Hypoperfusion assessed by pressure reactivity index is associated with delayed cerebral ischemia after subarachnoid hemorrhage:an observational study

Background:Dysfunction of cerebral autoregulation is one of the pathophysiological mechanisms that causes delayed cerebral ischemia(DCI)after subarachnoid hemorrhage(SAH).Pressure reactivity index(PRx)have been confirmed to reflect the level of cerebral autoregulation and used to derive optimal cerebral perfusion pressure(CPPopt).The goal of this study is to explore the associations between autoregulation,CPPopt,PRx,and DCI.Methods:Continuous intracranial pressure(ICP),arterial blood pressure(ABP),and cerebral perfusion pressure(CPP)signals acquired from 61 aSAH patients were retrospectively analyzed.PRx was calculated and collected by Pneumatic computer system.The CPP at the lowest PRx was determined as the CPPopt.The duration of a hypoperfusion event(dHP)was defined as the cumulative time that the PRx was>0.3 and the CPP was<CPPopt.The duration of CPP more than 10 mmHg below CPPopt(ΔCPPopt<−10 mmHg)was also used to assess hypoperfusion.The percent of the time of hypoperfusion by dHP andΔCPPopt<−10 mmHg(%dHP and%ΔCPPopt)were compared between DCI group and control group,utilizing univariate and multivariable logistic regression.It was the clinical prognosis at 3 months after hemorrhage that was assessed with the modified Rankin Scale,and logistic regression and ROC analysis were used for predictive power for unfavorable outcomes(mRs 3–5).Results:Data from 52 patients were included in the final analysis of 61 patients.The mean%dHP in DCI was 29.23%and 10.66%in control.The mean%ΔCPPopt<−10 mmHg was 22.28%,and 5.90%in control.The%dHP(p<0.001)and the%ΔCPPopt<−10mmHg(p<0.001)was significantly longer in the DCI group.In multivariate logistic regression model,%ΔCPPopt<−10 mmHg(p<0.001)and%dHP(p<0.001)were independent risk factor for predicting DCI,and%ΔCPPopt<−10 mmHg(p=0.010)and%dHP(p=0.026)were independent risk factor for predicting unfavorable outcomes.Conclusions:The increase of duration of hypoperfusion events and duration of CPP below CPPopt over 10 mmHg,evaluated as time of lowered CPP,is highly indicative of DCI and unfavorable outcomes.

Correlation study of relative parameters of intracranial pressure and prognosis of patient with craniocerebral injury

Objective:To analyze the correlation of the relative parameters of intracranial pressure to the prognosis in patients with craniocerebral injury.Methods:The clinical data of 80 patients with closed craniocerebral injury were retrospectively analyzed,and all of these patients underwent conventional examinations of arterial blood pressure and intracranial pressure.Neumatic DCR system was used to monitor relative parameters of intracranial pressure from patients.According to the score of Glasgow outcome scale(GOS)upon discharge,they were divided into favorable prognosis group(GOSⅢ-Ⅴ,n=46)and unfavorable prognosis group(GOSⅠ-Ⅱ,n=34).The relative parameters of intracranial pressure of two groups were compared so as to analyze the correlation of the prognosis in patients to ICP-related parameters.Results:Pressure reactivity index(PRx)and intracranial pressure(ICP)of favorable prognosis group were significantly higher than those of unfavorable prognosis group(t=12.27,t=5.22,p<0.05).Meanwhile,cerebral perfusion pressure(CPP)and ICP-ABP wave amplitude correlation(IAAC)of favorable prognosis group were significantly lower than those of unfavorable prognosis group(t=14.54,t=14.78,p<0.05).The average age,gender,duration of admission to neurosurgical intensive care unit(NICU)and GCS(Glasgow coma scale)score on admission of the two groups were not statistically significant.Conclusions:The prognosis and ICP-related parameters(such as PRx,ICP,CPP,etc.)in patients with craniocerebral injury are risk factors for the prognosis effect.Therefore,to monitor the above-mentioned indicators has an important clinical value for assessing the prognosis of craniocerebral injury.

High frequency heart rate variability evoked by repetitive transcranial magnetic stimulation over the medial prefrontal cortex: A preliminary investigation on brain processing of acute stressor-evoked cardiovascular reactivity

Introduction: Transcranial Magnetic Stimulation (TMS) is a non-invasive technique for brain stimulation. Repetitive TMS (rTMS) over the medial Prefrontal Cortex (mPFC), Broadman Area 10 (BA10) may stimulate transynaptically perigenual Anterior Cingulate Cortex (pACC, BA 33), insula, amigdala, hypothalamus and connected branches of the Autonomic Nervous System (ANS) involved in stressorevoked cardiovascular reactivity. Stressors are associated with an increase in sympathetic cardiac control, a decrease in parasympathetic control, or both, and, consequently, an increase in systolic/stroke volume, total vascular impedance/resistance and heart rate, a decrease of baroreflex sensitivity, i.e., an increase in blood pressure/arterial tension. Objectives and Aims: The present work aims, using TMS and accordingly to Gianaros modeling, based on functional neuroimaging studies and previous neuroanatomical data from animal models, to probe the connectivity of brain systems involved in stressor-evoked cardiovascular reactivity and to explore TMS potential as a tool for detection and stratification of individual differences concerning this reactivity and hemorreological risk factors correlated with the development of Coronary Heart Disease (CHD). Methods: Both subjects, a 52 years old male and a 40 years old female with previous increased Low Frequency (LF)/High Frequency (HF) Heart Rate Variability (HRV) ratios (respectively, 4.209/3.028) without decompensated cardiorespiratory symptoms, gave informed consent, and ethico-legal issues have been observed. Electroencephalographic (EEG) monitoring has been performed for safety purposes. Immediately after administration, over the mPFC, of 15 pulses of rTMS, during 60 second, with an inductive electrical current, at the stimulating coil, of 85.9 Ampère per μsecond and 66 Ampère per μsecond, respectively, for male and female subjects (a “figure-of-eight” coil and magnetic stimulator MagLite, Dantec/Medtronic, have been used), HRV spectrum analysis (cStress software) has been performed (during 5 minutes, in supine position). Results: In both subjects, LF power, HF power and LF/HF ratio results, before and after rTMS administration, pointed towards sympathetic attenuation and parasympathetic augmentation (respectively, in male/female subject: decreased LF power—65.1 nu/69.3 nu, before rTMS;56.1 nu/41.6 nu, after rTMS;increased HF power—15.5 nu/22.9 nu, before rTMS;30.9 nu/45.5 nu, after rTMS). Conclusions: In this preliminary investigation, the existence of a link between “mind” and heart’s function has been put in evidence, through a reversible “virtual” lesion, of brain systems involved in cardiovascular control, caused by TMS. Repetitive TMS over mPFC decreased brain function involved in stressorevoked cardiovascular reactivity, suggesting the importance of TMS in the management of stress-related cardiovascular disorders.

Approaches to neuroprotection in pediatric neurocritical care

Acute neurologic injuries represent a common cause of morbidity and mortality in children presenting to the pediatric intensive care unit.After primary neurologic insults,there may be cerebral brain tissue that remains at risk of secondary insults,which can lead to worsening neurologic injury and unfavorable outcomes.A fundamental goal of pediatric neurocritical care is to mitigate the impact of secondary neurologic injury and improve neurologic outcomes for critically ill children.This review describes the physiologic framework by which strategies in pediatric neurocritical care are designed to reduce the impact of secondary brain injury and improve functional outcomes.Here,we present current and emerging strategies for optimizing neuroprotective strategies in critically ill children.