Abstract TP339: Simultaneous Multiple Intracerebral Hemorrhages (SMICH)

Background and Purpose: Simultaneous multiple intracerebral hemorrhages (SMICH) are uncommon. Few single center studies have analyzed characteristics and outcome of SMICH. We analyzed clinical characteristics and outcome of SMICH patients from two comprehensive stroke centers. Methods: Baseline imaging from consecutive intracerebral hemorrhage (ICH) patients (n=1552) from Helsinki ICH study and Royal Melbourne Hospital ICH study were screened for SMICH. ICH etiology was classified according to the SMASH-U classification system. ICH due to trauma, tumor and aneurysmal rupture were excluded. Baseline clinical and radiological characteristics and 90-day mortality were compared between SMICH and single ICH patients. Association of SMICH with 90-day mortality was assessed in multivariable logistic regression models adjusted for predictors of ICH outcome. Results: 1452 patients were included in the analysis and 85 (5.9%) were classified as SMICH. SMICH were more often female (58% vs 42%;p=0.004), had lower baseline Glasgow Coma Scale (12 vs 14;p=0.008), and more frequent lobar location (59% v 34%;p<0.001) compared to single ICH. The SMASH-U etiology of SMICH patients was less often hypertensive (20% vs 37%;p=0.001), more other systemic coagulopathy (12% vs 3%;p<0.001) and trended towards more cerebral amyloid angiopathy (32% vs 23%;p=0.071). SMICH was not associated with 90-day mortality on univariate (37% vs 35%;p=0.635), multivariable (OR 0.783 95%CI 0.401-1.529;p=0.473), or propensity score matched analyses (OR 0.817 95% CI 0.400-1.668,p=0.578). Conclusion: SMICH occurs in approximately 1 in 20 ICH with more often lobar located hematomas, less often hypertensive and associated with more systemic coagulopathy. The mortality is similar to single ICH. Given varied etiologies, SMICH management should target the underlying pathology.

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Aβ (Amyloid Beta) and Tau Tangle Pathology Modifies the Association Between Small Vessel Disease and Cortical Microinfarcts

Stroke ◽

10.1161/strokeaha.120.031073 ◽

2021 ◽

Author(s):

A. Kapasi ◽

S.E. Leurgans ◽

Z. Arvanitakis ◽

L.L. Barnes ◽

D.A. Bennett ◽

...

Keyword(s):

Logistic Regression ◽

Older People ◽

Cerebral Amyloid Angiopathy ◽

Regression Models ◽

Small Vessel ◽

Amyloid Angiopathy ◽

Logistic Regression Models ◽

Aβ Amyloid ◽

Tangle Pathology ◽

Cerebral Amyloid

Background and Purpose: There is increasing recognition of the importance of cortical microinfarcts to overall brain health, cognition, and Alzheimer dementia. Cerebral small vessel pathologies are associated with microinfarcts and frequently coexist with Alzheimer disease; however, the extent to which Aβ (amyloid beta) and tau pathology modulates microvascular pathogenesis is not fully understood. Study objective was to examine the relationship of small vessel pathologies, arteriolosclerosis, and cerebral amyloid angiopathy, with cortical microinfarcts in people with differing levels of Aβ or tau tangle burden. Methods: Participants were 1489 autopsied older people (mean age at death, 89 years; 67% women) from 1 of 3 ongoing clinical-pathological cohort studies of aging. Neuropathological evaluation identified cortical Aβ and tau tangle burden using immunohistochemistry in 8 brain regions, provided semiquantitative grading of cerebral vessel pathologies, and identified the presence of cortical microinfarcts. Logistic regression models adjusted for demographics and atherosclerosis and examined whether Aβ or tau tangle burden modified relations between small vessel pathologies and cortical microinfarcts. Results: Cortical microinfarcts were present in 17% of older people, moderate-to-severe cerebral amyloid angiopathy pathology in 36%, and arteriolosclerosis in 34%. In logistic regression models, we found interactions with Aβ and tau tangles, reflecting that the association between arteriolosclerosis and cortical microinfarcts was stronger in the context of greater Aβ (estimate, 0.15; SE=0.07; P =0.02) and tau tangle burden (estimate, 0.13; SE=0.06; P =0.02). Interactions also emerged for cerebral amyloid angiopathy, suggesting that the association between cerebral amyloid angiopathy and cortical microinfarcts is more robust in the presence of higher Aβ (estimate, 0.27; SE=0.07; P <0.001) and tangle burden (estimate, 0.16; SE=0.06; P =0.005). Conclusions: These findings suggest that in the presence of elevated Aβ or tangle pathology, small vessel pathologies are associated with greater microvascular tissue injury, highlighting a potential link between neurodegenerative and vascular mechanisms.

