TY - JOUR
T1 - Magnetic resonance imaging-based scores of small vessel diseases
T2 - Associations with intracerebral haemorrhage location
AU - Schwarz, Ghil
AU - Banerjee, Gargi
AU - Hostettler, Isabel Charlotte
AU - Ambler, Gareth
AU - Seiffge, David J.
AU - Brookes, Tenzin S.
AU - Wilson, Duncan
AU - Cohen, Hannah
AU - Yousry, Tarek
AU - Salman, Rustam Al-shahi
AU - Lip, Gregory Y.h.
AU - Brown, Martin M.
AU - Muir, Keith W.
AU - Houlden, Henry
AU - Jäger, Rolf
AU - Werring, David J.
AU - Staals, Julie
N1 - Funding Information:
H.C. reports grants and other support from Bayer Healthcare and UCB outside the submitted work. T.Y. reports personal fees and other support from GlaxoSmithKline , Biogen Idec , Novartis, ESOR, Merck, Hikma and Parexel outside the submitted work. G.Y.H.L. reports consultancy and speaker fees from Bayer, Bayer/Janssen, BMS/Pfizer, Biotronik, Medtronic, Boehringer Ingelheim, Microlife, Roche and Daiichi-Sankyo outside the submitted work; no fees are directly received personally. K.W.M. reports personal fees from Bayer, personal fees and non-financial support from Boehringer Ingelheim and personal fees from Daiichi-Sankyo outside the submitted work. DJS: Scientific advisory boards: Bayer and Pfizer. Compensation for educational efforts: Stago. DJS is supported by a fellowship from the Swiss National Science Foundation (SNF), the Bangerter-Rhyner Foundation, the Bayer Foundation 2017 “Thrombosis Research Award” and the Swiss Society of Neurology. D.J.W. reports personal fees from Bayer, Alnylam and Portola outside the submitted work. The remaining authors declare no financial or other conflicts of interest.
Funding Information:
H.C. reports grants and other support from Bayer Healthcare and UCB outside the submitted work. T.Y. reports personal fees and other support from GlaxoSmithKline, Biogen Idec, Novartis, ESOR, Merck, Hikma and Parexel outside the submitted work. G.Y.H.L. reports consultancy and speaker fees from Bayer, Bayer/Janssen, BMS/Pfizer, Biotronik, Medtronic, Boehringer Ingelheim, Microlife, Roche and Daiichi-Sankyo outside the submitted work; no fees are directly received personally. K.W.M. reports personal fees from Bayer, personal fees and non-financial support from Boehringer Ingelheim and personal fees from Daiichi-Sankyo outside the submitted work. DJS: Scientific advisory boards: Bayer and Pfizer. Compensation for educational efforts: Stago. DJS is supported by a fellowship from the Swiss National Science Foundation (SNF), the Bangerter-Rhyner Foundation, the Bayer Foundation 2017 “Thrombosis Research Award” and the Swiss Society of Neurology. D.J.W. reports personal fees from Bayer, Alnylam and Portola outside the submitted work. The remaining authors declare no financial or other conflicts of interest.
Funding Information:
DJW received funding from the Stroke Foundation/British Heart Foundation. This work was undertaken at UCLH/UCL which receives a proportion of funding from the Department of Health's National Institute for Health Research (NIHR) Biomedical Research Centres funding scheme. GB holds a Stroke Association and NIHR Clinical Lectureship, and has received funding from the Rosetrees Trust. ICH and HH received funding from the Alzheimer Research UK and Dunhill Medical Trust Foundation.
Publisher Copyright:
© 2022 The Author(s)
PY - 2022/3/15
Y1 - 2022/3/15
N2 - Introduction: Total small vessel disease (SVD) score and cerebral amyloid angiopathy (CAA) score are magnetic resonance imaging-based composite scores built to preferentially capture deep perforator arteriopathy-related and CAA-related SVD burden, respectively. Non-lobar intracerebral haemorrhage (ICH) is related to deep perforator arteriopathy, while lobar ICH can be associated with deep perforator arteriopathy or CAA; however, the associations between ICH location and these scores are not established. Methods: In this post-hoc analysis from a prospective cohort study, we included 153 spontaneous non-cerebellar ICH patients. Wald test, univariable and multivariable logistic regression analysis were performed to investigate the association between each score (and individual score components) and ICH location. Results: Total SVD score was associated with non-lobar ICH location (Wald test: unadjusted, p = 0.017; adjusted, p = 0.003); however, no individual component of total SVD score was significantly associated with non-lobar ICH. CAA score was not significantly associated with lobar location (Wald test: unadjusted, p = 0.056; adjusted, p = 0.126); cortical superficial siderosis (OR 8.85 [95%CI 1.23–63.65], p = 0.030) and ≥ 2 strictly lobar microbleeds (OR 1.63 [95%CI 1.04–2.55], p = 0.035) were related with lobar ICH location, while white matter hyperintensities showed an inverse relation (OR 0.53 [95%CI 0.26–1.08; p = 0.081]). Conclusions: Total SVD score was associated with non-lobar ICH location. The lack of significant association between CAA score and lobar ICH may in part be due to the mixed aetiology of lobar ICH, and to the inclusion of white matter hyperintensities, a non-specific marker of SVD type, in the CAA score.
AB - Introduction: Total small vessel disease (SVD) score and cerebral amyloid angiopathy (CAA) score are magnetic resonance imaging-based composite scores built to preferentially capture deep perforator arteriopathy-related and CAA-related SVD burden, respectively. Non-lobar intracerebral haemorrhage (ICH) is related to deep perforator arteriopathy, while lobar ICH can be associated with deep perforator arteriopathy or CAA; however, the associations between ICH location and these scores are not established. Methods: In this post-hoc analysis from a prospective cohort study, we included 153 spontaneous non-cerebellar ICH patients. Wald test, univariable and multivariable logistic regression analysis were performed to investigate the association between each score (and individual score components) and ICH location. Results: Total SVD score was associated with non-lobar ICH location (Wald test: unadjusted, p = 0.017; adjusted, p = 0.003); however, no individual component of total SVD score was significantly associated with non-lobar ICH. CAA score was not significantly associated with lobar location (Wald test: unadjusted, p = 0.056; adjusted, p = 0.126); cortical superficial siderosis (OR 8.85 [95%CI 1.23–63.65], p = 0.030) and ≥ 2 strictly lobar microbleeds (OR 1.63 [95%CI 1.04–2.55], p = 0.035) were related with lobar ICH location, while white matter hyperintensities showed an inverse relation (OR 0.53 [95%CI 0.26–1.08; p = 0.081]). Conclusions: Total SVD score was associated with non-lobar ICH location. The lack of significant association between CAA score and lobar ICH may in part be due to the mixed aetiology of lobar ICH, and to the inclusion of white matter hyperintensities, a non-specific marker of SVD type, in the CAA score.
KW - CAA score
KW - Cerebral amyloid angiopathy
KW - Intracerebral haemorrhage
KW - MRI-based score
KW - Small vessel disease
KW - Total SVD score
U2 - 10.1016/j.jns.2022.120165
DO - 10.1016/j.jns.2022.120165
M3 - Article
VL - 434
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
SN - 0022-510X
M1 - 120165
ER -