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Association of compromised cerebral perfusion with lenticulostriate artery impairments in the subacute phase of branch atheromatous disease

BACKGROUND PURPOSE: Whether altered cerebral perfusion is associated with the pathogenesis of single subcortical infarctions (SSIs) in the lenticulostriate artery (LSA) territory remains unclear. OBJECTIVE: We aimed to assess whether cerebral perfusion abnormalities are related to LSA impairments in...

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Detalles Bibliográficos
Autores principales: Jiang, Shuai, Cui, Jing-Yu, Yan, Yu-Ying, Yang, Tang, Tao, Wen-Dan, Wu, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9260584/
https://www.ncbi.nlm.nih.gov/pubmed/35813607
http://dx.doi.org/10.1177/17562864221109746
Descripción
Sumario:BACKGROUND PURPOSE: Whether altered cerebral perfusion is associated with the pathogenesis of single subcortical infarctions (SSIs) in the lenticulostriate artery (LSA) territory remains unclear. OBJECTIVE: We aimed to assess whether cerebral perfusion abnormalities are related to LSA impairments in the subacute phase of SSIs and then to examine their correlations with etiological subtypes of SSIs. METHODS: A total of 110 patients with acute SSIs in the LSA territory were prospectively recruited between July 2017 and October 2021, and they underwent magnetic resonance perfusion-weighted imaging (PWI) and whole-brain vessel-wall imaging (VWI) within 7 days of stroke onset. Based on VWI, patients were assigned to one of two SSI subtypes: branch atheromatous disease (BAD, n = 78, 70.9%) or lacunar infarction related to cerebral small vessel disease (CSVD-related LI, n = 32, 29.1%). Perfusion maps and LSA morphology were also quantitatively assessed. RESULTS: Based on PWI, 22 patients (20%) had hypoperfusion and 88 (80%) showed normal perfusion. Compared with normal individuals, patients with hypoperfusion showed shorter average LSA length (23.48 ± 4.81 mm versus 25.47 ± 3.74 mm, p = 0.037). Compared with patients with CSVD-related LI, patients with BAD had significantly lower relative cerebral blood flow [0.95 (IQR 0.81–1.12) versus 1.04 (IQR 0.92–1.22); p = 0.036] and cerebral blood volume [0.95 (IQR 0.84–1.15) versus 1.14 (IQR 0.97–1.27); p = 0.020] after adjusting for hypertension, number of LSA branches, and infarct volume. CONCLUSION: Compromised cerebral perfusion is associated with impairments in the LSA and with BAD pathogenesis. Perfusion magnetic resonance imaging can provide important insights into acute SSI pathophysiology, and it may be useful for determining the clinical significance of perfusion abnormalities in BAD occurrence.