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Hereditary cerebral amyloid angiopathy, Piedmont-type mutation

Neurology Genetics ◽

10.1212/nxg.0000000000000411 ◽

2020 ◽

Vol 6 (2) ◽

pp. e411 ◽

Cited By ~ 2

Author(s):

Mariel G. Kozberg ◽

Susanne J. van Veluw ◽

Matthew P. Frosch ◽

Steven M. Greenberg

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Ex Vivo ◽

Amyloid Plaques ◽

Amyloid Angiopathy ◽

Pathologic Examination ◽

Potential Association ◽

History Of ◽

Intracerebral Hemorrhages ◽

Β Amyloid ◽

Cerebral Amyloid

ObjectiveWe present here a case report of a patient with a family history of intracerebral hemorrhages (ICHs) who presented with multiple large lobar hemorrhages in rapid succession, with cognitive sparing, who was found to have a mutation in the β-amyloid coding sequence of amyloid precursor protein (Leu705Val), termed the Piedmont-type mutation, the second ever reported case of this form of hereditary cerebral amyloid angiopathy (CAA).MethodsTargeted pathologic examination was performed aided by the use of ex vivo MRI.ResultsSevere CAA was observed mainly involving the leptomeningeal vessels and, to a far lesser extent, cortical vessels, with no amyloid plaques or neurofibrillary tangles.ConclusionsThis leptomeningeal pattern of β-amyloid deposition coupled with multiple large hemorrhages demonstrates unique pathophysiologic characteristics of CAA associated with the Piedmont-type mutation, suggesting a potential association between leptomeningeal CAA and larger ICHs.

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Predictors of localization, outcome, and etiology of spontaneous intracerebral hemorrhages: focus on cerebral amyloid angiopathy

Journal of Neural Transmission ◽

10.1007/s00702-020-02174-2 ◽

2020 ◽

Vol 127 (6) ◽

pp. 963-972 ◽

Cited By ~ 1

Author(s):

Bernadett Fakan ◽

Zita Reisz ◽

Denes Zadori ◽

Laszlo Vecsei ◽

Peter Klivenyi ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Amyloid Angiopathy ◽

Intracerebral Hemorrhages ◽

Cerebral Amyloid

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Cerebral amyloid angiopathy as a cause of multiple intracerebral hemorrhages

Neurology ◽

10.1212/wnl.34.6.730 ◽

1984 ◽

Vol 34 (6) ◽

pp. 730-730 ◽

Cited By ~ 68

Author(s):

C. Gilles ◽

J. M. Brucher ◽

P. Khoubesserian ◽

J. J. Vanderhaeghen

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Amyloid Angiopathy ◽

Intracerebral Hemorrhages ◽

Cerebral Amyloid

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Clinical characteristics of ATTR-type leptomeningeal amyloidosis/cerebral amyloid angiopathy

Journal of the Neurological Sciences ◽

10.1016/j.jns.2017.08.3297 ◽

2017 ◽

Vol 381 ◽

pp. 383

Author(s):

S. Kodama ◽

D. Miyazaki ◽

T. Yoshinaga ◽

M. Yazaki ◽

Y. Sekijima

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Clinical Characteristics ◽

Amyloid Angiopathy ◽

Cerebral Amyloid

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Spatial and temporal intracerebral hemorrhage patterns in Dutch-type hereditary cerebral amyloid angiopathy

International Journal of Stroke ◽

10.1177/17474930211057022 ◽

2021 ◽

pp. 174749302110570

Author(s):

Sabine Voigt ◽

Siham Amlal ◽

Emma A Koemans ◽

Ingeborg Rasing ◽

Ellis S van Etten ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Temporal Pattern ◽

