Cerebral amyloid angiopathy: a long-term consequence of traumatic brain injury?

We report the case of long-term follow-up of brain magnetic imaging of cerebral amyloid angiopathy. Cerebral amyloid angiopathy is often considered a major cause of spontaneous intracerebral hemorrhage in the elderly. This case illustrates the markedly progressive clinical and radiological features of the vasculopathic process in 10 years.

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Cerebrovascular and Neurodegenerative Pathologies in Long-Term Stable Mild Cognitive Impairment

Journal of Alzheimer s Disease ◽

10.3233/jad-200829 ◽

2021 ◽

pp. 1-15

Author(s):

Manu J. Sharma ◽

Brandy L. Callahan

Keyword(s):

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Cerebral Amyloid Angiopathy ◽

Neurofibrillary Tangles ◽

Small Vessel Disease ◽

Significant Proportion ◽

Amyloid Angiopathy ◽

Prodromal Phase ◽

Cerebral Amyloid

Background: Mild cognitive impairment (MCI) is considered by some to be a prodromal phase of a progressive disease (i.e., neurodegeneration) resulting in dementia; however, a substantial portion of individuals (ranging from 5–30%) remain cognitively stable over the long term (sMCI). The etiology of sMCI is unclear but may be linked to cerebrovascular disease (CVD), as evidence from longitudinal studies suggest a significant proportion of individuals with vasculopathy remain stable over time. Objective: To quantify the presence of neurodegenerative and vascular pathologies in individuals with long-term (>5-year) sMCI, in a preliminary test of the hypothesis that CVD may be a contributor to non-degenerative cognitive impairment. We expect frequent vasculopathy at autopsy in sMCI relative to neurodegenerative disease, and relative to individuals who convert to dementia. Methods: In this retrospective study, using data from the National Alzheimer’s Coordinating Center, individuals with sMCI (n = 28) were compared to those with MCI who declined over a 5 to 9-year period (dMCI; n = 139) on measures of neurodegenerative pathology (i.e., Aβ plaques, neurofibrillary tangles, TDP-43, and cerebral amyloid angiopathy) and CVD (infarcts, lacunes, microinfarcts, hemorrhages, and microbleeds). Results: Alzheimer’s disease pathology (Aβ plaques, neurofibrillary tangles, and cerebral amyloid angiopathy) was significantly higher in the dMCI group than the sMCI group. Microinfarcts were the only vasculopathy associated with group membership; these were more frequent in sMCI. Conclusion: The most frequent neuropathology in this sample of long-term sMCI was microinfarcts, tentatively suggesting that silent small vessel disease may characterize non-worsening cognitive impairment.

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Index event of cerebral amyloid angiopathy (CAA) determines long-term prognosis and recurrent events (retrospective analysis and clinical follow-up)

Neurological Research and Practice ◽

10.1186/s42466-021-00152-x ◽

2021 ◽

Vol 3 (1) ◽

Author(s):

Andrea Wagner ◽

Christiane Groetsch ◽

Sibylle Wilfling ◽

Karl-Michael Schebesch ◽

Mustafa Kilic ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Recurrent Events ◽

Clinical Presentation ◽

Secondary Prophylaxis ◽

Amyloid Angiopathy ◽

Index Event ◽

Asymptomatic Patients ◽

Cerebral Amyloid

Abstract Background The modified Boston criteria (mBC) define the probability for the diagnosis of cerebral amyloid angiopathy (CAA). Its initial clinical presentation differs from asymptomatic cerebral microbleedings (cMBs), acute ischemic stroke (AIS), cortical hemosiderosis (cSS), to lobar ICH (lICH). Methods Retrospective analyses and clinical follow-ups of individuals with at least mBC “possible” CAA from 2005 to 2018. Results 149 patients were classified in subgroups due to the index event: lICH (n = 91), AIS (n = 32), > 3 cMBs only (n = 16) and cSS (n = 10). Patients in the lICH subgroup had a significantly higher percentage of single new lICHs compared to other groups, whereas patients in the AIS-group had a significantly higher percentage of multiple new AIS. cMBs as index event predisposed for AIS during follow up (p < 0.0016). Patients of the cMBs- or cSS-group showed significantly more TFNEs (transient focal-neurological episodes) and lower numbers of asymptomatic patients (for epilepsy and TFNEs) at the index event than patients with lICH or AIS (p < 0.0013). At long-term follow-up, the cMBs- and cSS-group were characterized by more TFNEs and fewer asymptomatic patients. Conclusions A new classification system of CAA should add subgroups according to the initial clinical presentation to the mBCs allowing individual prognosis, acute treatment and secondary prophylaxis.

