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Alterations in the coupling functions between cerebral oxyhaemoglobin and arterial blood pressure signals in post-stroke subjects

Cerebral autoregulation (CA) is the complex homeostatic regulatory relationship between blood pressure (BP) and cerebral blood flow (CBF). This study aimed to analyze the frequency-specific coupling function between cerebral oxyhemoglobin concentrations (delta [HbO(2)]) and mean arterial pressure (M...

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Detalles Bibliográficos
Autores principales: Su, Honglun, Huo, Congcong, Wang, Bitian, Li, Wenhao, Xu, Gongcheng, Liu, Qianying, Li, Zengyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5905974/
https://www.ncbi.nlm.nih.gov/pubmed/29668713
http://dx.doi.org/10.1371/journal.pone.0195936
Descripción
Sumario:Cerebral autoregulation (CA) is the complex homeostatic regulatory relationship between blood pressure (BP) and cerebral blood flow (CBF). This study aimed to analyze the frequency-specific coupling function between cerebral oxyhemoglobin concentrations (delta [HbO(2)]) and mean arterial pressure (MAP) signals based on a model of coupled phase oscillators and dynamical Bayesian inference. Delta [HbO(2)] was measured by 24-channel near-infrared spectroscopy (NIRS) and arterial BP signals were obtained by simultaneous resting-state measurements in patients with stroke, that is, 9 with left hemiparesis (L–H group), 8 with right hemiparesis (R–H group), and 17 age-matched healthy individuals as control (healthy group). The coupling functions from MAP to delta [HbO(2)] oscillators were identified and analyzed in four frequency intervals (I, 0.6–2 Hz; II, 0.145–0.6 Hz; III, 0.052–0.145 Hz; and IV, 0.021–0.052 Hz). In L–H group, the CS from MAP to delta [HbO(2)] in interval III in channel 8 was significantly higher than that in healthy group (p = 0.003). Compared with the healthy controls, the coupling in MAP→delta [HbO(2)] showed higher amplitude in interval I and IV in patients with stroke. The increased CS and coupling amplitude may be an evidence of impairment in CA, thereby confirming the presence of impaired CA in patients with stroke. In interval III, the CS in L–H group from MAP to delta [HbO(2)] in channel 16 (p = 0.001) was significantly lower than that in healthy controls, which might indicate the compensatory mechanism in CA of the unaffected side in patients with stroke. No significant difference in region-wise CS between affected and unaffected sides was observed in stroke groups, indicating an evidence of globally impaired CA. These findings provide a method for the assessment of CA and will contribute to the development of therapeutic interventions in stroke patients.