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

ABSTRACT: 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 [HbO2]) and mean arterial pressure (MAP) signals based on a model of coupled phase oscillators and dynamical Bayesian inference. Delta [HbO2] 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 [HbO2] 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 [HbO2] 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 [HbO2] 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 [HbO2] 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.

SUBMITTER: Su H

PROVIDER: S-EPMC5905974 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThis study aimed to assess brain oxygenation status and cerebral autoregulation function in subjects with cognitive dysfunction.MethodsThe Montreal Cognitive Assessment (MoCA) was applied to divide the subjects into three groups: cognitive impairment (Group CI, 72.50 ± 10.93 y), mild cognitive impairment (Group MCI, 72.02 ± 9.90 y), and normal cognition (Group NC, 70.72 ± 7.66 y). Near-infrared spectroscopy technology and a non-invasive blood pressure device were used to simultaneously measure changes in cerebral tissue oxygenation signals in the bilateral prefrontal lobes (LPFC/RPFC) and arterial blood pressure (ABP) signals from subjects in the resting state (15 min). The coupling between ABP and cerebral oxyhemoglobin concentrations (Δ [O2Hb]) was calculated in very-low-frequency (VLF, 0.02-0.07 Hz) and low-frequency (LF, 0.07-0.2 Hz) bands based on the dynamical Bayesian inference approach. Pearson correlation analyses were used to study the relationships between MoCA scores, tissue oxygenation index, and strength of coupling function.ResultsIn the interval VLF, Group CI (p = 0.001) and Group MCI (p = 0.013) exhibited significantly higher coupling strength from ABP to Δ [O2Hb] in the LPFC than Group NC. In the interval LF, coupling strength from ABP to Δ [O2Hb] in the LPFC was significantly higher in Group CI than in Group NC (p = 0.001). Pearson correlation results showed that MoCA scores had a significant positive correlation with the tissue oxygenation index and a significant negative correlation with the coupling strength from ABP to Δ [O2Hb].ConclusionThe significantly increased coupling strength may be evidence of impaired cerebral autoregulation function in subjects with cognitive dysfunction. The Pearson correlation results suggest that indicators of brain oxygenation status and cerebral autoregulation function can reflect cognitive function. This study provides insights into the mechanisms underlying the pathophysiology of cognitive impairment and provides objective indicators for screening cognitive impairment in the elderly population.

Project description:Background and Purpose: Stroke induces immediate profound alterations of the peripheral immune system rendering patients more susceptible to post-stroke infections. The precise mechanisms maintaining stroke-induced immune alterations (SIIA) remain unknown. High-Mobility-Group-Protein B1 (HMGB-1) is elevated for at least 7 days post-stroke and has been suggested to mediate SIIA. Patients with rapid clinical recovery of neurological deficits rarely develop severe infections. We therefore investigated whether rapid neurological recovery (either spontaneous or secondary to neurovascular recanalization therapy) alters the course of SIIA. National Institutes of Health Stroke Scale (NIHSS) served as surrogate marker for neurological improvement. Methods: Fluorescence-activated cell sorting was used to define leukocyte subpopulations. C-reactive protein (CRP), procalcitonin (PCT), HMGB-1, GM-CSF; IFN-?, IFN-?, IL-1?, IL-1RA, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-17, IL-17F, IL-18, TNF-?, MIF, IL-8, MCP-1, MCP-4, MIP-3?, MIP-3?, Eotaxin, soluble IL-6 receptor, E-selectin, and P-selectin were analyzed by ELISA or Multiplex Assays. Serum miRNA expression changes were analyzed by qPCR. Results: Cellular parameters were similar in the improved and non-improved cohort on admission. In patients with rapid clinical recovery absolute and relative leukocyte, neutrophil, and lymphocyte numbers normalized promptly overnight. In contrast, HMGB-1 serum levels did not differ between the two groups. Nine miRNA were found to be differentially expressed between improved and non-improved patients. Conclusions: SIIA are detectable on admission of acute stroke patients. While it was assumed that post-stroke immunosuppression is rapidly reversed with improvement this is the first data set that shows that improvement actually is associated with a rapid reversal of SIIA demonstrating that SIIA require a constant signal to persist. The observation that HMGB-1 serum concentrations were similar in improved and non-improved cohorts argues against a role for this pro-inflammatory mediator in the maintenance of SIIA. Serum miRNA observed to be regulated in stroke in other publications was counter regulated with improvement in our cohort.

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

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