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Cerebral amyloid angiopathy in streptozotocin rat model of sporadic Alzheimer’s disease: a long-term follow up study

Journal of Neural Transmission ◽

10.1007/s00702-011-0651-4 ◽

2011 ◽

Vol 118 (5) ◽

pp. 765-772 ◽

Cited By ~ 67

Author(s):

Melita Salkovic-Petrisic ◽

Jelena Osmanovic-Barilar ◽

Martina K. Brückner ◽

Siegfried Hoyer ◽

Thomas Arendt ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Rat Model ◽

Amyloid Angiopathy ◽

Sporadic Alzheimer’S Disease ◽

Follow Up Study ◽

Long Term Follow Up ◽

Streptozotocin Rat Model ◽

Cerebral Amyloid

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Decreased Basal Ganglia Volume in Cerebral Amyloid Angiopathy

Journal of Stroke ◽

10.5853/jos.2020.04280 ◽

2021 ◽

Vol 23 (2) ◽

pp. 223-233

Author(s):

Panagiotis Fotiadis ◽

Marco Pasi ◽

Andreas Charidimou ◽

Andrew D. Warren ◽

Kristin M. Schwab ◽

...

Keyword(s):

Brain Injury ◽

Basal Ganglia ◽

Cerebral Amyloid Angiopathy ◽

Magnetic Resonance Images ◽

Tissue Loss ◽

Independent Effect ◽

Amyloid Angiopathy ◽

Intracranial Volume ◽

Cerebral Amyloid ◽

N 93

Background and Purpose Cerebral amyloid angiopathy (CAA) is a common pathology of the leptomeningeal and cortical small vessels associated with hemorrhagic and non-hemorrhagic brain injury. Given previous evidence for CAA-related loss of cortical thickness and white matter volume, we hypothesized that CAA might also cause tissue loss in the basal ganglia.Methods We compared basal ganglia volumes expressed as a percentage of total intracranial volume (pBGV) of non-demented patients with sporadic and hereditary CAA to age-matched healthy control (HC) and Alzheimer’s disease (AD) cohorts.Results Patients with sporadic CAA had lower pBGV (n=80, 1.16%±0.14%) compared to HC (n=80, 1.30%±0.13%, P<0.0001) and AD patients (n=80, 1.23%±0.11%, P=0.001). Similarly, patients with hereditary CAA demonstrated lower pBGV (n=25, 1.26%±0.17%) compared to their matched HC (n=25, 1.36%±0.15%, P=0.036). Using a measurement of normalized basal ganglia width developed for analysis of clinical-grade magnetic resonance images, we found smaller basal ganglia width in patients with CAA-related lobar intracerebral hemorrhage (ICH; n=93, 12.35±1.47) compared to age-matched patients with hypertension-related deep ICH (n=93, 13.46±1.51, P<0.0001) or HC (n=93, 15.45±1.22, P<0.0001). Within the sporadic CAA research cohort, decreased basal ganglia volume was independently correlated with greater cortical gray matter atrophy (r=0.45, P<0.0001), increased basal ganglia fractional anisotropy (r=–0.36, P=0.001), and worse performance on language processing (r=0.35, P=0.003), but not with cognitive tests of executive function or processing speed.Conclusions These findings suggest an independent effect of CAA on basal ganglia tissue loss, indicating a novel mechanism for CAA-related brain injury and neurologic dysfunction.

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