Cerebral amyloid angiopathy – The modified Boston criteria in clinical practice

Caetano, André; Ladeira, Filipa; Barbosa, Raquel; Viana-Baptista, Miguel

doi:10.1016/j.jns.2017.11.021

Cited by 14 publications

(13 citation statements)

References 17 publications

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“…Similar microhemorrhages in people are characteristic for cerebral amyloid angiopathy, the diagnosis of which generally relies upon MRI findings and supporting clinical features (Sharma et al, 2018;Yamada, 2015;Boulouis, Charidimou & Greenberg, 2016;Smith, 2018). Indeed, according to the Boston criteria for diagnosing human cerebral amyloid angiopathy, supportive clinical data and MRI evidence of microhemorrhages, combined with the absence of any other identifiable cause for hemorrhage, supports a diagnosis of "probable cerebral amyloid angiopathy" in the dogs in our study (Yamada, 2015;Boulouis, Charidimou & Greenberg, 2016;Chardimou et al, 2017;Charidimou, 2015;Caetano et al, 2018).…”

Section: Discussionsupporting

confidence: 76%

Interthalamic adhesion size in aging dogs with presumptive spontaneous brain microhemorrhages: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction

Dewey

Rishniw

Johnson

et al. 2020

PeerJ

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Objective Spontaneous brain microhemorrhages in elderly people are present to some degree in Alzheimer’s disease patients but have been linked to brain atrophy in the absence of obvious cognitive decline. Brain microhemorrhages have recently been described in older dogs, but it is unclear whether these are associated with brain atrophy. Diminution of interthalamic adhesion size-as measured on MRI or CT-has been shown to be a reliable indicator of brain atrophy in dogs with canine cognitive dysfunction (CCD) in comparison with successfully aging dogs. We hypothesized that aging dogs with brain microhemorrhages presenting for neurologic dysfunction but without obvious features of cognitive decline would have small interthalamic adhesion measurements, like dogs with CCD, compared with control dogs. The objective of this study was to compare interthalamic adhesion size between three groups of aging (>9 years) dogs: (1) neurologically impaired dogs with presumptive spontaneous brain microhemorrhages and no clinical evidence of cognitive dysfunction (2) dogs with CCD (3) dogs without clinical evidence of encephalopathy on neurologic examination (control dogs). MR images from 52 aging dogs were reviewed and measurements were obtained of interthalamic adhesion height (thickness) and mid-sagittal interthalamic adhesion area for all dogs, in addition to total brain volume. Interthalamic adhesion measurements, either absolute or normalized to total brain volume were compared between groups. Signalment (age, breed, sex), body weight, presence and number of SBMs, as well as other abnormal MRI findings were recorded for all dogs. Results All interthalamic adhesion measurement parameters were significantly (P < 0.05) different between control dogs and affected dogs. Both dogs with cognitive dysfunction (12/15; 80%) and dogs with isolated brain microhemorrhages had more microhemorrhages than control dogs (3/25; 12%). Affected dogs without cognitive dysfunction had significantly more microhemorrhages than dogs with cognitive dysfunction. In addition to signs of cognitive impairment for the CCD group, main clinical complaints for SBM and CCD dogs were referable to central vestibular dysfunction, recent-onset seizure activity, or both. Geriatric dogs with spontaneous brain microhemorrhages without cognitive dysfunction have similar MRI abnormalities as dogs with cognitive dysfunction but may represent a distinct disease category.

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Section: Discussionsupporting

confidence: 76%

Interthalamic adhesion size in aging dogs with presumptive spontaneous brain microhemorrhages: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction

Dewey

Rishniw

Johnson

et al. 2020

PeerJ

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“…Additional neuroimaging markers that aid clinical diagnosis include perivascular changes that occur in the vicinity around CAA-affected vessels. For example, cortical superficial siderosis indicates perivascular iron accumulation in pial arteries and arterioles reflecting cerebral microbleeds [12,14,23]. Another noted perivascular change associated with CAA is the presence of dilated perivascular spaces, particularly around penetrating arterioles with amyloid deposition [8,24].…”

Section: Discussionmentioning

confidence: 99%

“…Previously, a set of criteria was established, known as the 'Boston Criteria', that determines a diagnosis of probable CAA based on the presence and anatomical location of cerebral microbleeds [11]. An updated version of the "Boston Criteria" was proposed incorporating additional key imaging biomarkers that detect other cerebral vascular injuries associated with amyloid containing vessels including cortical superficial siderosis, enlarged perivascular spaces and white matter hyperintensities [12][13][14]. Also, anatomical distribution patterns of amyloid accumulation in whole brain detected by positron emission tomography (PET) and Aβ specific radiotracer imaging studies has been informative [15,16].…”

