scholarly journals Vessel Wall Enhancement on Black-Blood MRI Predicts Acute and Future Stroke in Cerebral Amyloid Angiopathy

Author(s):  
J.S. McNally ◽  
A. Sakata ◽  
M.D. Alexander ◽  
L.D. Dewitt ◽  
J.A. Sonnen ◽  
...  
2020 ◽  
Vol 41 (3) ◽  
pp. 446-448
Author(s):  
Q. Hao ◽  
N.M. Tsankova ◽  
H. Shoirah ◽  
C.P. Kellner ◽  
K. Nael

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Adam De Havenon ◽  
Remy Lobo ◽  
Laura Eisenmenger ◽  
Nabeel Chauhan ◽  
Dana Dewitt ◽  
...  

Introduction: Arterial wall enhancement detected on vessel wall MRI (vwMRI) has been associated with increased stroke risk in the setting of intracranial atherosclerosis. Other pathologies affect the vessel wall, including cerebral amyloid angiopathy (CAA). CAA is secondary to Aβ vessel wall deposition resulting in microvessel leakage, microbleeds and ischemic stroke. Our goal was to determine if vwMRI could detect vessel wall inflammation and leptomeningeal contrast leakage in CAA, and if these are associated with recent infarction. Methods: In this retrospective study, 28 vwMRI scans in 23 patients demonstrated probable CAA from 2015-16. Probable CAA was diagnosed by peripherally located microhemorrhages detected on susceptibility-weighted imaging. Vessel wall and leptomeningeal enhancement was determined using a validated pre and post contrast flow-suppressed T1-weighted sequence. Recent infarcts were detected by DTI trace (20 direction B2000). A mixed effects logistic regression model was used to determine the association of vessel wall or leptomeningeal enhancement with recent infarct in CAA patients, accounting for up to 3 scans per patient. Results: In the 28 vwMRI scans, ischemic stroke was detected in 17 (61%), leptomeningeal enhancement in 13 (46%), and vessel wall enhancement in 14 (50%). The figure shows a representative patient with a recent infarct and biopsy-proven CAA with vessel wall enhancement (arrow) detected on vwMRI. Vessel wall enhancement was associated with recent infarct with an odds ratio (OR) = 10.8, p= 0.012. Leptomeningeal enhancement was associated with recent infarct with an OR = 3.8, p= 0.11. Conclusions: Both vessel wall and leptomeningeal enhancement are present in CAA, though vessel wall enhancement is more associated with recent infarction. Larger, prospective studies may be needed to determine future stroke risk and additional risk factors predicting ischemic stroke in CAA.


Neuroreport ◽  
1996 ◽  
Vol 7 (2) ◽  
pp. 562-564 ◽  
Author(s):  
Reinhard Prior ◽  
Donatella DʼUrso ◽  
Rainer Frank ◽  
Ingrid Prikulis ◽  
Goran Pavlakovic

2009 ◽  
Vol 32 (6S) ◽  
pp. 5
Author(s):  
A Gangloff ◽  
L Nadeau

Objective: Evaluation of the UK NEQAS 2008 guidelines for the interpretation of spectrophotometric xanthochromia. Method: A search of the laboratory database for all the xanthochromia test results between May 1st 2008 and May 1st 2009 was performed. Medical charts were reviewed for patients of Hôpital de l’Enfant-Jésus (HEJ) that had at least one detectable pigment (bilirubin, oxyhemoglobin, or methemoglobin). Xanthochromia results obtained with 4 different criteria (Chalmers original, Modified Chalmers, Duiser and UK NEQAS 2008) were compared. Results: We reviewed 41 medical charts (2 patients with duplicate lumbar punctures (LP) for a total of 43 LP). For these 41 patients there were 11 positive xanthochromia results, 5 of which were in concordance with a final diagnosis of subarachnoid hemorrhage (SAH). The diagnosis of the 6 other positive xanthochromia results were as follow: meningeal spread of a lymphoma, cerebral amyloid angiopathy, exertional headache, viral encephalitis with a possibility of petechiaes on the cerebral CT and second LP. Interpretation (negative/positive) of 40/43 LP was identical for the 4 methods. 2 LP were positive with Duiser and UK NEQAS 2008 but negative with Chalmers approaches (final diagnosis: SAH and cerebral amyloid angiopathy). 1 LP was positive only by the Duiser method (viral encephalitis). Conclusions: UK NEQAS 2008 guidelines identified all SAH but are sensitive to traumatic and pathologic meningeal lesions. Except for a case of viral encephalitis with a suspicion of cerebral petechiaes on CT, UK NEQAS 2008 gave xanthochromia results similar to the one in use at HEJ (Duiser). Chalmers original and Modified Chalmers methods missed one of the five SAH.


2020 ◽  
Vol 25 (4) ◽  
pp. 31-37
Author(s):  
A. A. Kornilova ◽  
O. V. Lagoda ◽  
M. M. Tanashyan

The present article addresses the definition of cerebral amyloid angiopathy (CAA) and its symptoms based on the analysis of the medical case; the issues of diagnosis and treatment of this pathology are discussed. The Boston criteria, which became the basis for diagnosis, study of clinical manifestations and progression of CAA and approaches to its therapy, are presented. Methods and modes of neuroimaging, including magnetic resonance imaging (MRI), which verify micro cerebral haemorrhage, are described. At the same time, the role and significance of cardiac arrhythmias in the genesis of ischemic stroke are discussed, and scales for assessing the risk of its occurrence are presented. The observation of the neurological, somatic, neuroimaging, neuropsychological status of a 62-year-old patient confirms quite rare combination of probable CAA, paroxysmal atrial fibrillation and repeated hemorrhagic functional apoplexy (FA). The relevance of the case described, is a complex clinical dilemma based on mutually exclusive recommendations for the pharmacological correction of such conditions. It is emphasized that in many multicenter clinical studies on the effectiveness of antithrombotic medication (antiaggregants, anticoagulants) in the treatment and prevention of ischaemic functional apoplexy , an important exclusion criterion is a hemorrhagic stroke in past history (including the multiple changes in haemostasis indicators). Taking into account the obtained clinical and laboratory data in the dynamics, the tactics of treating the described patient were determined. The results of studies related to the treatment of comorbid pathology that should become the subject of the development of a personalized algorithm for managing patients in each specific case, are discussed.


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