TY - JOUR
T1 - Nonfocal transient neurological attacks are associated with cerebral small vessel disease
AU - Oudeman, Eline A.
AU - Greving, Jacoba P.
AU - van den Berg-Vos, Renske M.
AU - Biessels, Geert Jan
AU - Bron, Esther E.
AU - van Oostenbrugge, Robert
AU - de Bresser, Jeroen
AU - Jaap Kappelle, L.
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Background and Purpose-Nonfocal transient neurological attacks (TNAs), such as unsteadiness, bilateral weakness,or confusion, are associated with an increased risk of stroke and dementia. Cerebral ischemia plays a role in theirpathogenesis, but the precise mechanisms are unknown. We hypothesized that cerebral small vessel disease is involvedin the pathogenesis of TNAs and assessed the relation between TNAs and manifestations of cerebral small vessel diseaseon magnetic resonance imaging.Methods-We included participants from the HBC (Heart-Brain Connection) study. In this study, hemodynamic andcardiovascular contributions to cognitive impairment have been studied in patients with heart failure, carotid arteryocclusion, or possible vascular cognitive impairment, as well as in a reference group. We excluded participantswith a history of stroke or transient ischemic attacks. The occurrence of the following 8 TNAs was assessed with astandardized interview: unconsciousness, confusion, amnesia, unsteadiness, bilateral leg weakness, blurred vision,nonrotatory dizziness, and paresthesias. The occurrence of TNAs was related to the presence of lacunes or white matterhyperintensities (Fazekas score, =2; early confluent or confluent lesions) in logistic regression analysis, adjusted for age,sex, and hypertension.Results-Of 304 participants (60% men; mean age, 67±9 years), 63 participants (21%) experienced =1 TNAs. Lacunesand early confluent or confluent white matter hyperintensities were more common in participants with TNAs than inparticipants without TNAs (35% versus 20%; adjusted odds ratio, 2.32 [95% CI, 1.22-4.40] and 48% versus 27%;adjusted odds ratio, 2.65 [95% CI, 1.44-4.90], respectively).Conclusions-In our study, TNAs are associated with the presence of lacunes and early confluent or confluent white matterhyperintensities of presumed vascular origin, which indicates that cerebral small vessel disease might play a role in thepathogenesis of TNAs.
AB - Background and Purpose-Nonfocal transient neurological attacks (TNAs), such as unsteadiness, bilateral weakness,or confusion, are associated with an increased risk of stroke and dementia. Cerebral ischemia plays a role in theirpathogenesis, but the precise mechanisms are unknown. We hypothesized that cerebral small vessel disease is involvedin the pathogenesis of TNAs and assessed the relation between TNAs and manifestations of cerebral small vessel diseaseon magnetic resonance imaging.Methods-We included participants from the HBC (Heart-Brain Connection) study. In this study, hemodynamic andcardiovascular contributions to cognitive impairment have been studied in patients with heart failure, carotid arteryocclusion, or possible vascular cognitive impairment, as well as in a reference group. We excluded participantswith a history of stroke or transient ischemic attacks. The occurrence of the following 8 TNAs was assessed with astandardized interview: unconsciousness, confusion, amnesia, unsteadiness, bilateral leg weakness, blurred vision,nonrotatory dizziness, and paresthesias. The occurrence of TNAs was related to the presence of lacunes or white matterhyperintensities (Fazekas score, =2; early confluent or confluent lesions) in logistic regression analysis, adjusted for age,sex, and hypertension.Results-Of 304 participants (60% men; mean age, 67±9 years), 63 participants (21%) experienced =1 TNAs. Lacunesand early confluent or confluent white matter hyperintensities were more common in participants with TNAs than inparticipants without TNAs (35% versus 20%; adjusted odds ratio, 2.32 [95% CI, 1.22-4.40] and 48% versus 27%;adjusted odds ratio, 2.65 [95% CI, 1.44-4.90], respectively).Conclusions-In our study, TNAs are associated with the presence of lacunes and early confluent or confluent white matterhyperintensities of presumed vascular origin, which indicates that cerebral small vessel disease might play a role in thepathogenesis of TNAs.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85075814797&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/31637974
U2 - https://doi.org/10.1161/STROKEAHA.119.025328
DO - https://doi.org/10.1161/STROKEAHA.119.025328
M3 - Article
C2 - 31637974
SN - 0039-2499
VL - 50
SP - 3540
EP - 3544
JO - Stroke
JF - Stroke
IS - 12
ER -