Section: Introductionmentioning

confidence: 99%

Reduced Levels of Cerebrospinal Fluid/Plasma Aβ40 as an Early Biomarker for Cerebral Amyloid Angiopathy in RTg-DI Rats

Zhu

Hoos

et al. 2020

IJMS

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The accumulation of fibrillar amyloid β-protein (Aβ) in blood vessels of the brain, the condition known as cerebral amyloid angiopathy (CAA), is a common small vessel disease that promotes cognitive impairment and is strongly associated with Alzheimer’s disease. Presently, the clinical diagnosis of this condition relies on neuroimaging markers largely associated with cerebral macro/microbleeds. However, these are markers of late-stage disease detected after extensive cerebral vascular amyloid accumulation has become chronic. Recently, we generated a novel transgenic rat model of CAA (rTg-DI) that recapitulates multiple aspects of human CAA disease with the progressive accumulation of cerebral vascular amyloid, largely composed of Aβ40, and the consistent emergence of subsequent microbleeds. Here, we investigated the levels of Aβ40 in the cerebrospinal fluid (CSF) and plasma of rTg-DI rats as CAA progressed from inception to late stage disease. The levels of Aβ40 in CSF and plasma precipitously dropped at the early onset of CAA accumulation at three months of age and continued to decrease with the progression of disease. Notably, the reduction in CSF/plasma Aβ40 levels preceded the emergence of cerebral microbleeds, which first occurred at about six months of age, as detected by in vivo magnetic resonance imaging and histological staining of brain tissue. These findings support the concept that reduced CSF/plasma levels of Aβ40 could serve as a biomarker for early stage CAA disease prior to the onset of cerebral microbleeds for future therapeutic intervention.

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“…[5][6][7][8] Indeed, according to the Boston criteria for diagnosing human cerebral amyloid angiopathy, supportive clinical data and MRI evidence of microhemorrhages, combined with the absence of any other identifiable cause for hemorrhage, supports a diagnosis of "probable cerebral amyloid angiopathy". 6,7,[26][27][28] Could microhemorrhages in dogs be caused by cerebral amyloid angiopathy and could this, in turn, lead to cognitive dysfunction? In humans, the relationship between cerebral amyloid angiopathy and Alzheimer's disease is well-established, but not straightforward; investigators have identified cerebral amyloid angiopathy as a risk factor for development of Alzheimer's disease, and Alzheimer's disease patients are commonly afflicted with concurrent cerebral amyloid angiopathy.…”

Section: Discussionmentioning

confidence: 99%

Presumptive spontaneous brain microhemorrhages in geriatric dogs: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction

Dewey

Rishniw

Johnson

et al. 2019

Preprint

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The objective of this study was to compare specific brain MRI anatomic measurements between three groups of geriatric ( > 8yrs) dogs: 1) neurologically impaired dogs with presumptive spontaneous brain microhemorrhages and no clinical evidence of canine cognitive dysfunction 2) dogs with canine cognitive dysfunction 3) dogs without clinical evidence of cognitive impairment or abnormalities on neurologic examination (control dogs). MR images from 46 geriatric dogs were reviewed and measurements were obtained of interthalamic adhesion height (thickness) and mid-sagittal interthalamic adhesion area for all dogs, in addition to total brain volume. Interthalamic adhesion measurements, either absolute or normalized to total brain volume were compared between groups. Signalment (age, breed, sex), body weight, presence and number of SBMs, as well as other abnormal MRI findings were recorded for all dogs. All interthalamic adhesion measurement parameters were significantly (p<0.05) different between control dogs and affected dogs. Both dogs with cognitive dysfunction (12/13; 92 %) and dogs with isolated brain microhemorrhages had more microhemorrhages than control dogs (3/19; 16%). Affected dogs without cognitive dysfunction had more microhemorrhages than dogs with cognitive dysfunction. In addition to signs of cognitive impairment for the CCD group, main clinical complaints for SBM and CCD dogs were referable to central vestibular dysfunction, recent-onset seizure activity, or both. Geriatric dogs with spontaneous brain microhemorrhages without cognitive dysfunction have similar MRI abnormalities as dogs with cognitive dysfunction but may represent a distinct diseasecategory.

show abstract

Cerebral amyloid angiopathy – The modified Boston criteria in clinical practice

Cited by 14 publications

References 17 publications

Interthalamic adhesion size in aging dogs with presumptive spontaneous brain microhemorrhages: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction

Interthalamic adhesion size in aging dogs with presumptive spontaneous brain microhemorrhages: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction

Reduced Levels of Cerebrospinal Fluid/Plasma Aβ40 as an Early Biomarker for Cerebral Amyloid Angiopathy in RTg-DI Rats

Presumptive spontaneous brain microhemorrhages in geriatric dogs: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction

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