Occipital Lobe ◽

Time Interval ◽

Amyloid Angiopathy ◽

Degree Relative ◽

Amyloid Load ◽

Intracerebral Hemorrhages ◽

Cerebral Amyloid ◽

Histopathological Studies

Aim To investigate whether there is a topographical and temporal pattern of index and recurrent intracerebral hemorrhages (ICH) in Dutch-type hereditary Cerebral Amyloid Angiopathy (D-CAA) to increase our understanding on CAA-related ICH development. Methods We included patients with DNA confirmed D-CAA or a history with ≥1 lobar ICH and ≥1 first-degree relative with D-CAA. Topographical pattern was studied by location (proportion frontal/parietal/temporal/occipital; infra/supratentorial and occurrence ratios relative to lobe volume) and volume of index and recurrent ICHs were determined on CT. Temporal pattern was examined by time between recurrent ICHs was retrieved from medical records. Results We included 72 patients with D-CAA (mean age at index ICH 55 years) with in total 214 ICH. The median follow-up time was 7 years (range 0.8 to 28 years). All ICH were lobar and supratentorial. The index ICH was most frequently located in the occipital lobe (34% vs. 22% in the other three lobes; with index ICH occurrence ratios relative to lobe volume of 1.9 for occipital, 1.0 for temporal, 1.2 for parietal, and 0.5 for frontal, p = 0.001). In 16/47 (34%) patients with multiple ICH, the second ICH was located in the same lobe as the index ICH. The median time-interval between subsequent ICH was #1-2 ICH 27 months, #2-3 ICH 14 months, and #3-4 ICH 7 months (p = 0.6) There was no difference in volume between index and recurrent ICHs. Conclusions We found that index and recurrent ICHs in D-CAA have a preference for the occipital lobe and are least frequent in the frontal lobe, which adds to the existing knowledge of histopathological studies on amyloid load in CAA. Surprisingly, there was no acceleration in time nor gradual increase of hematoma volume between subsequent ICHs.

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Original article The association between cerebral amyloid angiopathy and atherosclerosis in patients with intracerebral hemorrhages

Folia Neuropathologica ◽

10.5114/fn.2013.37709 ◽

2013 ◽

Vol 3 ◽

pp. 243-249

Author(s):

Tadeusz Andrzej Mendel ◽

Teresa Wierzba-Bobrowicz ◽

Tomasz Stępień ◽

Grażyna Maria Szpak

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Amyloid Angiopathy ◽

Intracerebral Hemorrhages ◽

Cerebral Amyloid

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Lacunes, Microinfarcts, and Vascular Dysfunction in Cerebral Amyloid Angiopathy

Neurology ◽

10.1212/wnl.0000000000011631 ◽

2021 ◽

Vol 96 (12) ◽

pp. e1646-e1654

Author(s):

Elif Gokcal ◽

Mitchell J. Horn ◽

Susanne J. van Veluw ◽

Aina Frau-Pascual ◽

Alvin S. Das ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Regression Models ◽

Cox Regression ◽

Vascular Dysfunction ◽

Blood Oxygen Level Dependent ◽

White Matter Hyperintensity ◽

Amyloid Angiopathy ◽

Cerebral Amyloid ◽

Relationship Of ◽

The Relationship

ObjectiveTo analyze the relationship of lacunes with cortical cerebral microinfarcts (CMIs), to assess their association with vascular dysfunction, and to evaluate their effect on the risk of incident intracerebral hemorrhage (ICH) in cerebral amyloid angiopathy (CAA).MethodsThe count and topography of lacunes (deep/lobar), CMIs, and white matter hyperintensity (WMH) volume were retrospectively analyzed in a prospectively enrolled CAA cohort that underwent high-resolution research MRIs. The relationship of lacunes with CMIs and other CAA-related markers including time to peak (TTP) of blood oxygen level–dependent signal, an established measure of vascular dysfunction, was evaluated in multivariate models. Adjusted Cox regression models were used to investigate the relationship between lacunes and incident ICH.ResultsThe cohort consisted of 122 patients with probable CAA without dementia (mean age, 69.4 ± 7.6 years). Lacunes were present in 31 patients (25.4%); all but one were located in lobar regions. Cortical CMIs were more common in patients with lacunes compared to patients without lacunes (51.6% vs 20.9%, p = 0.002). TTP was not associated with either lacunes or CMIs (both p > 0.2) but longer TTP response independently correlated with higher WMH volume (p = 0.001). Lacunes were associated with increased ICH risk in univariate and multivariate Cox regression models (p = 0.048 and p = 0.026, respectively).ConclusionsOur findings show a high prevalence of lobar lacunes, frequently coexisting with CMIs in CAA, suggesting that these 2 lesion types may be part of a common spectrum of CAA-related infarcts. Lacunes were not related to vascular dysfunction but predicted incident ICH, favoring severe focal vessel involvement rather than global ischemia as their mechanism.

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