohamed Ridha ◽  
Yasmin Aziz ◽  
Joseph Broderick
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Cavernous Malformation ◽  
Pathogenic Mutation ◽  
Cerebral Cavernous Malformation ◽  
Amyloid Angiopathy ◽  
History Of ◽  
Cerebral Amyloid ◽  
Cerebral Microhemorrhages ◽  
Familial Cerebral Cavernous Malformation ◽  
Work Up

A 67-year-old man was referred from ophthalmology for possible cerebral amyloid angiopathy (CAA) discovered during work-up of possible optic neuropathy. MRI (figure 1) demonstrated innumerable periventricular, brainstem, and cortical cerebral microhemorrhages (CMH). Scattered, non-specific white matter hyperintensities was seen on T2-weighted imaging without surrounding hypointense rim. He had no hypertension, and the distribution was uncharacteristic for CAA. Despite absent family history of stroke or seizure, testing for familial cerebral cavernous malformation (FCCM) identified a pathogenic mutation of KRIT1 (c.382G>T).

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